HIV

How Can I Tell if I Have HIV?

You cannot rely on symptoms to tell whether you have HIV. The only way to know for sure if you have
HIV is to get tested
You cannot rely on symptoms to tell whether you have HIV. The only way to know for sure if you have
HIV is to get tested. Knowing your status is important because it helps you make healthy decisions to
prevent getting or transmitting HIV.

The symptoms of HIV vary, depending on the individual and what stage of the disease you are in: the
early stage, the clinical latency stage, or AIDS (the late stage of HIV infection). Below are the symptoms
that some individuals may experience in these three stages. Not all individuals will experience these
symptoms.

Early Stage of HIV

About 40% to 90% of people have flu-like symptoms within 2-4 weeks after HIV infection. Other people
do not feel sick at all during this stage, which is also known as acute HIV infection. Early infection is
defined as HIV infection in the past six months (recent) and includes acute (very recent) infections. Flu-
like symptoms can include:

Fever
Chills
Rash
Night sweats
Muscle aches
Sore throat
Fatigue
Swollen lymph nodes
Mouth ulcers

These symptoms can last anywhere from a few days to several weeks. During this time, HIV infection
may not show up on some types of HIV tests, but people who have it are highly infectious and can
spread the infection to others.

You should not assume you have HIV just because you have any of these symptoms. Each of these
symptoms can be caused by other illnesses. And some people who have HIV do not show any symptoms
at all for 10 years or more.

If you think you may have been exposed to HIV, get an HIV test
However, if you think you may have been exposed to HIV and could be in the early stage of HIV
infection, get an HIV test. Most HIV tests detect antibodies (proteins your body makes as a reaction
against the presence of HIV), not HIV itself. But it take can take a few weeks or longer for your body to
produce these antibodies.
Some places use HIV tests that can detect acute and recent infections, but others do not. So be sure to
let your testing site know if you think you may have been recently infected with HIV. Tests that can
detect acute infection look for HIV RNA or p24 antigen. Most doctors and clinics that provide a full range
of health care services can do this test, but some places that only do HIV testing may not have it. So you
may want to contact the site before you go to ask if they can test you for acute HIV infection.

Knowing your HIV status helps you make healthy decisions to prevent getting or transmitting HIV
After you get tested, it’s important to find out the result of your test. If you’re HIV-positive, you should
see a doctor and start HIV treatment as soon as possible. You are at high risk of transmitting HIV to
others during the early stage of HIV infection, even if you have no symptoms. For this reason, it is very
important to take steps to reduce your risk of transmission. If you’re HIV-negative, explore HIV-
prevention options, like pre-exposure prophylaxis (PrEP), that can help you stay negative.

Clinical Latency Stage

After the early stage of HIV infection, the disease moves into a stage called the clinical latency stage
(also called “chronic HIV infection”). During this stage, HIV is still active but reproduces at very low
levels. People with chronic HIV infection may not have any HIV-related symptoms, or only mild ones.

For people who aren’t taking medicine to treat HIV (called antiretroviral therapy or ART), this period can
last a decade or longer, but some may progress through this phase faster. People who are taking
medicine to treat HIV, and who take their medications the right way, every day, may be in this stage for
several decades because treatment helps keep the virus in check. (Read more about HIV treatment.)

It’s important to remember that people can still transmit HIV to others during this phase even if they
have no symptoms, although people who are on ART and stay virally suppressed (having a very low level
of virus in their blood) are much less likely to transmit HIV than those who are not virally suppressed.

Progression to AIDS

If you have HIV and you are not on ART, eventually the virus will weaken your body’s immune system
and you will progress to AIDS (acquired immunodeficiency syndrome), the late stage of HIV infection.

Symptoms can include:

Rapid weight loss

Recurring fever or profuse night sweats
Extreme and unexplained tiredness
Prolonged swelling of the lymph glands in the armpits, groin, or neck
Diarrhea that lasts for more than a week
Sores of the mouth, anus, or genitals

HIV is a virus spread through certain body fluids that attacks the body’s immune system, specifically the
CD4 cells, often called T cells. Over time, HIV can destroy so many of these cells that the body can’t fight
off infections and disease. These special cells help the immune system fight off infections. Untreated,
HIV reduces the number of CD4 cells (T cells) in the body. This damage to the immune system makes it
harder and harder for the body to fight off infections and some other diseases. Opportunistic infections
or cancers take advantage of a very weak immune system and signal that the person has AIDS. Learn
more about the stages of HIV and how to know whether you’re infected.

What Is HIV?

HIV stands for human immunodeficiency virus. It is the virus that can lead to acquired immunodeficiency
syndrome, or AIDS, if not treated. Unlike some other viruses, the human body can’t get rid of HIV
completely, even with treatment. So once you get HIV, you have it for life.

HIV attacks the body’s immune system, specifically the CD4 cells (T cells), which help the immune
system fight off infections. Untreated, HIV reduces the number of CD4 cells (T cells) in the body, making
the person more likely to get other infections or infection-related cancers. Over time, HIV can destroy so
many of these cells that the body can’t fight off infections and disease. These opportunistic infections or
cancers take advantage of a very weak immune system and signal that the person has AIDS, the last
stage of HIV infection.

No effective cure currently exists, but with proper medical care, HIV can be controlled. The medicine
used to treat HIV is called antiretroviral therapy or ART. If taken the right way, every day, this medicine
can dramatically prolong the lives of many people infected with HIV, keep them healthy, and greatly
lower their chance of infecting others. Before the introduction of ART in the mid-1990s, people with HIV
could progress to AIDS in just a few years. Today, someone diagnosed with HIV and treated before the
disease is far advanced can live nearly as long as someone who does not have HIV.

What Is AIDS?

AIDS is the most severe phase of HIV infection. People with AIDS have such badly damaged immune
systems that they get an increasing number of severe illnesses, called opportunistic infections.

What Are the Stages of HIV Infection?

Without treatment, HIV advances in stages, overwhelming your immune system and getting worse over
time. The three stages of HIV infection are: (1) acute HIV infection, (2) clinical latency, and (3) AIDS
(acquired immunodeficiency syndrome).

However, there’s good news: by using HIV medicines (called antiretroviral therapy or ART) consistently,
you can prevent HIV from progressing to AIDS. ART helps control the virus so that you can live a longer,
healthier life and greatly reduces the risk of transmitting HIV to others.

These are the three stages of HIV infection:

Acute HIV Infection Stage

Within 2 to 4 weeks after infection, many, but not all, people develop flu-like symptoms, often described
as “the worst flu ever.” Symptoms can include fever, swollen glands, sore throat, rash, muscle and joint
aches and pains, and headache. This is called “acute retroviral syndrome” (ARS) or “primary HIV
infection,” and it’s the body’s natural response to the HIV infection. People who think that they may
have been infected recently and are in the acute stage of HIV infection should seek medical care right
away. Starting treatment at this stage can have significant benefits to your health.
During this early period of infection, large amounts of virus are being produced in your body. The virus
uses CD4 cells to replicate and destroys them in the process. Because of this, your CD4 cells can fall
rapidly. Eventually your immune response will begin to bring the level of virus in your body back down
to a level called a viral set point, which is a relatively stable level of virus in your body. At this point, your
CD4 count begins to increase, but it may not return to pre-infection levels. It may be particularly
beneficial to your health to begin ART during this stage.

During the acute HIV infection stage, you are at very high risk of transmitting HIV to your sexual or
needle-sharing partners because the levels of HIV in your blood stream are extremely high. For this
reason, it is very important to take steps to reduce your risk of transmission.

Clinical Latency Stage

After the acute stage of HIV infection, the disease moves into a stage called the “clinical latency” stage.
“Latency” means a period where a virus is living or developing in a person without producing symptoms.
During the clinical latency stage, people who are infected with HIV experience no symptoms, or only
mild ones. (This stage is sometimes called “asymptomatic HIV infection” or “chronic HIV infection.”)

During the clinical latency stage, the HIV virus continues to reproduce at very low levels, even if it
cannot be detected with standard laboratory tests. If you take ART, you may live with clinical latency for
decades and never progress to AIDS because treatment helps keep the virus in check. (Read more about
HIV treatment.)

People in this symptom-free stage are still able to transmit HIV to others. The risk of transmission is
greatly reduced by HIV treatment. In studies looking at the effects of HIV treatment on transmission, no
new HIV infections have been linked to someone with very low or undetectable (suppressed) viral load.

For people who are not on ART, the clinical latency stage lasts an average of 10 years, but some people
may progress through this stage faster. As the disease progressions, eventually your viral load will begin
to rise and your CD4 count will begin to decline. As this happens, you may begin to have constitutional
symptoms of HIV as the virus levels increase in your body before you develop AIDS.

AIDS

This is the stage of HIV infection that occurs when your immune system is badly damaged and you
become vulnerable to opportunistic infections. When the number of your CD4 cells falls below 200 cells
per cubic millimeter of blood (200 cells/mm3), you are considered to have progressed to AIDS. (In
someone with a healthy immune system, CD4 counts are between 500 and 1,600 cells/mm3.) You are
also considered to have progressed to AIDS if you develop one or more opportunistic illnesses,
regardless of your CD4 count.

Without treatment, people who progress to AIDS typically survive about 3 years. Once you have a
dangerous opportunistic illness, life-expectancy without treatment falls to about 1 year. ART can be
helpful for people who have AIDS when diagnosed and can be lifesaving. Treatment is likely to benefit
people with HIV no matter when it is started, but people who start ART soon after they get HIV
experience more benefits from treatment than do people who start treatment after they have
developed AIDS.
In the United States, most people with HIV do not develop AIDS because effective ART stops disease
progression. People with HIV who are diagnosed early can have a life span that is about the same as
someone like them who does not HIV.

People living with HIV may progress through these stages at different rates, depending on a variety of
factors, including their genetic makeup, how healthy they were before they were infected, how much
virus they were exposed to and its genetic characteristics, how soon after infection they are diagnosed
and linked to care and treatment, whether they see their healthcare provider regularly and take their
HIV medications as directed, and different health-related choices they make, such as decisions to eat a
healthful diet, exercise, and not smoke.

Is There a Cure for HIV?

No effective cure currently exists for HIV. But with proper medical care, HIV can be controlled.
Treatment for HIV is called antiretroviral therapy or ART. If taken the right way, every day, ART can
dramatically prolong the lives of many people infected with HIV, keep them healthy, and greatly lower
their chance of infecting others. Before the introduction of ART in the mid-1990s, people with HIV could
progress to AIDS (the last stage of HIV infection) in a few years. Today, someone diagnosed with HIV and
treated before the disease is far advanced can live nearly as long as someone who does not have HIV.

Philippines gripped by dengue vaccine fears

3 February 2018

Domingo expressed concerns about potential epidemics in the Philippines

Fears over a dengue vaccine in the Philippines have led to a big drop in immunisation rates for
preventable diseases, officials have warned.
Health Under-Secretary Enrique Domingo said many parents were refusing to get their children
vaccinated for polio, chicken pox and tetanus.
The fears centre on Dengvaxia, a drug developed by French company Sanofi.
Sanofi and local experts say there is no evidence linking the deaths of 14 children to the drug.
However, the company had warned last year that the vaccine could make the disease worse in some
people not infected before.
Dengue fever affects more than 400 million people each year around the world. Dengvaxia is the world's
first vaccine against dengue.
The mosquito-borne disease is a leading cause of serious illness and death among children in some Asian
and Latin American countries, according to the World Health Organization (WHO).
What did Mr Domingo say about immunisation rates?
"Our programmes are suffering... (people) are scared of all vaccines now", he warned.
Mr Domingo added that vaccination rates for some preventable diseases had dropped as much as 60%
in recent years - significantly lower that the nationwide target of 85%.
Asian Tiger MosquitoImage copyrightAFP
Image caption
Dengue is a potentially deadly mosquito-borne disease
Mr Domingo expressed concerns about potential epidemics in the Philippines - a nation of about 100
million people, many of whom are impoverished.
What triggered fears about Dengvaxia?
More than 800,000 children were vaccinated across the country in 2016-17. Fourteen of them have
died.
Dengvaxia immunisations were halted last year, as the Philippines launched an investigation into what
caused the deaths.
On Saturday, Doctors for Public Welfare (DPW) said a clinical review conducted by Philippine General
Hospital forensic pathologists had determined that the deaths were not linked to the vaccine, the
Philippine Daily Inquirer reported.
What about Sanofi's reaction?
In a statement, the French company said: "The University of the Philippines-Philippine General Hospital
expert panel confirmed... that there is currently no evidence directly linking the Dengvaxia vaccine to
any of the 14 deaths.
"In Dengvaxia clinical trials conducted over more than a decade and the over one million doses of the
vaccine administered, no deaths related to the vaccine have been reported to us.
"Clinical evidence confirms dengue vaccination in the Philippines will provide a net reduction in dengue
disease."
Last November, Sanofi announced that its vaccine could worsen the potentially deadly disease in people
not previously infected.
"For those not previously infected by dengue virus, however, the analysis found that in the longer term,
more cases of severe disease could occur following vaccination upon a subsequent dengue infection,"
the firm said in a statement.
Sanofi says Dengvaxia has been registered in 19 countries and launched in 11 of them.
In its latest advice on the vaccine, the WHO said that "until a full review has been conducted, WHO
recommends vaccination only in individuals with a documented past dengue infection".
Presentational grey line
Recent vaccine controversies:
'Anti-vax' movement: activities in the past few years by fringe campaigners against immunisation -
particularly for measles - lead to falling immunisation rates in France, Italy and the US
Polio: Islamist militants in Pakistan have carried out attacks against workers vaccinating children in
recent years. The militants say immunisation is a Western campaign to sterilise Pakistani children
MMR (measles, mumps and rubella): starts with a publication of a 1998 paper falsely linking the vaccine
to autism. This leads to a drop in immunisation rates in the UK and the Republic of Ireland.
 Ebola virus disease
Fact sheet
Updated January 2018

Key facts
 Ebola virus disease (EVD), formerly known as Ebola haemorrhagic fever, is a severe, often fatal illness in
humans.
 The virus is transmitted to people from wild animals and spreads in the human population through human-to-
human transmission.
 The average EVD case fatality rate is around 50%. Case fatality rates have varied from 25% to 90% in past
outbreaks.
 The first EVD outbreaks occurred in remote villages in Central Africa, near tropical rainforests. The 2014–2016
outbreak in West Africa involved major urban areas as well as rural ones.
 Community engagement is key to successfully controlling outbreaks. Good outbreak control relies on applying a
package of interventions, namely case management, infection prevention and control practices, surveillance and
contact tracing, a good laboratory service, safe and dignified burials and social mobilisation.
 Early supportive care with rehydration, symptomatic treatment improves survival. There is as yet no licensed
treatment proven to neutralize the virus but a range of blood, immunological and drug therapies are under
development.

Background
The Ebola virus causes an acute, serious illness which is often fatal if untreated. Ebola virus disease (EVD) first
appeared in 1976 in 2 simultaneous outbreaks, one in what is now, Nzara, South Sudan, and the other in
Yambuku, Democratic Republic of Congo. The latter occurred in a village near the Ebola River, from which the
disease takes its name.
The 2014–2016 outbreak in West Africa was the largest and most complex Ebola outbreak since the virus was
first discovered in 1976. There were more cases and deaths in this outbreak than all others combined. It also
spread between countries, starting in Guinea then moving across land borders to Sierra Leone and Liberia.
The virus family Filoviridae includes three genera: Cuevavirus, Marburgvirus, and Ebolavirus. Within the genus
Ebolavirus, five species have been identified: Bundibugyo ebolavirus, Reston ebolavirus, Sudan ebolavirus, Taï
Forest ebolavirus and Zaire ebolavirus. Bundibugyo ebolavirus, Zaire ebolavirus, and Sudan ebolavirus have
been associated with large outbreaks in Africa. The virus causing the 2014–2016 West African outbreak belongs
to the Zaire ebolavirus species.
Transmission
It is thought that fruit bats of the Pteropodidae family are natural Ebola virus hosts. Ebola is introduced into the
human population through close contact with the blood, secretions, organs or other bodily fluids of infected
animals such as chimpanzees, gorillas, fruit bats, monkeys, forest antelope and porcupines found ill or dead or in
the rainforest.
Ebola then spreads through human-to-human transmission via direct contact (through broken skin or mucous
membranes) with the blood, secretions, organs or other bodily fluids of infected people, and with surfaces and
materials (e.g. bedding, clothing) contaminated with these fluids.
Health-care workers have frequently been infected while treating patients with suspected or confirmed EVD.
This has occurred through close contact with patients when infection control precautions are not strictly
practiced.
Burial ceremonies that involve direct contact with the body of the deceased can also contribute in the
transmission of Ebola.
Sexual transmission
More surveillance data and research are needed on the risks of sexual transmission, and particularly on the
prevalence of viable and transmissible virus in semen over time. In the interim, and based on present evidence,
WHO recommends that:
 All Ebola survivors and their sexual partners should receive counselling to ensure safe sexual practices and be
provided with condoms when discharged from Ebola treatment units and when enrolled in national semen and
body fluid testing programmes.
 Male Ebola survivors should be offered semen testing when discharged from Ebola treatment units,, and then,
for those who test positive, every month thereafter until their semen tests negative for virus twice by RT-PCR,
with a minimum interval of two weeks between tests.
 Ebola survivors and their sexual partners should either:
o abstain from all types of sex, or
o observe safe sex through correct and consistent condom use until their semen has twice tested negative.
 Having tested negative twice as described above, survivors can safely resume normal sexual practices with
reduced risk of sexual transmission.
 In exceptional circumstances where a male survivor does not have access to semen testing, he should continue to
practice safe sex and hygiene for at least 12 months from onset of symptoms; this interval may be adjusted as
 additional information becomes available on the prevalence and infectivity of Ebola virus in the semen of
survivors over time.
 Until such time as their semen has twice tested negative for Ebola, survivors should practice good hand and
personal hygiene by immediately and thoroughly washing with soap and water after any physical contact with
semen, including after masturbation. During this period used condoms should be handled safely, and safely
disposed of, so as to prevent contact with seminal fluids.
 All survivors, their partners and families should be shown respect, dignity and compassion.
 For more, read the Guidance on clinical care for survivors of Ebola virus disease
Symptoms of Ebola virus disease
The incubation period, that is, the time interval from infection with the virus to onset of symptoms is 2 to 21
days. Humans are not infectious until they develop symptoms. First symptoms are the sudden onset of fever
fatigue, muscle pain, headache and sore throat. This is followed by vomiting, diarrhoea, rash, symptoms of
impaired kidney and liver function, and in some cases, both internal and external bleeding (e.g. oozing from the
gums, blood in the stools). Laboratory findings include low white blood cell and platelet counts and elevated
liver enzymes.
Persistent virus in people recovering from Ebola virus disease
Ebola virus is known to persist in immune-privileged sites in some people who have recovered from Ebola virus
disease. These sites include the testicles, the inside of the eye, and the central nervous system. In women who
have been infected whilepregnant, the virus persists in the placenta, amniotic fluid and fetus. In women who
have been infected while breastfeeding, the virus may persist in breast milk.
Studies of viral persistence indicate that in a small percentage of survivors, some body fluids may test positive
on reverse transcriptase polymerase chain reaction (RT-PCR) for Ebola virus for longer than 9 months.
Relapse-symptomatic illness in someone who has recovered from EVD due to increased replication of the virus
in a specific site is a rare event, but has been documented. Reasons for this phenomenon are not yet fully
understood.
Diagnosis
It can be difficult to clinically distinguish EVD from other infectious diseases such as malaria, typhoid fever,
meningitis and other viral haemorrhagic fevers. Confirmation that symptoms are caused by Ebola virus infection
are made using the following diagnostic methods:
 antibody-capture enzyme-linked immunosorbent assay (ELISA)
 antigen-capture detection tests
 serum neutralization test
 reverse transcriptase polymerase chain reaction (RT-PCR) assay
 electron microscopy
 virus isolation by cell culture.
Careful consideration should be given to the selection of diagnostic tests, which take into account technical
specifications, disease incidence and prevalence, and social and medical implications of test results. It is strongly
recommended that diagnostic tests, which have undergone an independent and international evaluation, be
considered for use.
 Diagnostic tests evaluated through the WHO Emergency Use Assessment and Listing process
Current WHO recommended tests include:
 Automated or semi-automated nucleic acid tests (NAT) for routine diagnostic management.
 Rapid antigen detection tests for use in remote settings where NATs are not readily available. These tests are
recommended for screening purposes as part of surveillance activities, however reactive tests should be
confirmed with NATs.
 The preferred specimens for diagnosis include:
o Whole blood collected in ethylenediaminetetraacetic acid (EDTA) from live patients exhibiting symptoms.
o Oral fluid specimen stored in universal transport medium collected from deceased patients or when blood
collection is not possible.
 Samples collected from patients are an extreme biohazard risk; laboratory testing on non-inactivated samples
should be conducted under maximum biological containment conditions. All biological specimens should be
packaged using the triple packaging system when transported nationally and internationally.
Treatment and vaccines
Supportive care-rehydration with oral or intravenous fluids- and treatment of specific symptoms, improves
survival. There is as yet no proven treatment available for EVD. However, a range of potential treatments
including blood products, immune therapies and drug therapies are currently being evaluated.
An experimental Ebola vaccine proved highly protective against the deadly virus in a major trial in Guinea. The
vaccine, called rVSV-ZEBOV, was studied in a trial involving 11 841 people during 2015. Among the 5837
people who received the vaccine, no Ebola cases were recorded 10 days or more after vaccination. In
comparison, there were 23 cases 10 days or more after vaccination among those who did not receive the vaccine.
The trial was led by WHO, together with Guinea’s Ministry of Health, Médecins sans Frontières and the
Norwegian Institute of Public Health, in collaboration with other international partners. A ring vaccination
protocol was chosen for the trial, where some of the rings are vaccinated shortly after a case is detected, and
other rings are vaccinated after a delay of 3 weeks.
Prevention and control
Good outbreak control relies on applying a package of interventions, namely case management, surveillance and
contact tracing, a good laboratory service, safe and dignified burials and social mobilisation. Community
engagement is key to successfully controlling outbreaks. Raising awareness of risk factors for Ebola infection
and protective measures (including vaccination) that individuals can take is an effective way to reduce human
transmission. Risk reduction messaging should focus on several factors:
 Reducing the risk of wildlife-to-human transmission from contact with infected fruit bats or monkeys/apes
and the consumption of their raw meat. Animals should be handled with gloves and other appropriate protective
clothing. Animal products (blood and meat) should be thoroughly cooked before consumption.
 Reducing the risk of human-to-human transmission from direct or close contact with people with Ebola
symptoms, particularly with their bodily fluids. Gloves and appropriate personal protective equipment should be
worn when taking care of ill patients at home. Regular hand washing is required after visiting patients in
hospital, as well as after taking care of patients at home.
 Reducing the risk of possible sexual transmission, based on further analysis of ongoing research and
consideration by the WHO Advisory Group on the Ebola Virus Disease Response, WHO recommends that male
survivors of Ebola virus disease practice safe sex until their semen tests negative twice for Ebola virus. Contact
with body fluids should be avoided and washing with soap and water is recommended. WHO does not
recommend isolation of male or female convalescent patients whose blood has been tested negative for Ebola
virus.
For more, read the Guidance on clinical care for survivors of Ebola virus disease
 Outbreak containment measures, including prompt and safe and dignified burial of the dead, identifying
people who may have been in contact with someone infected with Ebola and monitoring their health for 21 days,
the importance of separating the healthy from the sick to prevent further spread, and the importance of good
hygiene and maintaining a clean environment.
Controlling infection in health-care settings:
Health-care workers should always take standard precautions when caring for patients, regardless of their
presumed diagnosis. These include basic hand hygiene, respiratory hygiene, use of personal protective
equipment (to block splashes or other contact with infected materials), safe injection practices and safe burial
practices.
Health-care workers caring for patients with suspected or confirmed Ebola virus should apply extra infection
control measures to prevent contact with the patient’s blood and body fluids and contaminated surfaces or
materials such as clothing and bedding. When in close contact (within 1 metre) of patients with EBV, health-care
 workers should wear face protection (a face shield or a medical mask and goggles), a clean, non-sterile long-
sleeved gown, and gloves (sterile gloves for some procedures).
Laboratory workers are also at risk. Samples taken from humans and animals for investigation of Ebola infection
should be handled by trained staff and processed in suitably equipped laboratories.
WHO response
WHO aims to prevent Ebola outbreaks by maintaining surveillance for Ebola virus disease and supporting at-risk
countries to developed preparedness plans. The document provides overall guidance for control of Ebola and
Marburg virus outbreaks:
 Ebola and Marburg virus disease epidemics: preparedness, alert, control, and evaluation
When an outbreak is detected WHO responds by supporting surveillance, community engagement, case
management, laboratory services, contact tracing, infection control, logistical support and training and assistance
with safe burial practices.
WHO has developed detailed advice on Ebola infection prevention and control:
 Infection prevention and control guidance for care of patients with suspected or confirmed Filovirus
haemorrhagic fever in health-care settings, with focus on Ebola

Zika virus
Fact sheet
Updated 6 September 2016

Key facts
 Zika virus disease is caused by a virus transmitted primarily by Aedesmosquitoes.
 People with Zika virus disease can have symptoms including mild fever, skin rash, conjunctivitis, muscle and
joint pain, malaise or headache. These symptoms normally last for 2-7 days.
 There is scientific consensus that Zika virus is a cause of microcephaly and Guillain-Barré syndrome. Links to
other neurological complications are also being investigated.

Introduction
Zika virus is a mosquito-borne flavivirus that was first identified in Uganda in 1947 in monkeys through a
network that monitored yellow fever. It was later identified in humans in 1952 in Uganda and the United
 Republic of Tanzania. Outbreaks of Zika virus disease have been recorded in Africa, the Americas, Asia and the
Pacific. From the 1960s to 1980s, human infections were found across Africa and Asia, typically accompanied
by mild illness. The first large outbreak of disease caused by Zika infection was reported from the Island of Yap
(Federated States of Micronesia) in 2007. In July 2015 Brazil reported an association between Zika virus
infection and Guillain-Barré syndrome. In October 2015 Brazil reported an association between Zika virus
infection and microcephaly.
 More on the history of Zika virus
Signs and Symptoms
The incubation period (the time from exposure to symptoms) of Zika virus disease is not clear, but is likely to be
a few days. The symptoms are similar to other arbovirus infections such as dengue, and include fever, skin
rashes, conjunctivitis, muscle and joint pain, malaise, and headache. These symptoms are usually mild and last
for 2-7 days.
Complications of Zika virus disease
Based on a systematic review of the literature up to 30 May 2016, WHO has concluded that Zika virus infection
during pregnancy is a cause of congenital brain abnormalities, including microcephaly; and that Zika virus is a
trigger of Guillain-Barré syndrome. Intense efforts are continuing to investigate the link between Zika virus and
a range of neurological disorders, within a rigorous research framework.
 Q&A: Zika virus and complication
Transmission
Zika virus is primarily transmitted to people through the bite of an infected mosquito from the Aedes genus,
mainly Aedes aegypti in tropical regions. Aedes mosquitoes usually bite during the day, peaking during early
morning and late afternoon/evening. This is the same mosquito that transmits dengue, chikungunya and yellow
fever. Sexual transmission of Zika virus is also possible. Other modes of transmission such as blood transfusion
are being investigated.
Diagnosis
Infection with Zika virus may be suspected based on symptoms and recent history of travel (e.g. residence in or
travel to an area with active Zika virus transmission). A diagnosis of Zika virus infection can only be confirmed
through laboratory tests on blood or other body fluids, such as urine, saliva or semen.
 Laboratory testing for Zika virus infection
Treatment
Zika virus disease is usually mild and requires no specific treatment. People sick with Zika virus should get
plenty of rest, drink enough fluids, and treat pain and fever with common medicines. If symptoms worsen, they
should seek medical care and advice. There is currently no vaccine available.
Prevention
Mosquito bites
Protection against mosquito bites is a key measure to prevent Zika virus infection. This can be done by wearing
clothes (preferably light-coloured) that cover as much of the body as possible; using physical barriers such as
window screens or closing doors and windows; sleeping under mosquito nets; and using insect repellent
containing DEET, IR3535 or icaridin according to the product label instructions. Special attention and help
should be given to those who may not be able to protect themselves adequately, such as young children, the sick
or elderly. Travellers and those living in affected areas should take the basic precautions described above to
protect themselves from mosquito bites.
It is important to cover, empty or clean potential mosquito breeding sites in and around houses such as buckets,
drums, pots, gutters, and used tyres. Communities should support local government efforts to reduce mosquitoes
in their locality. Health authorities may also advise that spraying of insecticides be carried out.
 Vector control operations framework for Zika virus
Sexual transmission
Zika virus can be transmitted through sexual intercourse. This is of concern due to an association between Zika
virus infection and adverse pregnancy and fetal outcomes.
For regions with active transmission of Zika virus, all people with Zika virus infection and their sexual partners
(particularly pregnant women) should receive information about the risks of sexual transmission of Zika virus.
WHO recommends that sexually active men and women be correctly counselled and offered a full range of
contraceptive methods to be able to make an informed choice about whether and when to become pregnant in
order to prevent possible adverse pregnancy and fetal outcomes. Women who have had unprotected sex and do
not wish to become pregnant due to concerns about Zika virus infection should have ready access to emergency
contraceptive services and counselling. Pregnant women should practice safer sex (including correct and
consistent use of condoms) or abstain from sexual activity for at least the whole duration of the pregnancy.
For regions with no active transmission of Zika virus, WHO recommends practising safer sex or abstinence for a
period of six months for men and women who are returning from areas of active transmission to prevent Zika
virus infection through sexual intercourse. Sexual partners of pregnant women, living in or returning from areas
where local transmission of Zika virus occurs should practice safer sex or abstain from sexual activity
throughout the pregnancy.
 Prevention of sexual transmission of Zika virus
WHO response
WHO is supporting countries to control Zika virus disease by taking actions outlined in the “Zika Strategic
Response Framework":
 Define and prioritize research into Zika virus disease by convening experts and partners.
 Enhance surveillance of Zika virus and potential complications.
 Strengthen capacity in risk communication to engage communities to better understand risks associated with
Zika virus.
 Strengthen the capacity of laboratories to detect the virus.
 Support health authorities to implement vector control strategies aimed at reducing Aedes mosquito populations.
 Prepare recommendations for the clinical care and follow-up of people with complications related to Zika virus
infection, in collaboration with experts and other health agencies.
 Zika Strategic Response Framework
 Genetic engineering
WRITTEN BY:

 The Editors of Encyclopaedia Britannica

LAST UPDATED: 2-9-2018 See Article History

Genetic engineering, the artificial manipulation, modification, and

recombination of DNA or othernucleic acid molecules in order to modify an
organism or population of organisms.

genetic engineeringA genetically engineered salmon (top) and a natural salmon of the same age
(bottom). The ability to engineer and precisely edit the genomes of animals, while potentially beneficial,
has raised ethical questions.Paul Darrow—The New York Times/Redux
 What’s the Difference Between a Gene and an Allele?

Genes and alleles are genetic sequences, and both determine biological traits. So,

what makes them different?

READ MORE

Historical Developments
The term genetic engineering initially referred to various techniques used for
the modification or manipulation of organisms through the processes
of heredity and reproduction. As such, the term embraced both artificial selection
and all the interventions of biomedical techniques, among themartificial
insemination, in vitro fertilization (e.g., “test-tube” babies), cloning,
and gene manipulation. In the latter part of the 20th century, however, the term
came to refer more specifically to methods ofrecombinant DNA
technology (or gene cloning), in which DNA molecules from two or more sources
are combined either within cells or in vitro and are then inserted into host
organisms in which they are able to propagate.

genetic engineeringAn overview of genetic engineering, particularly as applied to microbes.© Open

University

The possibility for recombinant DNA technology emerged with the discovery
of restriction enzymesin 1968 by Swiss microbiologist Werner Arber. The
following year American microbiologist Hamilton O. Smith purified so-called type
II restriction enzymes, which were found to be essential to geneticengineering for
their ability to cleave a specific site within the DNA (as opposed to type I
restriction enzymes, which cleave DNA at random sites). Drawing on Smith’s
work, American molecular biologist Daniel Nathans helped advance the
technique of DNA recombination in 1970–71 and demonstrated that type II
enzymes could be useful in genetic studies. Genetic engineering based on
recombination was pioneered in 1973 by American biochemists Stanley N.
Cohen and Herbert W. Boyer, who were among the first to cut DNA into
fragments, rejoin different fragments, and insert the new genes into E.
coli bacteria, which then reproduced.
Process And Techniques
Most recombinant DNA technology involves the insertion of foreign genes into
the plasmids of common laboratory strains of bacteria. Plasmids are small rings
of DNA; they are not part of the bacterium’s chromosome (the main repository
of the organism’s genetic information). Nonetheless, they are capable of
directing protein synthesis, and, like chromosomal DNA, they are reproduced
and passed on to the bacterium’s progeny. Thus, by incorporating foreign
DNA (for example, a mammalian gene) into a bacterium, researchers can
obtain an almost limitless number of copies of the inserted gene. Furthermore,
if the inserted gene is operative (i.e., if it directs protein synthesis), the
modified bacterium will produce the protein specified by the foreign DNA.
A subsequent generation of genetic engineering techniques that emerged in
the early 21st century centred on gene editing. Gene editing, based on a
technology known as CRISPR-Cas9, allows researchers to customize a living
organism’s genetic sequence by making very specific changes to its DNA.
Gene editing has a wide array of applications, being used for the genetic
modification of crop plants and livestock and of laboratory model organisms
(e.g., mice). The correction of genetic errors associated with disease in
animals suggests that gene editing has potential applications in gene
therapy for humans.
World Science Festival

Applications
Genetic engineering has advanced the understanding of many theoretical and
practical aspects of gene function and organization. Through recombinant
DNA techniques, bacteria have been created that are capable of synthesizing
human insulin, human growth hormone, alpha interferon, a hepatitis B vaccine, and
other medically useful substances. Plants may be genetically adjusted to
enable them to fix nitrogen, and genetic diseases can possibly be corrected by
replacing dysfunctional genes with normally functioning genes. Nevertheless,
special concern has been focused on such achievements for fear that they
might result in the introduction of unfavourable and possibly dangerous traits
into microorganisms that were previously free of them—e.g., resistance to
antibiotics, production of toxins, or a tendency to cause disease. Likewise, the
application of gene editing in humans has raisedethical concerns, particularly
regarding its potential use to alter traits such as intelligence and beauty.
Controversy
In 1980 the “new” microorganisms created by recombinant DNA research
were deemed patentable, and in 1986 the U.S. Department of
Agriculture approved the sale of the first living genetically altered organism—
a virus, used as a pseudorabies vaccine, from which a single gene had been
cut. Since then several hundred patents have been awarded for genetically
altered bacteria and plants. Patents on genetically engineered and genetically
modified organisms, particularly crops and other foods, however, were
a contentious issue, and they remained so into the first part of the 21st century.

FAST FACTS: What you

need to know about
vaccine company Sanofi
Pasteur
More than a year after its release of Dengvaxia, the world’s first dengue vaccine, Sanofi
advises the public the vaccine poses more risks for recipients who have had no prior
infection
Sofia Tomacruz

Published 8:19 PM, December 01, 2017

Updated 6:39 PM, D

RISK. Pharmaceutical companuy Sanofi pasteur issued new findings against it Dengvaxia vaccine. Photo
by Rappler

MANILA, Philippines – French pharmaceutical giant Sanofi Pasteur has found itself in
hot water since releasing findings against its own Dengvaxia dengue vaccine on
Thursday, November 30.

More than a year after its release of the world’s first dengue vaccine, Sanofi advised the
public that clinical studies revealed the vaccine poses more risks for recipients who had
no prior infection. (READ: Dengue vaccine more risky for people without prior infection –
Sanofi)

According to the Department of Heatlh (DOH), more than 700,000 Filipino youth have
been given the vaccine under the government’s mass immunization program, which
was launched in April 2016. (READ: More than 700,000 Filipino youth got risky dengue
vaccine – DOH)

Largest vaccine company

Sanofi Pasteur is the world’s largest vaccine company and serves as the vaccines
division of multinational pharmaceutical company Sanofi.

It set out to create the dengue vaccine more than 20 years ago to address the disease
in regions such as Latin America and Asia, where the virus is endemic.
Previous reports said 40,000 people from 15 countries participated in clinical tests,
which revealed an 80% reduction in the risk of hospitalization after being administered
the shot.

The vaccine provided protection from all 4 dengue strains, with previous
recommendations stating that healthy individuals aged 9 to 45 years old could be
administered the shot in 3 doses at 6-month intervals.

Eleven countries, including the Philippines, have approved the commercial release of
Dengvaxia: Brazil, Costa Rica, El Salvador, Guatemala, Mexico, Paraguay, Peru,
Indonesia, Singapore, and Thailand.
The company includes in its history affiliations with key scientists and companies, which
created the first vaccines for tetanus, polio, rabies, and typhoid, among others. It’s also
credited as the world’s largest producer and provider of seasonal influenza vaccines
and poliomyelitis vaccines.

According to its official website, it provides more than one billion doses of vaccines each
year, administering several kinds of immunization shots to more than 500 million people
worldwide.

Prevent deaths?

The advisory issued by Sanofi Pasteur on Thursday is just the latest in a string of issues
surrounding the dengue vaccine. (TIMELINE: Dengue immunization program for public
school students)

The vaccine was approved for sale in the Philippines a few weeks after then President
Benigno Aquino III received executives from the company in a courtesy call in Paris,
France, in December 2015.

Months after the Philippine government approved the commercial sale of Dengvaxia,
the DOH found itself quelling fears that the vaccine was not safe. This was after reports
surfaced that 4 people who had taken the shot died. Janette Garin, who was then DOH
secretary, said the deaths were unrelated to the vaccine.

The DOH approved the purchase of the vaccines in December 2015 after it reported
a rise in dengue cases – with over 78,000 cases reported in September 2015. The
World Heath Organization (WHO) said the vaccine was safe and effective, and
recommended it be administered in places with at least 50% disease incidence in the
population.

By April 2016, DOH embarked on its vaccination program, where more than one million
children were supposed to be the first recipients of the anti-dengue vaccine in the
country.

Since then, the treatment has faced several controversies. It was flagged as unsafe in
July 2016 by then-DOH secretary Paulyn Ubial. It has also been subject to a probe by
the House of Representatives.

During its approval, the vaccine was considered a major step in the prevention of
dengue, with hopes that the drug could eventually help prevent millions of deaths. But
thousands who have been given the shot with no prior history of the disease now face
the risk of developing severe dengue.
What is Cloning
Clones are organisms that are exact genetic copies. Every single bit of their DNA is identical.

Clones can happen naturally—identical twins are just one of many examples. Or they can be
made in the lab. Below, find out how natural identical twins are similar to and different from
clones made through modern cloning technologies.
Twin girls
How Is Cloning Done?
Many people first heard of cloning when Dolly the Sheep showed up on the scene in 1997.
Artificial cloning technologies have been around for much longer than Dolly, though.

There are two ways to make an exact genetic copy of an organism in a lab: artificial embryo
twinning and somatic cell nuclear transfer.

1. Artificial Embryo Twinning

Artificial embryo twinning is a relatively low-tech way to make clones. As the name suggests,
this technique mimics the natural process that creates identical twins.

In nature, twins form very early in development when the embryo splits in two. Twinning
happens in the first days after egg and sperm join, while the embryo is made of just a small
number of unspecialized cells. Each half of the embryo continues dividing on its own,
ultimately developing into separate, complete individuals. Since they developed from the
same fertilized egg, the resulting individuals are genetically identical.

Artificial embryo twinning uses the same approach, but it is carried out in a Petri dish instead
of inside the mother. A very early embryo is separated into individual cells, which are allowed
to divide and develop for a short time in the Petri dish. The embryos are then placed into a
surrogate mother, where they finish developing. Again, since all the embryos came from the
same fertilized egg, they are genetically identical.

2. Somatic Cell Nuclear Transfer

Somatic cell nuclear transfer (SCNT), also called nuclear transfer, uses a different approach
than artificial embryo twinning, but it produces the same result: an exact genetic copy, or
clone, of an individual. This was the method used to create Dolly the Sheep.

What does SCNT mean? Let's take it apart:

Somatic cell: A somatic cell is any cell in the body other than sperm and egg, the two types of
reproductive cells. Reproductive cells are also called germ cells. In mammals, every somatic
cell has two complete sets of chromosomes, whereas the germ cells have only one complete
set.
Nuclear: The nucleus is a compartment that holds the cell's DNA. The DNA is divided into
packages called chromosomes, and it contains all the information needed to form an
organism. It's small differences in our DNA that make each of us unique.

Transfer: Moving an object from one place to another. To make Dolly, researchers isolated a
somatic cell from an adult female sheep. Next they removed the nucleus and all of its DNA
from an egg cell. Then they transferred the nucleus from the somatic cell to the egg cell. After
a couple of chemical tweaks, the egg cell, with its new nucleus, was behaving just like a freshly
fertilized egg. It developed into an embryo, which was implanted into a surrogate mother and
carried to term. (The transfer step is most often done using an electrical current to fuse the
membranes of the egg and the somatic cell.)

The lamb, Dolly, was an exact genetic replica of the adult female sheep that donated the
somatic cell. She was the first-ever mammal to be cloned from an adult somatic cell.
Watch these videos of enucleation and nuclear transfer.

How does SCNT differ from the natural way of making an embryo?
Natural fertilization, where egg and sperm join, and SCNT both make the same thing: a
dividing ball of cells, called an embryo. So what exactly is the difference between the two?

An embryo's cells all have two complete sets of chromosomes. The difference between
fertilization and SCNT lies in where those two sets come from.

In fertilization, the sperm and egg have one set of chromosomes each. When the sperm and
egg join, they grow into an embryo with two sets—one from the father's sperm and one from
the mother's egg.

In SCNT, the egg cell's single set of chromosomes is removed. It is replaced by the nucleus
from a somatic cell, which already contains two complete sets of chromosomes. So, in the
resulting embryo, both sets of chromosomes come from the somatic cell.

Is cloning an organism the same as cloning a gene?

You may have heard about researchers cloning, or identifying, genes that are responsible for
various medical conditions or traits. What's the difference?

When scientists clone an organism, they are making an exact genetic copy of the whole
organism, as described above.
 When scientists clone a gene, they isolate and make exact copies of just one of an organism's
genes. Cloning a gene usually involves copying the DNA sequence of that gene into a smaller,
more easily manipulated piece of DNA, such as a plasmid. This process makes it easier to study
the function of the individual gene in the laboratory.

Herpes simplex virus

Updated January 2017

Key facts
 The herpes simplex virus, or herpes, is categorized into 2 types: herpes simplex virus type 1 (HSV-1) and herpes
simplex virus type 2 (HSV-2).
 HSV-1 is mainly transmitted by oral-to-oral contact to cause oral herpes (which can include symptoms known as
“cold sores”), but can also cause genital herpes.
 HSV-2 is a sexually transmitted infection that causes genital herpes.
 Both HSV-1 and HSV-2 infections are lifelong.
 An estimated 3.7 billion people under age 50 (67%) have HSV-1 infection globally.
 An estimated 417 million people aged 15-49 (11%) worldwide have HSV-2 infection.
 Most oral and genital herpes infections are asymptomatic.
 Symptoms of herpes include painful blisters or ulcers at the site of infection.
 Herpes infections are most contagious when symptoms are present but can still be transmitted to others in the
absence of symptoms.
 Infection with HSV-2 increases the risk of acquiring and transmitting HIV infection.

Introduction
Infection with the herpes simplex virus, commonly known as herpes, can be due to either herpes simplex virus
type 1 (HSV-1) or herpes simplex virus type 2 (HSV-2). HSV-1 is mainly transmitted by oral to oral contact to
cause infection in or around the mouth (oral herpes). HSV-2 is almost exclusively sexually transmitted, causing
infection in the genital or anal area (genital herpes). However, HSV-1 can also be transmitted to the genital area
through oral-genital contact to cause genital herpes.
Both oral herpes infections and genital herpes infections are mostly asymptomatic but can cause mild symptoms
or painful blisters or ulcers at the site of infection.
 Herpes simplex virus - type 1 (HSV-1)
 Herpes simplex virus - type 2 (HSV-2)
Herpes simplex virus type 1 (HSV-1)
HSV-1 is a highly contagious infection, which is common and endemic throughout the world. Most HSV-1
infections are acquired during childhood, and infection is lifelong. The vast majority of HSV-1 infections are
oral herpes (infections in or around the mouth, sometimes called orolabial, oral-labial or oral-facial herpes), but a
proportion of HSV-1 infections are genital herpes (infections in the genital or anal area).
Scope of the problem
In 2012, an estimated 3.7 billion people under the age of 50, or 67% of the population, had HSV-1 infection.
Estimated prevalence of the infection was highest in Africa (87%) and lowest in the Americas (40-50%).
With respect to genital HSV-1 infection, 140 million people aged 15-49-years were estimated to have genital
HSV-1 infection worldwide in 2012, but prevalence varied substantially by region. Most genital HSV-1
infections are estimated to occur in the Americas, Europe and Western Pacific, where HSV-1 continues to be
acquired well into adulthood. In other regions, for example in Africa, most HSV-1 infections are acquired in
childhood, before the age of sexual debut.
Signs and symptoms
Oral herpes infection is mostly asymptomatic, and the majority of people with HSV-1 infection are unaware they
are infected. Symptoms of oral herpes include painful blisters or open sores called ulcers in or around the mouth.
Sores on the lips are commonly referred to as “cold sores.” Infected persons will often experience a tingling,
itching or burning sensation around their mouth, before the appearance of sores. After initial infection, the
blisters or ulcers can periodically recur. The frequency of recurrences varies from person to person.
Genital herpes caused by HSV-1 can be asymptomatic or can have mild symptoms that go unrecognized. When
symptoms do occur, genital herpes is characterised by 1 or more genital or anal blisters or ulcers. After an initial
genital herpes episode, which may be severe, symptoms may recur, but genital herpes caused by HSV-1 often
does not recur frequently.
Transmission
HSV-1 is mainly transmitted by oral-to-oral contact to cause oral herpes infection, via contact with the HSV-1
virus in sores, saliva, and surfaces in or around the mouth. However, HSV-1 can also be transmitted to the
genital area through oral-genital contact to cause genital herpes.
HSV-1 can be transmitted from oral or skin surfaces that appear normal and when there are no symptoms
present. However, the greatest risk of transmission is when there are active sores.
 Individuals who already have HSV-1 oral herpes infection are unlikely to be subsequently infected with HSV-1
in the genital area.
In rare circumstances, HSV-1 infection can be transmitted from a mother with genital HSV-1 infection to her
infant during delivery.
Possible complications
Severe disease
In immunocompromised people, such as those with advanced HIV infection, HSV-1 can have more severe
symptoms and more frequent recurrences. Rarely, HSV-1 infection can also lead to more severe complications
such as encephalitis or keratitis (eye infection).
Neonatal herpes
Neonatal herpes can occur when an infant is exposed to HSV in the genital tract during delivery. This is a rare
condition, occurring in an estimated 10 out of every 100,000 births globally, but can lead to lasting neurologic
disability or death. The risk for neonatal herpes is greatest when a mother acquires HSV infection for the first
time in late pregnancy. Women who have genital herpes before they become pregnant are at very low risk of
transmitting HSV to their infants.
Psychosocial impact
Recurrent symptoms of oral herpes may be uncomfortable and can lead to some social stigma and psychological
distress. With genital herpes, these factors can have an important impact on quality of life and sexual
relationships. However, in time, most people with either kind of herpes adjust to living with the infection.
Treatment
Antiviral medications, such as acyclovir, famciclovir, and valacyclovir, are the most effective medications
available for people infected with HSV. These can help to reduce the severity and frequency of symptoms, but
cannot cure the infection.
 WHO guidelines for the treatment of Genital Herpes Simplex Virus
Prevention
HSV-1 is most contagious during an outbreak of symptomatic oral herpes, but can also be transmitted when no
symptoms are felt or visible. People with active symptoms of oral herpes should avoid oral contact with others
and sharing objects that have contact with saliva. They should also abstain from oral sex, to avoid transmitting
herpes to the genitals of a sexual partner. Individuals with symptoms of genital herpes should abstain from
sexual activity whilst experiencing any of the symptoms.
People who already have HSV-1 infection are not at risk of getting it again, but they are still at risk of acquiring
herpes simplex virus type 2 (HSV-2) genital infection (see below).
The consistent and correct use of condoms can help to prevent the spread of genital herpes. However, condoms
can only reduce the risk of infection, as outbreaks of genital herpes can occur in areas not covered by a condom.
Pregnant women with symptoms of genital herpes should inform their health care providers. Preventing
acquisition of a new genital herpes infection is particularly important for women in late pregnancy, as this is
when the risk for neonatal herpes is greatest.
Additional research is underway to develop more effective prevention methods against HSV infection, such as
vaccines. Several candidate HSV vaccines are currently being studied.
Herpes simplex virus type 2 (HSV-2)
HSV-2 infection is widespread throughout the world and is almost exclusively sexually transmitted, causing
genital herpes. HSV-2 is the main cause of genital herpes, which can also be caused by herpes simplex virus type
1 (HSV-1). Infection with HSV-2 is lifelong and incurable.
Scope of the problem
Genital herpes caused by HSV-2 is a global issue, and an estimated 417 million people worldwide were living
with the infection in 2012. Prevalence of HSV-2 infection was estimated to be highest in Africa (31.5%),
 followed by the Americas (14.4%). It was also shown to increase with age, though the highest numbers of people
newly-infected were adolescents.
More women are infected with HSV-2 than men; in 2012 it was estimated that 267 million women and 150
million men were living with the infection. This is because sexual transmission of HSV is more efficient from
men to women than from women to men.
Signs and symptoms
Genital herpes infections often have no symptoms, or mild symptoms that go unrecognised. Most infected
people are unaware that they have the infection. Typically, about 10-20% of people with HSV-2 infection report
a prior diagnosis of genital herpes.
When symptoms do occur, genital herpes is characterised by one or more genital or anal blisters or open sores
called ulcers. In addition to genital ulcers, symptoms of new genital herpes infections often include fever, body
aches, and swollen lymph nodes.
After an initial genital herpes infection with HSV-2, recurrent symptoms are common but often less severe than
the first outbreak. The frequency of outbreaks tends to decrease over time. People infected with HSV-2 may
experience sensations of mild tingling or shooting pain in the legs, hips, and buttocks before the occurrence of
genital ulcers.
Transmission
HSV-2 is mainly transmitted during sex, through contact with genital surfaces, skin, sores or fluids of someone
infected with the virus. HSV-2 can be transmitted from skin in the genital or anal area that looks normal and is
often transmitted in the absence of symptoms.
In rare circumstances, HSV-2 infection can be transmitted from a mother to her infant during delivery.
Possible complications
HSV-2 and HIV
HSV-2 and HIV have been shown to influence each other. HSV-2 infection increases the risk of acquiring a new
HIV infection by approximately three-fold. In addition, people with both HIV and HSV-2 infection are more
likely to spread HIV to others. HSV-2 is amongst the most common infections in people living with HIV,
occurring in 60-90% of HIV-infected persons.
Infection with HSV-2 in people living with HIV (and other immunocompromised individuals) often has a more
severe presentation and more frequent recurrences. In advanced HIV disease, HSV-2 can lead to more serious,
but rare, complications such as meningoencephalitis, esophagitis, hepatitis, pneumonitis, retinal necrosis, or
disseminated infection.
Neonatal herpes
Neonatal herpes can occur when an infant is exposed to HSV in the genital tract during delivery. This is a rare
condition, occurring in an estimated 10 out of every 100,000 births globally, but can lead to lasting neurologic
disability or death. The risk for neonatal herpes is greatest when a mother acquires HSV infection for the first
time in late pregnancy. Women who have genital herpes before they become pregnant are at very low risk of
transmitting HSV to their infants.
Psychosocial impact
Recurrent symptoms of genital herpes may be painful and the infection can lead to social stigma and
psychological distress. These factors can have an important impact on quality of life and sexual relationships.
However, in time, most people with herpes adjust to living with the infection.
Treatment
Antivirals, such as acyclovir, famciclovir, and valacyclovir are the most effective medications available for
people infected with HSV. These can help to reduce the severity and frequency of symptoms, but cannot cure the
infection.
 WHO guidelines for the treatment of Genital Herpes Simplex Virus
Prevention
Individuals with genital HSV infection should abstain from sexual activity whilst experiencing symptoms of
genital herpes. HSV-2 is most contagious during an outbreak of sores, but can also be transmitted when no
symptoms are felt or visible.
The consistent and correct use of condoms can help reduce the risk of spreading genital herpes. However,
condoms only provide partial protection, as HSV can be found in areas not covered by a condom. Medical male
circumcision can provide men life-long partial protection against HSV-2, in addition to HIV and human
papillomavirus (HPV).
Pregnant women with symptoms of genital herpes should inform their health care providers. Preventing
acquisition of a new genital herpes infection is particularly important for women in late pregnancy, as this is
when the risk for neonatal herpes is greatest.
Additional research is underway to develop more effective prevention methods against HSV infection, such as
vaccines or topical microbicides (compounds which can be applied inside the vagina or rectum to protect against
sexually transmitted infections).
WHO response to herpes (HSV-1 and HSV-2)
WHO and partners are working to accelerate research to develop new strategies for prevention and control of
genital and neonatal HSV-1 and HSV-2 infections. Such research includes the development of HSV vaccines
and topical microbicides. Several candidate vaccines and microbicides are currently being studied.

Marburg virus disease

Fact sheet
Updated October 2017

Key facts

Marburg virus disease (MVD), formerly known as Marburg haemorrhagic fever, is a severe,
often fatal illness in humans.
Rousettus aegyptiacus, fruit bats of the Pteropodidae family, are considered to be natural
hosts of Marburg virus. The Marburg virus is transmitted to people from fruit bats and spreads
among humans through human-to-human transmission.
The Marburg virus causes severe viral haemorrhagic fever in humans.
The average MVD case fatality rate is around 50%. Case fatality rates have varied from 24% to
88% in past outbreaks depending on virus strain and case management.
Community engagement is key to successfully controlling outbreaks. Good outbreak control
relies on applying a package of interventions, namely case management, infection prevention
and control practices, surveillance and contact tracing, a good laboratory service, safe burials
and social mobilization.
Early supportive care with rehydration, symptomatic treatment improves survival. There is as
yet no licensed treatment proven to neutralize the virus but a range of blood products,
immune therapies and drug therapies are currently under development.
Marburg virus is the causative agent of Marburg virus disease (MVD), a disease with a case
fatality ratio of up to 88%. Marburg virus disease was initially detected in 1967 after
simultaneous outbreaks in Marburg and Frankfurt in Germany; and in Belgrade, Serbia.

Marburg and Ebola viruses are both members of the Filoviridae family (filovirus). Though
caused by different viruses, the two diseases are clinically similar. Both diseases are rare and
have the capacity to cause dramatic outbreaks with high fatality rates.

Two large outbreaks that occurred simultaneously in Marburg and Frankfurt in Germany, and
in Belgrade, Serbia, in 1967, led to the initial recognition of the disease. The outbreak was
associated with laboratory work using African green monkeys (Cercopithecus aethiops)
imported from Uganda. Subsequently, outbreaks and sporadic cases have been reported in
Angola, Democratic Republic of the Congo, Kenya, South Africa (in a person with recent travel
history to Zimbabwe) and Uganda. In 2008, two independent cases were reported in travelers
who had visited a cave inhabited by Rousettus bat colonies in Uganda.

Transmission

Initially, human MVD infection results from prolonged exposure to mines or caves inhabited
by Rousettus bat colonies.

Marburg spreads through human-to-human transmission via direct contact (through broken
skin or mucous membranes) with the blood, secretions, organs or other bodily fluids of
infected people, and with surfaces and materials (e.g. bedding, clothing) contaminated with
these fluids.
Health-care workers have frequently been infected while treating patients with suspected or
confirmed MVD. This has occurred through close contact with patients when infection control
precautions are not strictly practiced. Transmission via contaminated injection equipment or
through needle-stick injuries is associated with more severe disease, rapid deterioration, and,
possibly, a higher fatality rate.

Burial ceremonies that involve direct contact with the body of the deceased can also
contribute in the transmission of Marburg.

People remain infectious as long as their blood contains the virus.

Sexual transmission

Marburg virus transmission via infected semen has been documented up to seven weeks after
clinical recovery. More surveillance data and research are needed on the risks of sexual
transmission, and particularly on the prevalence of viable and transmissible virus in semen
over time. In the interim, and based on present evidence, WHO recommends that:

All Marburg survivors and their sexual partners should receive counselling to ensure safer
sexual practices until their semen has twice tested negative for Marburg virus.
Survivors should be provided with condoms.
Male Marburg survivors should be enrolled in semen testing programmes when discharged
(starting with counselling) and offered semen testing when mentally and physically ready,
within three months of disease onset.
Marburg survivors and their sexual partners should either:
abstain from all sexual practices, or
observe safer sexual practices through correct and consistent condom use until their semen
has twice tested undetected ( negative) for Marburg virus.
Having tested undetected (negative), survivors can safely resume normal sexual practices with
minimized risk of Marburg virus transmission.
Male survivors of Marburg virus disease should practice safer sexual practices and hygiene for
12 months from onset of symptoms or until their semen twice tests undetected (negative) for
Marburg virus.
Until such time as their semen has twice tested undetected (negative) for Marburg, survivors
should practice good hand and personal hygiene by immediately and thoroughly washing with
soap and water after any physical contact with semen, including after masturbation. During
this period used condoms should be handled safely, and safely disposed of, so as to prevent
contact with seminal fluids.
All survivors, their partners and families should be shown respect, dignity and compassion.
Symptoms of Marburg virus disease

The incubation period (interval from infection to onset of symptoms) varies from 2 to 21 days.

Illness caused by Marburg virus begins abruptly, with high fever, severe headache and severe
malaise. Muscle aches and pains are a common feature. Severe watery diarrhoea, abdominal
pain and cramping, nausea and vomiting can begin on the third day. Diarrhoea can persist for
a week. The appearance of patients at this phase has been described as showing “ghost-like”
drawn features, deep-set eyes, expressionless faces, and extreme lethargy. In the 1967
European outbreak, non-itchy rash was a feature noted in most patients between 2 and 7 days
after onset of symptoms.

Many patients develop severe haemorrhagic manifestations between 5 and 7 days, and fatal
cases usually have some form of bleeding, often from multiple areas. Fresh blood in vomitus
and faeces is often accompanied by bleeding from the nose, gums, and vagina. Spontaneous
bleeding at venepuncture sites (where intravenous access is obtained to give fluids or obtain
blood samples) can be particularly troublesome. During the severe phase of illness, patients
have sustained high fevers. Involvement of the central nervous system can result in confusion,
irritability, and aggression. Orchitis (inflammation of one or both testicles) has been reported
occasionally in the late phase of disease (15 days).

In fatal cases, death occurs most often between 8 and 9 days after symptom onset, usually
preceded by severe blood loss and shock.

Persistent virus in people recovering from Marburg virus disease

Marburg virus is known to persist in immune-privileged sites in some people who have
recovered from Marburg virus disease. These sites include the testicles and the inside of the
eye.

In women who have been infected while pregnant, the virus persists in the placenta, amniotic
fluid and fetus.
In women who have been infected while breastfeeding, the virus may persist in breast milk.
Relapse-symptomatic illness in the absence of re-infection in someone who has recovered
from MVD is a rare event, but has been documented. Reasons for this phenomenon are not
yet fully understood.

Diagnosis

It can be difficult to clinically distinguish MVD from other infectious diseases such as malaria,
typhoid fever, shigellosis, meningitis and other viral haemorrhagic fevers. Confirmation that
symptoms are caused by Marburg virus infection are made using the following diagnostic
methods:

antibody-capture enzyme-linked immunosorbent assay (ELISA)

antigen-capture detection tests
serum neutralization test
reverse transcriptase polymerase chain reaction (RT-PCR) assay
electron microscopy
virus isolation by cell culture.
Samples collected from patients are an extreme biohazard risk; laboratory testing on non-
inactivated samples should be conducted under maximum biological containment conditions.
All biological specimens should be packaged using the triple packaging system when
transported nationally and internationally.

Treatment and vaccines

Supportive care – rehydration with oral or intravenous fluids – and treatment of specific
symptoms, improves survival. There is as yet no proven treatment available for MVD.
However, a range of potential treatments including blood products, immune therapies and
drug therapies are currently being evaluated.

Marburg virus in animals

Rousettus aegyptiacus bats are considered natural hosts for Marburg virus. There is no
apparent disease in the fruit bats. As a result, the geographic distribution of Marburg virus
may overlap with the range of Rousettus bats.

African green monkeys (Cercopithecus aethiops) imported from Uganda were the source of
infection for humans during the first Marburg outbreak.
Experimental inoculations in pigs with different Ebola viruses have been reported and show
that pigs are susceptible to filovirus infection and shed the virus. Therefore pigs should be
considered as a potential amplifier host during MHF outbreaks. Although no other domestic
animals have yet been confirmed as having an association with filovirus outbreaks, as a
precautionary measure they should be considered as potential amplifier hosts until proven
otherwise.

Precautionary measures are needed in pig farms in Africa to avoid pigs becoming infected
through contact with fruit bats. Such infection could potentially amplify the virus and cause or
contribute to MHF outbreaks.

Prevention and control

Good outbreak control relies on applying a package of interventions, namely case

management, surveillance and contact tracing, a good laboratory service, safe and dignified
burials, and social mobilization. Community engagement is key to successfully controlling
outbreaks. Raising awareness of risk factors for Marburg infection and protective measures
that individuals can take is an effective way to reduce human transmission.

Risk reduction messaging should focus on several factors:

Reducing the risk of bat-to-human transmission arising from prolonged exposure to mines or
caves inhabited by fruit bat colonies. During work or research activities or tourist visits in
mines or caves inhabited by fruit bat colonies, people should wear gloves and other
appropriate protective clothing (including masks). During outbreaks all animal products (blood
and meat) should be thoroughly cooked before consumption.
Reducing the risk of human-to-human transmission in the community arising from direct or
close contact with infected patients, particularly with their body fluids. Close physical contact
with Marburg patients should be avoided. Gloves and appropriate personal protective
equipment should be worn when taking care of ill patients at home. Regular hand washing
should be performed after visiting sick relatives in hospital, as well as after taking care of ill
patients at home.
Communities affected by Marburg should make efforts to ensure that the population is well
informed, both about the nature of the disease itself and about necessary outbreak
containment measures.
Outbreak containment measures include prompt and safe burial of the dead, identifying
people who may have been in contact with someone infected with Marburg and monitoring
their health for 21 days, separating the healthy from the sick to prevent further spread, and
maintaining good hygiene and a clean environment need to be observed.
Reducing the risk of possible sexual transmission. Based on further analysis of ongoing
research, WHO recommends that male survivors of Marburg virus disease practice safe sex
and hygiene for 12 months from onset of symptoms or until their semen twice tests negative
for Marburg virus. Contact with body fluids should be avoided and washing with soap and
water is recommended. WHO does not recommend isolation of male or female convalescent
patients whose blood has been tested negative for Marburg virus.
Controlling infection in healthcare settings

Healthcare workers should always take standard precautions when caring for patients,
regardless of their presumed diagnosis. These include basic hand hygiene, respiratory hygiene,
use of personal protective equipment (to block splashes or other contact with infected
materials), safe injection practices and safe and dignified burial practices.

Healthcare workers caring for patients with suspected or confirmed Marburg virus should
apply extra infection control measures to prevent contact with the patient’s blood and body
fluids and contaminated surfaces or materials such as clothing and bedding. When in close
contact (within 1 metre) of patients with MVD, health-care workers should wear face
protection (a face shield or a medical mask and goggles), a clean, non-sterile long-sleeved
gown, and gloves (sterile gloves for some procedures).

Laboratory workers are also at risk. Samples taken from humans and animals for investigation
of Marburg infection should be handled by trained staff and processed in suitably equipped
laboratories.

WHO response

WHO aims to prevent Marburg outbreaks by maintaining surveillance for Marburg virus
disease and supporting at-risk countries to develop preparedness plans. The following
document provides overall guidance for control of Ebola and Marburg virus outbreaks:

Ebola and Marburg virus disease epidemics: preparedness, alert, control, and evaluation
 When an outbreak is detected WHO responds by supporting surveillance, community
engagement, case management, laboratory services, contact tracing, infection control,
logistical support and training and assistance with safe burial practices.

WHO has developed detailed advice on Marburg infection prevention and control:

Introduction to molecular biology

Deoxyribonucleic acid (DNA) is the molecule which carries the genetic instructions for
almost every living thing. Its unique chemistry not only allows this information to be
copied and passed on to an organism’s descendents, it also allows scientists
opportunities to investigate and manipulate an organism at a molecular level. As a
result, molecular biology techniques are at the forefront of most cutting edge scientific
research. In this project you will investigate a number of commonly used molecular
biology techniques involving DNA.
What is molecular biology?

Molecular biology is the study of living things at the level of the molecules which control
them and make them up. While traditional biology concentrated on studying whole living
organisms and how they interact within populations (a “top down” approach), molecular
biology strives to understand living things by examining the components that make them
up (a “bottom up” approach). Both approaches to biology are equally valid, although
improvements to technology have permitted scientists to concentrate more on the
molecules of life in recent years.

Molecular biology is a specialised branch of biochemistry, the study of the chemistry of

molecules which are specifically connected to living processes. Of particular importance
to molecular biology are the nucleic acids (DNA and RNA) and the proteins which are
constructed using the genetic instructions encoded in those molecules. Other
biomolecules, such as carbohydrates and lipids may also be studied for the interactions
they have with nucleic acids and proteins. Molecular biology is often separated from the
field of cell biology, which concentrates on cellular structures (organelles and the like),
molecular pathways within cells and cell life cycles.

The molecules which form the basis of life provide scientists with a more predictable
and mechanistic tool for scientists to study. Working with whole organisms (or even just
whole cells) can be unpredictable, with the outcome of experiments relying on the
interaction of thousands of molecular pathways and external factors. Molecular biology
provides scientists with a toolkit with which they may “tinker” with the way life works.
They may use them to determine the function of single genes or proteins, and find out
what would happen if that gene or protein was absent or faulty. Molecular biology is
used to examine when and why certain genes are switched “on” or “off”. An
understanding of each of the factors has granted scientists a deeper understanding of
how living things work, and used this knowledge to develop treatments for when living
things don’t work so well.

Common molecular biology techniques

The following list covers some of the more commonly used molecular
biology techniques – it is by no means exhaustive.
  Electrophoresis – a process which separates molecules such as DNA or proteins out
according to their size, electrophoresis is a mainstay of molecular biology laboratories.
While knowing the size of a molecule might not seem like all that much information, it
can be used to identify molecules or fragments of molecules and as a check to make
sure that we have the correct molecule present.

 Polymerase Chain Reaction (PCR) – a process used to amplify very small amounts of
DNA to amounts which can be used in further experiments. It is used as a basic tool in
molecular biology to ensure that we have sufficient DNA to carry out further techniques
such as genetic modification, however it has wider practical uses such as in forensics
(identification using DNA profiling) and disease diagnosis. PCR can also be used to
introduce small point mutations into a gene in a process called site-directed
mutagenesis.

 Restriction Digest – the process of cutting DNA up into smaller fragments

using enzymes which only act at a particular genetic sequence.

 Ligation – the process of joining two pieces of DNA together. Ligation is useful when
introducing a new piece of DNA into another genome.

 Blotting – a technique used to specifically identify biomolecules

following electrophoresis. The molecule of interest is indicated using either a labeled
probe (a complementary strand of nucleic acid) or a labeled antibody raised against a
specific protein.

 Cloning – the technique of introducing a new gene into a cell or organism. This can be
used to see what effect the expression of that gene has on the organism, to turn the
organism into a factory which will produce large quantities of the gene or the protein it
codes for, or (within the inclusion of a label) to indicate where the products of that gene
are expressed in the organism. Insertion of genetic material into a bacterium is
called transformation, while insertion into a eukaryotic cell is called transfection. If a virus
is used to introduce this material, the process is called transduction.

Each of these techniques is used in conjunction with other techniques to help scientists
solve a particular research question. For example, following using PCR to create large
quantities of a particular gene a scientist may ligate a gene for a particular protein into
a plasmid vector (a short circular strand of DNA which acts as a carrier), perform a
 quick restriction digest and electrophoresis to ensure that the gene has been inserted
properly, and then use that plasmid to transform a bacterial cell which is used to
produce large quantities of the vector. After purification of the vector from the bacteria, it
is then used to transfect a mammalian cell in culture. The scientist then uses protein
electrophoresis and western blotting to demonstrate the expression of the gene product.

Kaposi Sarcoma

Kaposi sarcoma (KS) is a cancer that causes patches of abnormal tissue to grow under the skin, in the lining of
the mouth, nose, and throat, in lymph nodes, or in other organs. These patches, or lesions, are usually red or
purple. They are made of cancer cells, blood vessels, and blood cells.

KS is caused by infection with human herpesvirus-8 (HHV-8). Most people infected with HHV-8 don't get KS.
It usually happens in

 People with weak immune systems, due to HIV/AIDS, drugs taken after an organ transplant, or another disease
 Older men of Jewish or Mediterranean descent
 Young men in Africa
The skin lesions may not cause symptoms. But they can spread to other parts of the body, especially in people
with HIV/AIDS. If they spread to the digestive tract or lungs, they can cause bleeding. Lesions on the lungs
can also make it hard to breathe.
Treatment depends on where the lesions are and how bad they are. Options include radiation therapy, surgery,
chemotherapy, and biologic therapy. People with HIV/AIDS also take HIV/AIDS Medicines.

What Is Kaposi Sarcoma?

Cancer starts when cells in the body begin to grow out of control. Cells in
nearly any part of the body can become cancer, and can spread to other
areas of the body. To learn more about how cancers start and spread,
see What Is Cancer?

Kaposi sarcoma (KS) is a cancer that develops from the cells that line lymph
or blood vessels. It usually appears as tumors on the skin or on mucosal
surfaces such as inside the mouth, but tumors can also develop in other parts
of the body, such as in the lymph nodes (bean-sized collections of immune
cells throughout the body), the lungs, or digestive tract.

The abnormal cells of KS form purple, red, or brown blotches or tumors on the
skin. These affected areas are called lesions. The skin lesions of KS most
often appear on the legs or face. They may look bad, but they usually cause
no symptoms. Some lesions on the legs or in the groin area may cause the
legs and feet to swell painfully.

KS can cause serious problems or even become life threatening when the
lesions are in the lungs, liver, or digestive tract. KS in the digestive tract, for
example, can cause bleeding, while tumors in the lungs may cause trouble
breathing.

Types of Kaposi sarcoma

The different types of KS are defined by the different populations it develops
in, but the changes within the KS cells are very similar.
Epidemic (AIDS-related) Kaposi sarcoma
The most common type of KS in the United States is epidemic or AIDS-related
KS. This type of KS develops in people who are infected with HIV, the virus
that causes AIDS.

A person infected with HIV (that is, who is HIV-positive) does not necessarily
have AIDS. The virus can be present in the body for a long time, often many
years, before causing major illness. The disease known as AIDS begins when
the virus has seriously damaged the immune system, which results in certain
types of infections or other medical complications, including KS. When HIV
damages the immune system, people who also are infected with a certain
virus (the Kaposi sarcoma associated herpesvirus or KSHV) are more likely to
develop KS.

KS is considered an “AIDS defining” illness. This means that when KS occurs

in someone infected with HIV, that person officially has AIDS (and is not just
HIV-positive).

In the United States, treating HIV infection with highly active antiretroviral
therapy (HAART) has resulted in fewer cases of epidemic KS. Still, some
patients develop symptoms of KS in the first few months of HAART treatment.

For most patients with HIV, HAART can often keep advanced KS from
developing. Still, KS can still occur in people whose HIV is well controlled with
HAART. Once KS develops it is still important to continue HAART.

In areas of the world where HAART is not easy to obtain, KS in AIDS patients
can advance quickly.

Classic (Mediterranean) Kaposi sarcoma

Classic KS occurs mainly in older people of Mediterranean, Eastern
European, and Middle Eastern heritage. Classic KS is more common in men
than in women.

Patients typically have one or more lesions on the legs, ankles, or the soles of
the feet. Compared to other types of KS, the lesions in this type do not grow
as quickly, and new lesions do not develop as often.

The immune system of people with classic KS is not as weak as it is in those

who have epidemic KS, but it may be weaker than normal. Getting older can
naturally weaken the immune system a little. When this occurs, people who
already have a KSHV (Kaposi sarcoma associated herpesvirus) infection are
more likely to develop KS.

Endemic (African) Kaposi sarcoma

Endemic KS occurs in people living in Equatorial Africa and is sometimes
called African KS. KSHV (Kaposi sarcoma associated herpesvirus) infection is
much more common in Africa than in other parts of the world, so the risk of KS
is higher. Other factors in Africa that weaken the immune system (such as
malaria, other chronic infections, and malnutrition) also probably contribute to
the development of KS, since the disease affects a broader group of people
that includes children and women.

Endemic KS tends to occur in younger people (usually under age 40). Rarely
a more aggressive form of endemic KS is seen in children before puberty.
This type usually affects the lymph nodes and other organs and can progress
quickly.

Endemic KS used to be the most common type of KS in Africa. Then, as AIDS

became more common in Africa, the epidemic type became more common.
 Iatrogenic (transplant-related) Kaposi
sarcoma
When KS develops in people whose immune systems have been suppressed
after an organ transplant, it is called iatrogenic, or transplant-related KS. Most
transplant patients need to take drugs to keep their immune system from
rejecting (attacking) the new organ. But by weakening the body’s immune
system, these drugs increase the chance that someone infected with KSHV
(Kaposi sarcoma associated herpesvirus) will develop KS. Stopping the
immune-suppressing drugs or lowering their dose often makes KS lesions go
away or get smaller.

Kaposi sarcoma in HIV negative men who

have sex with men
There have been reports of KS developing in men who have sex with men
who are not infected with HIV. In this group, the cases of KS are often mild,
similar to cases of classic KS.

 Written by

Prader-Willi syndrome
 Symptoms & causes
 Diagnosis & treatment

Overview

Prader-Willi (PRAH-dur VIL-e) syndrome is a rare genetic disorder that results in a

number of physical, mental and behavioral problems. A key feature of Prader-Willi
syndrome is a constant sense of hunger that usually begins at about 2 years of age.
People with Prader-Willi syndrome want to eat constantly because they never feel full
(hyperphagia), and they usually have trouble controlling their weight. Many
complications of Prader-Willi syndrome are due to obesity.

Best managed by a team approach, various specialists can work with you to manage
symptoms of this complex disorder, reduce the risk of developing complications and
improve the quality of life for your loved one with Prader-Willi syndrome.

Symptoms

Signs and symptoms of Prader-Willi syndrome can vary among individuals. Symptoms
may slowly change over time from childhood to adulthood.

Infants

Signs and symptoms that may be present from birth include:

 Poor muscle tone. A primary sign during infancy is poor muscle tone (hypotonia). Babies
may rest with their elbows and knees loosely extended instead of fixed, and they may feel
floppy or like rag dolls when they're held.

 Distinct facial features. Children may be born with almond-shaped eyes, a narrowing of
the head at the temples, a turned-down mouth and a thin upper lip.

 Poor sucking reflex. Infants may have a poor sucking reflex due to decreased muscle
tone. Poor sucking makes feeding difficult and can result in failure to thrive.

 Generally poor responsiveness. A baby may seem unusually tired, respond poorly to
stimulation, have a hard time waking up or have a weak cry.

 Underdeveloped genitals. Males may have a small penis and scrotum. The testicles may
be small or not descended from the abdomen into the scrotum (cryptorchidism). In
females, the clitoris and labia may be small.

Early childhood to adulthood

Other features of Prader-Willi syndrome appear during early childhood and remain
throughout life, requiring careful management. These features may include:
 Food craving and weight gain. A classic sign of Prader-Willi syndrome is a constant
craving for food, resulting in rapid weight gain, starting around age 2 years. Constant
hunger leads to eating often and consuming large portions. Unusual food-seeking
behaviors, such as hoarding food, or eating frozen food or even garbage, may develop.

 Underdeveloped sex organs. A condition called hypogonadism occurs when sex organs
(testes in men and ovaries in women) produce little or no sex hormones. This results in
underdeveloped sex organs, incomplete or delayed puberty, and in nearly all cases,
infertility. Without treatment, women may not start menstruating until their 30s or may
never menstruate, and men may not have much facial hair and their voices may never fully
deepen.

 Poor growth and physical development. Underproduction of growth hormone can result
in short adult height, low muscle mass and high body fat. Other endocrine problems may
include underproduction of thyroid hormone (hypothyroidism) or central adrenal
insufficiency, which prevents the body from responding appropriately during stress or
infections.

 Cognitive impairment. Mild to moderate intellectual disability, such as issues with

thinking, reasoning and problem-solving, is a common feature of the disorder. Even those
without significant intellectual disability have some learning disabilities.

 Delayed motor development. Toddlers with Prader-Willi syndrome often reach

milestones in physical movement — for example, sitting up or walking — later than other
children do.

 Speech problems. Speech is often delayed. Poor articulation of words may be an

ongoing problem into adulthood.

 Behavioral problems. Children and adults may at times be stubborn, angry, controlling or
manipulative. They may throw temper tantrums, especially when denied food, and may not
tolerate changes in routine. They may also develop obsessive-compulsive or repetitive
behaviors, or both. Other mental health disorders, such as anxiety and skin picking, may
develop.

 Sleep disorders. Children and adults with Prader-Willi syndrome may have sleep
disorders, including disruptions of the normal sleep cycle and a condition in which
breathing pauses during sleep (sleep apnea). These disorders can result in excessive
daytime sleepiness and worsen behavior problems.

 Other signs and symptoms. These may include small hands and feet, curvature of the
spine (scoliosis), hip problems, reduced saliva flow, nearsightedness and other vision
 problems, problems regulating body temperature, a high pain tolerance, or a lack of
pigment (hypopigmentation) causing hair, eyes and skin to be pale.

When to see a doctor

Regularly scheduled well-baby visits can help identify early signs of poor growth and
development, which can be signs of Prader-Willi syndrome or other disorders.

If you have concerns about your baby's health between well-baby visits, schedule an
appointment with your child's doctor.

Request an Appointment at Mayo Clinic

Causes

Prader-Willi syndrome is a genetic disorder, a condition caused by an error in one or

more genes. Although the exact mechanisms responsible for Prader-Willi syndrome
haven't been identified, the problem lies in the genes located in a particular region of
chromosome 15.

With the exception of genes related to sex characteristics, all genes come in pairs —
one copy inherited from your father (paternal gene) and one copy inherited from your
mother (maternal gene). For most types of genes, if one copy is "active," or expressed,
then the other copy also is expressed, although it's normal for some types of genes to
act alone.

Prader-Willi syndrome occurs because certain paternal genes that should be expressed
are not for one of these reasons:

 Paternal genes on chromosome 15 are missing.

 The child inherited two copies of chromosome 15 from the mother and no chromosome 15
from the father.

 There's some error or defect in paternal genes on chromosome 15.

In Prader-Willi syndrome, a defect on chromosome 15 disrupts the normal functions of a

portion of the brain called the hypothalamus, which controls the release of hormones. A
hypothalamus that isn't functioning properly can interfere with processes that result in
problems with hunger, growth, sexual development, body temperature, mood and sleep.

In most cases, Prader-Willi syndrome is caused by a random genetic error and is not
inherited. Determining which genetic defect caused Prader-Willi syndrome can be
helpful in genetic counseling.

Obesity-related complications

In addition to having constant hunger, people with Prader-Willi syndrome have low
muscle mass, so they need fewer than average calories, and they may not be physically
active. This combination of factors makes them prone to obesity and the medical
problems related to obesity, such as:

 Type 2 diabetes

 High blood pressure, high cholesterol and heart disease

 Sleep apnea

 Other complications, such as an increased risk of liver disease and gallbladder stones

Complications of inadequate hormone production

Complications arising from inadequate hormone production may include:

 Sterility. Although there have been a few reports of women with Prader-Willi syndrome
becoming pregnant, most people with this disorder are unable to have children.

 Osteoporosis. Osteoporosis causes bones to become weak and brittle, so they may
break easily. People with Prader-Willi syndrome are at an increased risk of developing
osteoporosis because they have low levels of sex hormones and may also have low levels
of growth hormone — both hormones help maintain strong bones.

Other complications

Other complications that can result from Prader-Willi syndrome include:

 Effects of binge eating. Eating large amounts of food quickly, called binge eating, can
cause the stomach to become abnormally enlarged. People with Prader-Willi syndrome
 may not report pain and they rarely vomit. Binge eating can also cause choking. Rarely, a
person may eat so much that it causes stomach rupture.

 Reduced quality of life. Behavioral problems can interfere with family functioning,
successful education and social participation. They can also reduce the quality of life for
children, teenagers and adults with Prader-Willi syndrome.

Prevention

If you have a child with Prader-Willi syndrome and would like to have another baby,
consider seeking genetic counseling. A genetic counselor may help determine your risk
of having another child with Prader-Willi syndrome.

By Mayo Clinic Staff

Black Death
PANDEMIC, MEDIEVAL EUROPE
WRITTEN BY: The Editors of Encyclopaedia Britannica
See Article History
Alternative Title: Great Mortality
Black Death, pandemic that ravaged Europe between 1347 and 1351, taking a proportionately
greater toll of life than any other known epidemic or war up to that time.

plague epidemiology: genomic information

plague epidemiology: genomic information
Researchers using genomic information to trace the transmission routes in past epidemics of
plague.
University College Cork, Ireland
The Black Death is widely believed to have been the result of plague, caused by infection with
the bacterium Yersinia pestis. Modern genetic analyses indicate that the strain of Y. pestis
introduced during the Black Death is ancestral to all extant circulating Y. pestis strains known
to cause disease in humans. Hence, the origin of modern plague epidemics lies in the medieval
period. Other scientific evidence has indicated that the Black Death may have been viral in
origin.

Yersinia pestis
Yersinia pestis
A microscopic image shows Yersinia pestis, the bacterium that causes plague.
© Photodisc/Thinkstock
READ MORE ON THIS TOPIC
plague
plague: History
…plague pandemic was the dreaded Black Death of Europe in the 14th century. The number of
deaths was enormous, reaching two-thirds or three-fourths of the population in various parts
of Europe. It has been calculated that one-fourth to one-third of the total population of
Europe, or 25 million persons, died…

READ MORE
Origin And Incidence

Having originated in China and Inner Asia, the Black Death decimated the army of the Kipchak
khan Janibeg while he was besieging the Genoese trading port of Kaffa (now Feodosiya) in
Crimea (1347). With his forces disintegrating, Janibeg catapulted plague-infested corpses into
the town in an effort to infect his enemies. From Kaffa, Genoese ships carried the epidemic
westward to Mediterranean ports, whence it spread inland, affecting Sicily (1347); North
Africa, mainland Italy, Spain, and France (1348); and Austria, Hungary, Switzerland, Germany,
and the Low Countries (1349). A ship from Calais carried the plague to Melcombe Regis,
Dorset, in August 1348. It reached Bristol almost immediately and spread rapidly throughout
the southwestern counties of England. London suffered most violently between February and
May 1349, East Anglia and Yorkshire during that summer. The Black Death reached the
extreme north of England, Scotland, Scandinavia, and the Baltic countries in 1350.

The second pandemic of the Black Death in Europe (1347–51)

The second pandemic of the Black Death in Europe (1347–51)
Encyclopædia Britannica, Inc.
There were recurrences of the plague in 1361–63, 1369–71, 1374–75, 1390, and 1400.
Modern research has suggested that, over that period of time, plague was introduced into
Europe multiple times, coming along trade routes in waves from Central Asia as a result of
climate fluctuations that affected populations of rodents infested with plague-carrying fleas.

Oriental rat flea

Oriental rat flea
Oriental rat flea (Xenopsylla cheopis), primary vector for the transmission of the bacterium
Yersinia pestis between rats and humans.
Centers for Disease Control and Prevention (CDC)
The rate of mortality from the Black Death varied from place to place: whereas some districts,
such as the duchy of Milan, Flanders, and Béarn, seem to have escaped comparatively lightly,
others, such as Tuscany, Aragon, Catalonia, and Languedoc, were very hard hit. Towns, where
the danger of contagion was greater, were more affected than the countryside, and within the
towns the monastic communities provided the highest incidence of victims. Even the great
and powerful, who were more capable of flight, were struck down: among royalty, Eleanor,
queen of Peter IV of Aragon, and King Alfonso XI of Castile succumbed, and Joan, daughter of
the English king Edward III, died at Bordeaux on the way to her wedding with Alfonso’s son.
Canterbury lost two successive archbishops, John de Stratford and Thomas Bradwardine;
Petrarch lost not only Laura, who inspired so many of his poems, but also his patron, Giovanni
Cardinal Colonna. The papal court at Avignon was reduced by one-fourth. Whole communities
and families were sometimes annihilated.

Family diary (1340/1360) of Florentine merchant Pepo d'Antonio di Lando degli Albizzi, in
which he recorded the deaths of relatives from the Black Death in 1348.
Family diary (1340/1360) of Florentine merchant Pepo d'Antonio di Lando degli Albizzi, in
which he recorded the deaths of relatives from the Black Death in 1348.
The Newberry Library, Ryerson Fund, 1952
Consequences

The consequences of this violent catastrophe were many. A cessation of wars and a sudden
slump in trade immediately followed but were only of short duration. A more lasting and
serious consequence was the drastic reduction of the amount of land under cultivation, due to
the deaths of so many labourers. This proved to be the ruin of many landowners. The shortage
of labour compelled them to substitute wages or money rents in place of labour services in an
effort to keep their tenants. There was also a general rise in wages for artisans and peasants.
These changes brought a new fluidity to the hitherto rigid stratification of society.

Black Death
Black Death
Plague victims during the Black Death, 14th century.
Courtesy of the National Library of Medicine
The psychological effects of the Black Death were reflected north of the Alps (not in Italy) by a
preoccupation with death and the afterlife evinced in poetry, sculpture, and painting; the
Roman Catholic Church lost some of its monopoly over the salvation of souls as people turned
to mysticism and sometimes to excesses.

Anti-Semitism greatly intensified throughout Europe as Jews were blamed for the spread of
the Black Death. A wave of violent pogroms ensued, and entire Jewish communities were
killed by mobs or burned at the stake en masse.

The economy of Siena received a decisive check. The city’s population was so diminished that
the project of enlarging the cathedral was abandoned, and the death of many great painters,
such as Ambrogio and Pietro Lorenzetti, brought the development of the first Sienese school
to a premature end.

Black Death
Black Death
Blessed Bernard Tolomei Interceding for the Cessation of the Plague in Siena, oil on copper by
Giuseppe Maria Crespi, c. 1735.
Active Museum/Alamy
In England the immediate effects of the epidemic of 1349 seem to have been of short
duration, and the economic decline which reached its nadir in the mid-15th century should
probably be attributed rather to the pandemic recurrence of the plague.

The study of contemporary archives suggests a mortality varying in the different regions
between one-eighth and two-thirds of the population, and the French chronicler Jean
Froissart’s statement that about one-third of Europe’s population died in the epidemic may be
fairly accurate. The population in England in 1400 was perhaps half what it had been 100 years
earlier; in that country alone, the Black Death certainly caused the depopulation or total
disappearance of about 1,000 villages. A rough estimate is that 25 million people in Europe
 died from plague during the Black Death. The population of western Europe did not again
reach its pre-1348 level until the beginning of the 16th century.

Black Death
Black Death
A town crier calling for the families of victims of the Black Death to “bring out your dead” for
mass burial.

Controversial dengue vaccine in spotlight

after death of Filipino children
By Lindsay Murdoch

Bangkok: Philippine authorities are investigating the deaths of 14 children vaccinated

in the world's first wide-scale dengue vaccine program amid growing fears about its
safety and anger over its use on 837,000 children.
The administration of former president Benigno Aquino approved use of Dengvaxia
in early 2016 to combat the potentially deadly mosquito-borne virus despite
objections from government experts.
Eric John Vital, 12, holds his vaccination record as he joins other protesters demand
accountability at a rally outside the Department of Health in Manila.
Photo: BULLIT MARQUEZ

President Rodrigo Duterte's administration continued the vaccination drive after he

took office in June 2016 despite a warning from the World Health Organisation.

Health researchers fear the scandal will stoke mistrust in vaccines across the world.

Protesters rally, in Manila last month, against the controversial mass immunisation of
Filipino children with Dengvaxia made by Sanofi Pasteur.
Photo: AARON FAVILA

The Philippines stopped the sale and distribution of Dengvaxia late last year after its
French producer Sanofi Pasteur warned the vaccine could worsen symptoms for
people who had not been previously infected with the virus.

Dengue affects 390 million people globally every year and kills 25,000, mostly in
Asia and Latin America.

The company's disclosure provoked a public furore in the Philippines with some
parents blaming the vaccine for their children's deaths.

The Philippine Department of Health has revealed that at least 53 children who were
given the vaccine still developed dengue "although they recovered or were on their
way to recovery".

Former Philippine President Benigno Aquino at a Senate probe on the controversial

anti-dengue vaccine Dengvaxia last month.
Photo: BULLIT MARQUEZ

The government has assigned an independent panel of experts to investigate the

deaths of the 14 children and report its findings within two weeks.

Health Secretary Francisco Duque told reporters that at least four of the children died
of dengue.
Thomas Triomphe, Asia-Pacific head of Sanofi Pasteur, the manufacturer, prepares to
take his seat at the Philippine Senate probe.
Photo: BULLIT MARQUEZ

"We need to watch out for 837,000 students who have been vaccinated and to us this
is paramount," he said.

One death under investigation is that of 10-year-old Christine Mae de Guzman who
suffered a throbbing headache one day after receiving a second dose of the vaccine.

Protesters wear Guinea Pig masks to condemn the controversial mass immunisation of
Filipino children with Dengvaxia.
Photo: AARON FAVILA

Within days she had died, succumbing to dengue fever.

Christine's school in the province of Bataan, 100 kilometres north-west of Manila,

was one of the first to take part in the vaccination drive.

"Of course we approved of it," Christine's father Nelson de Guzman told reporters. "It
was for health."

The government has said it will sue Sanofi, accusing the pharmaceutical giant of
failing to comply with Philippine Food and Drug Administration (FDA) guidelines.

It is also demanding a refund for $US70 million ($89 million) worth of unused
Dengvaxia stock.

Sanofi maintains the vaccine does not kill people and that the drug is still effective for
people who have previously contracted dengue.

The vaccinated children, aged nine or above, were not tested for previous dengue
infection.

The company said in a statement it has complied with local regulations and FDA
requirements and that it will continue to cooperate in full transparency with Philippine
authorities, and to comply with the country's laws and regulations.
Dr Su-Peing Ng, head of the company's vaccine division, told reporters "there is no
cause for alarm" and "those vaccinated in high-exposure settings are much more
protected than those who were not."

Former president Aquino told a congressional hearing in December that the disease
was a significant enough problem that he met with Sanofi executives twice before
approving use of the vaccine.

More than 200,000 people contracted dengue in the Philippines last year, many of
them children.

Doctors at the Philippine Department of Health had raised concerns over the lack of
long-term safety data on its use before the program was launched.

Duterte has welcomed the investigations.

"If there is a failure let them sort it out," he said.

Dengvaxi has been introduced in 10 other countries but the Philippines is the only one
to launch a mass immunisation drive.

The Brazilian government has said it will continue a trial in Parana, a southern state
hard-hit by dengue epidemics, for children aged older than 15 but it would follow
Sanofi's recommendation to avoid vaccinating people who have never had dengue.

The World Health Organisation, which published guidelines on how to use the
vaccine in 2016, said it did not approve the mass vaccination program.

"This is a decision for governments and governments alone," said Dr Gundo Weiler,
the WHO's representative in the Philippines.

Leonila Dans, an epidemiologist and paediatrician at the University of the Philippines,

has described the vaccination program as devastating for the country, one of Asia's
poorest nations with a population of 100 million.

"Even those who are not vaccinated are very emotional about it, because they feel for
the kids who had the vaccine," she said.

Michel De Wilde, a former senior vice president of research and development at

Sanofi, who oversaw the vaccine's development until he left the company in 2013,
told the New York Times the program was a "huge disappointment and big lesson in
humility."
The company spent decades developing the live-virus vaccine which is administered
in three doses, taken six months apart.
 RELATED ARTICLE

HEALTHCARE

Natural-born killers: mosquito-borne diseases

Add to sh ortlist

Also called break-bone disease, dengue can cause high fevers, headaches, muscle and
joint pains and lingering weaknesses.

Sometimes the disease causes hemorrhage or shock, which can be fatal.

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21

What is Cloning? An exact genetic copy of an

organism (identical twins are natural clones)
Published byModified over 2 years ago

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Presentation on theme: "What is Cloning? An exact genetic copy of an

organism (identical twins are natural clones)"— Presentation
transcript:
1 What is Cloning? An exact genetic copy of an organism (identical twins are natural clones)
2 Two Ways to Do It Artificial embryo twinning Somatic cell nuclear transfer What????????

3 Artificial Embryo Twinning Separate an early embryo into two cells Allow each to divide and
develop on its own Place in a surrogate mother Allow to grow and develop

4 Somatic Cell Nuclear Transfer Somatic cells are cells in the body except the sperm and egg.
Every somatic cell has two sets of chromosomes in a mammal.  Isolate a somatic cell  Transfer
the nucleus to an egg cell that has had its original nucleus removed  The egg cell will develop like a
fertilized zygote (method used to create Dolly the sheep)

5 Dolly Dolly, the first mammal to be cloned from adult DNA, was put down by lethal injection Feb.
14, 2003. Prior to her death, Dolly had been suffering from lung cancer and crippling arthritis.
Although most Finn Dorset sheep live to be 11 to 12 years of age, postmortem examination of Dolly
seemed to indicate that, other than her cancer and arthritis, she appeared to be quite normal. The
unnamed sheep from which Dolly was cloned had died several years prior to her creation. Dolly was
a mother to six lambs, bred the old-fashioned way.

6 Cloned Foods Currently there are only a small number of cloned farm animals in the United
States.  According to a recent Washington Post, there are 150 cloned cows out of 9 million dairy
cows in the United States, which each clone costing about $20,000 to produce. The expense alone
should keep the number down.

7 Draft Risk Assessment Something we could do Copies of the Draft Risk Assessment may be
requested from the Communications Staff (HFV-12), Center for Veterinary Medicine, Food and Drug
Administration, 7519 Standish Place, Rockville, MD 20855, and may be viewed on the Internet at
http://www.fda.gov/cvm/cloning.htmhttp://www.fda.gov/cvm/cloning.htm FDA is seeking comments
from the public on the three documents for the next 90 days. To submit electronic comments on the
three documents, visit http://www.accessdata.fda.gov/scripts/oc/dockets/comments/commentdock
et.cfm?AGENCY=FDA. Written comments may be sent to: Division of Dockets Management (HFA-
305), Food and Drug Administration, 5630 Fishers Lane, Rm. 1061, Rockville, MD, 20852.
Comments must be received by Apr. 2, 2007 and should include the docket number 2003N- 0573.
http://www.accessdata.fda.gov/scripts/oc/dockets/comments/commentdock et.cfm?AGENCY=FDA

8 Genetically Modified Foods and Organisms Genes from different organisms that improve taste
and nutritional value or provide resistance to particular types of disease can be used to genetically
engineer food crops. Uses recombinant DNA technology  What????

9 1996 1 st biotech crops on 7 million acres 2006 = 252 million acres  This is 13% more than in
2005 http://www.bio.org/ataglance/acreage.asp

10 GM Foods In 2003, about 167 million acres (67.7 million hectares) grown by 7 million farmers in
18 countries were planted with transgenic crops, the principal ones being herbicide- and insecticide-
resistant  soybeans, corn, cotton, and canola. Other crops grown commercially or field-tested are 
a sweet potato resistant to a virus that could decimate most of the African harvest,  rice with
increased iron and vitamins that may alleviate chronic malnutrition in Asian countries, and  a variety
of plants able to survive weather extremes. US Department of Energy

11 U.S. Department of Energy Human Genome Program, http://www.ornl.gov/hgmis.

12 Cloning DNA in Plasmids By fragmenting DNA of any origin (human, animal, or plant) and
inserting it in the DNA of rapidly reproducing foreign cells, billions of copies of a single gene or DNA
segment can be produced in a very short time.  DNA to be cloned is inserted into a plasmid (a
small, self-replicating circular molecule of DNA) that is separate from chromosomal DNA.  When
the recombinant plasmid is introduced into bacteria, the newly inserted segment will be replicated
along with the rest of the plasmid. http://www.biology.arizona.edu/

13 Cut DNA with restriction enzyme Join vector and DNA fragment using DNA ligase Recombinant
molecule Introduce recombinant into bacterium image credit: U.S. Department of Energy Human
Genome Program, http://www.ornl.gov/hgmis.

14 Inserting Bt toxin gene into corn Isolate the genetic material in Bt Insert gene into DNA carrier
Vector carrier into the plasmid Plasmid inserts DNA into the corn cell genome Grow your corn! Art by
Jiang Long and Jen Philpot

15 Bt Corn A bacterium, Bacillus thuringiensis, and the gene of interest produces a protein that kills
Lepidoptera larvae (European corn borer). This protein is called the Bt delta endotoxin. Growers use
Bt corn as an alternative to spraying insecticides for control of European and southwestern corn
borer.

16 The Bt gene, from Bacillus thuringiensis, produces a toxin that protects against caterpillars,
reducing applications of insecticides and increasing yields. The glyphosate resistance gene protects
food plants against the broad- spectrum herbicide Roundup, which efficiently kills invasive weeds in
the field.  The major advantages of the "Roundup Ready®" system include better weed control,
reduction of crop injury, higher yield, and lower environmental impact than traditional herbicide
systems.  In 2004, approximately 85% of soy and 45% of corn grown in the U.S. were grown from
Roundup Ready® seed. Most Americans would probably be surprised to learn that more than 60%
of fresh vegetables and processed foods sold in supermarkets today are genetically modified by
gene transfer. http://www.dnalc.org/home.html

17 Taste Testing Soon Wednesday Sam Ball (Guest Speaker) about what we are doing on campus
for sustainability Next exam questions soon too http://vm.cfsan.fda.gov/~lrd/biotechm.html
What Is Breast Cancer?
Breast cancer starts when cells in the breast begin to grow out of control.
These cells usually form a tumor that can often be seen on an x-ray or felt as
a lump. The tumor is malignant (cancer) if the cells can grow into (invade)
surrounding tissues or spread (metastasize) to distant areas of the body.
Breast cancer occurs almost entirely in women, but men can get breast
cancer, too.

Cells in nearly any part of the body can become cancer and can spread to
other areas. To learn more about cancer and how all cancers start and
spread, see Cancer Basics.
Where breast cancer starts
Breast cancers can start from different parts of the breast. Most breast
cancers begin in the ducts that carry milk to the nipple (ductal cancers). Some
start in the glands that make breast milk (lobular cancers). There are also
other types of breast cancer that are less common.

A small number of cancers start in other tissues in the breast. These cancers
are called sarcomas and lymphomas and are not really thought of as breast
cancers.

Although many types of breast cancer can cause a lump in the breast, not all
do. Many breast cancers are found on screening mammograms which can
detect cancers at an earlier stage, often before they can be felt, and before
symptoms develop. There are other symptoms of breast cancer you should
watch for and report to a health care provider.

It’s also important to understand that most breast lumps are benign and not
cancer (malignant). Non-cancerous breast tumors are abnormal growths, but
they do not spread outside of the breast and they are not life threatening. But
some benign breast lumps can increase a woman's risk of getting breast
cancer. Any breast lump or change needs to be checked by a health care
professional to determine if it is benign or malignant (cancer) and if it might
affect your future cancer risk.
How breast cancer spreads
Breast cancer can spread when the cancer cells get into the blood or lymph
system and are carried to other parts of the body.

The lymph system is a network of lymph (or lymphatic) vessels found

throughout the body that connects lymph nodes (small bean-shaped
collections of immune system cells). The clear fluid inside the lymph vessels,
called lymph, contains tissue by-products and waste material, as well as
immune system cells. The lymph vessels carry lymph fluid away from the
breast. In the case of breast cancer, cancer cells can enter those lymph
vessels and start to grow in lymph nodes. Most of the lymph vessels of the
breast drain into:

 Lymph nodes under the arm (axillary nodes)

 Lymph nodes around the collar bone (supraclavicular [above the collar
bone] and infraclavicular [below the collar bone] lymph nodes)
  Lymph nodes inside the chest near the breast bone (internal mammary

lymph nodes)

If cancer cells have spread to your lymph nodes, there is a higher chance that
the cells could have traveled through the lymph system and spread
(metastasized) to other parts of your body. The more lymph nodes with breast
cancer cells, the more likely it is that the cancer may be found in other organs.
Because of this, finding cancer in one or more lymph nodes often affects your
treatment plan. Usually, you will need surgery to remove one or more lymph
nodes to know whether the cancer has spread.

Still, not all women with cancer cells in their lymph nodes develop metastases,
and some women with no cancer cells in their lymph nodes develop
metastases later.

 Written by