Viral Structure/Function

I.

Biology of Viruses
A. Structure 20-300nm
1. Capsid icosahedral vs helical envelope (in some)
2. Nucleic acid (DNA or RNA)
a) If it has BOTH it is not a virus, only have
one type (makes them unique)
3. Size - 20-300nm, some larger
B. Function of major structural units
1. Capsid (nucleocapsid) - Outermost structure
a) An accumulation of proteins that
encloses the nucleic acid
b) Made of subunits called capsomeres
c) Different configurations [most common]
(1) Icosahedral
configuration - benzene ring-like
(2) Helical - long stringy
viruses (Tobacco Mosaic Virus)
d) Purposes (1) Protection of nucleic
acid - Inside is a hunk nucleic acids, they can not survive long in
the environment
(2) On viruses that do not
have an envelope (naked), it will also contain specific receptor
sites for their specific host tissue
(a) Tissue
tropism is extremely important for viruses - not all
viruses will grow on all cells
(b) Recept
or sites that they have in their capsid or envelope make
them unique
(3) May contain other
components that allow the virus to enter its host cell
2. Envelope - a glycoprotein envelope that surrounds the
nucleocapsid
a) A bilayer of lipids, may possibly have
spikes, everything else is inside
b) Envelopes may be created in part by the
host, or may be material from the hosts own membrane that are ripped
off during budding
(1) The lipid containing
viruses, when they mature, tend to leak out and bud, pulling
chunks of the host lipid envelope with them
c) Spikes may contain different types of
compounds
(1) Influenzas - spikes
contain hemagglutinin - causes agglutination of RBCs
(a) H1N1
etc - what does it mean?
(i)
H
- Refers to the specific type of hemagglutinin
(ii)
N
- Refers to neuraminidase (also found in the

envelope)
3. Nucleic acid
a) Can be either DNA or RNA - only one
type
b) Shape
(1) DNA
(a) Animal
viruses tend NOT to be circular - sort of linear
(b) Can be
almost circular
(c) Bacteri
al viruses can be completely circular
c) Structure
(1) Single stranded DNA
(2) Double stranded
circular (very few cases)
(3) RNA single stranded positive or negative sense/polarity
(a) west
nile and polio are positive sense
(4) Segmented RNA - its in
pieces
(a) Exampl
e: Influenza type A has 8 segments, which is how it is
able to stay ahead of vaccines, it is constantly resorting.
(5) Double stranded RNA
(not many)

DNA viruses
Parvoviridae

Fifth disease

papovavirdae

Warts HPV

Adenoviridae

Respiratory, eye, some GI

Adeno 12 and 5 are carcinogenic

hepadnaviridae

Serum hepatitis, Hep B Classic

poxviridae

Small pox size of chlamydia

Herpes

herpes type 1 and 2 Varicella zoster, Epstein barr, cytomegalovirus,Chicken pox

RNA viruses

Viral parthenogenesis

picorna means
little

Polio, coxsackie, echo? Colds CNS GI ENTEROVIRUSES

corono

also common cold, SARS

paramyxo

measles, mumps

Othro myxo

influenza ABC

Arena

ZAR bugs? Lassa fever

Reo virus
double
stranded RNA
viruses

GI disease.. infant diarrhea

toga

Arthropod borne

flavi

Arthropod borne

BUNya

Arthropod borne

Rhabdo

rabies

retro

HIV 1 and 2

4. Viral Genomes
a) Wide diversity
b) Some have only 4 genes, some have
hundreds of genes
c) There may be virus associated
enzymes/enzyme activity which may be carried by the virus or dictated
by the virus for the host cell to make
d) Enzymes
(1) RNA dependent RNA
polymerase - Used for making specific viral RNA
(2) Reverse transcriptase Retroviruses - Can create DNA from RNA
(3) Protein
kinases/phosphatases
(4) Ribonuclease
(5) Neuraminidase - used
by viruses to get out of host cell
(a) Differen
t types
C. What viruses are not:
1. They are not: plants, animals, bacteria, or alive!
D. What viruses are:
1. Quintessential parasite - completely dedicated to their
host
a) Obligate intracellular parasites
b) More so than chlamydia, rickettsia etc.
2. No functions, can not synthesize proteins - devoid of
ribosomes
3. Can not generate or store ATP energy
4. Require their host to pretty much make all of their:

a) Amino acids for structural proteins and

enzymes
b) Need host to make nucleo-proteins (?)
c) Lipids are usually derived from host also
- either made by the host or ripped of the host as it replicates
5. Enzymes
a) Dont generally have enzymes
b) A few do have them:
(1) Contain in their coat
necessary Enzymes for early stages of their growth
(2) Enzymes in their
envelope, many are cell derived
E. Where did they come from?
1. 1930s thoughts:
a) Speculation was that they are an early
form of pro-life
b) Because they are incapable of
surviving without a host, it is unlikely they could have preceded cellular
life!
2. Now
a) Speculated that viruses represent rogue
genetic elements that eventually adopted a parasitic existence
b) May have been bacteria-like organisms
that became more and more dependant on their host until they could not
longer do anything
II.

Classification - Major Virus Families Containing Human Pathogens

A. How many virus families are there?
1. Varies from 12 to 18 to over 20 depending on how they
are grouped
2. We are going to go with 20 families, but:
a) There are are thousands of species
within each families
b) Each species can have up to thousands
of different serotypes
3. Classification is no longer based on symptoms or
where you got it
4. Now based on
a) Structure of genome - DNA? RNA?
Strands?
b) Ultra-Structure of particle - Size
c) Symmetry of the capsid
d) Envelope - or none?
e) Replication type - In cytoplasm? In
nucleus? Both?
f) Genomic sequences themselves are
being used to determine how viruses are related
g) Example: No two hepatitis are actually
in the same group :(
5. Most human viruses are RNA viruses
B. DNA Viruses
1. ssDNA Naked
a) Parvoviridae (Fifth Disease)
(1) Involve B-19, the agent
of Fifth Disease
2. dsDNA Naked

a) Papovaviridae (HPV warts)

(1) Papillomavirus
(2) All warts are generally
caused by these
b) Adenoviridae (Respiratory, conjunctivitis,
GI)
(1) Two of the first cancer
viruses were in this group
3. ds DNA Envelope
a) Hepadnaviridae (HBV Serum
Hepatitis)
(1) Hepatitis B virus sexual transmission or parenterally
b) Herpesviridae (HSV, EB, VZ,
Cytomegalo, etc.)
(1) Herpes 1 & 2, Epstein
Barr, Varicella Zoster
c) Poxviridae (Smallpox, Cowpox,
Molluscum contagiosum)
(1) 300nm, one of the
largest viruses
(2) Same size as chlamydia
C. RNA Viruses respiratory agents
1. ss RNA Naked
a) Picornaviridae (Rhinovirus, Enterovirus,
Hepatitis A virus)
(1) Little RNA virus
b) Caliciviridae (Norovirus, Hepatitis E)
c) Astroviridae (GI disease)
2. ss RNA Enveloped
a) Flaviviridiae (Yellow Fever, West Nile,
Dengue, Hepatitis C) - arthropod borne
b) Togaviridae (WEE, EEE, Rubella) arthropod borne
c) Retroviridae (HIV)
d) Filoviridae (Ebola, Marburg)
e) Coronaviridae (Respiratory (common
cold), GI, SARS)
f) Rhabdoviridae (Rabies)
(1) Bullet shaped viruses
g) Bunyaviridae (Hanta virus, CrimeanCongo hemorrhagic fever) - arthropod borne
h) Orthomyxoviridae (Influenza A-->C)
i) Paramyxoviridae (Measles, Respiratory,
Mumps, Respiratory Syncytial virus, Human metapneumovirus)
j) Arenaviridae (Lassa fever)
3. ds RNA Naked
a) Reoviridae (Respiratory, Rotavirus
(infant diarrhea) GI)
(1) Primarily GI diseases
III.
them

Virus Replication Cycle - they are nothing except things that make other things build
A. Replication cycles
1. Too varied to deal with here
2. The only time knowledge of the cycle is useful if there is

a treatment that is germane to that part (HIV)

3. Basic Steps
a) Infect the host
b) Replicate their parts - proteins,
enzymes, nucleic acids
c) Put everything together into new viruses
and get them out of the cell
d) Goal: Make more viruses and get out
(coughing, diarrhea);
B. Attachment receptor sites
1. First step - sometimes called adsorption
2. Adsorption of virus to the host cell is random - just need
to be in the right place at the right time
a) This is why you need a lot of virus to be
effective
3. Must have the appropriate: ionic conditions, pH,
temperature
4. No energy is needed
5. Attach to a specific specific receptor site that is keyed by
a receptor site on the most external structure of the virus
6. Generally, the receptor sites were not made for viruses,
the viruses has adapted to use a receptor site intended for something else
7. Estimated that every eukaryotic cell has 10^5 virus
binding sites
8. Some viruses use multiple receptor sites - HIV can use
multiple sites on CD4 cells
C. Penetration (translocation)
1. After attaching, the virus needs to get inside the cell
a) If you can stop this from happening, you
can stop the virus from being successful (there are some drugs that can
do this)
2. Methods:
a) Endocytosis - active process where
viruses are taken up in a vacuole
b) Viropexis - passive process of virus
moving through
c) Fuse with the membrane (HIV)
D. Uncoating
1. Nucleic acid within capsid/virus must be released
2. Host removes the lipid envelope/protein coat
E. Macromolecular synthesis
1. Translation of mRNA into virus specific viral proteins
(capsid, nucleic acid) depends on nucleic acid type of parent virus
a) Examples: DNA, SS (+) sense RNA, SS
(-) sense RNA (note: retro covered in Reproductive theme spring)
b) First must create mRNA
(1) For DNA viruses - its
the typical way, very much like any DNA synthesis, DNA makes
messenger RNA just like a eukaryotic system, the host makes it
using the viral DNA as the script
c) Early protein synthesis - regulatory
proteins, DNA replication
d) Late protein synthesis - Virus capsid
2. Usually occurs in the cytoplasm in organelles (?)
3. RNA viruses have positive/minus sense
a) Positive sense ssRNA viruses

(1) Virus genome is already

its own messenger RNA
(2) It is infectious - its all
ready to go and make more viruses
(3) It makes a negative
strand as an intermediate for the production of new positive
sense progeny strands
(4) Cant get a plus from a
plus.
b) Negative sense ssRNA viruses
(1) The RNA is not
considered infectious - a negative strand cant do anything by
itself
(2) It is used as a template
to make mRNA virus protein - host cell makes the RNA
(3) A positive strand is used
as an intermediate to produce negative strand progeny
F. Assembly, maturation and release
1. Maturation - putting together the protein & nucleic acid
to make the virus
a) Coalescing - bringing things together
b) Assembly - occurs in the cytoplasm
c) Release - varies depending on whether
it is enveloped or not
(1) No envelope - release
occurs spontaneously by lysis
(a) Crystalli
ne arrays build up in the host cell
(b) Releas
ed upon lysis of the cell - explosive releasing of 5001000 virus progeny per cell
(c) Inhibitin
g normal metabolic pathways, causing disintegration of
the cytoskeleton and membranes - cell is being primed
for explosion
(2) Envelope - released
more slowly through the process of budding
(a) Takes
longer to kill the host cell, but able to replicate/shed
longer
(b) Each
bud takes a little bit of the host cell with them as part of
the viral envelope
IV.

Prions abnormal, transmissible proteins

A. Non-degradable protein accumulates in brain -> neurological
degeneration CJD, Kuru, BSE (Mad Cow)
B. One theory (of about 10)
1. At its core, a prion is an abnormal/aberrant structure
through folding of a common prion structure that is found mostly in neural cells. It
is a normal, but transmissible agent that can induce other prions, normal ones, to
fold abnormally like they are,
a) Mostly occurs in brain/CNS
b) Damage of abnormal folding &
resistance to degradation causes signs and symptoms
c) Rapidly progressive

d) Frequently fatal
2. Two types

V.

a) PRPC - normal prions

b) PRPSC - abnormal
c) Sequences that make up the two
proteins are identical - exactly the same
(1) only differ by the
method that they are folded
(2) only difference in an
alpha helix vs beta helix
(a) immune
system recognizes it as normal
(b) no
inflammatory or antibody response
d) Pathogenic prions are folded in such a
way that they:
(1) resist normal
digestion by proteolytic enzymes
(2) resist degradation at
high temperatures
(3) tend to aggregate into
filaments - in brain cells, damage form this is thought to cause
symptoms
e) When confronted with abnormal prions,
normal prions are converting into abnormal ones
(1) Amplification effect
f) Introduction of non-biodegradable
material causes the neurological degeneration consistent with all of these
diseases
g) Transmitted by:
(1) direct inoculation into
CNS
(2) transmission by
ingestion
(a) eating
relatives (ewie)
(b) mad
cows
Viral Pathogenesis
A. Basic Steps
1. Infect at Portal of Entry
a) All viruses have at least one portal of
entry
b) Initial site may or may not be the
primary target site
(1) If its a skin virus, the
portal of entry is the skin, but it is also its target
(2) For something like
Polio, the portal of entry is GI, but its target is neural tissue
(3) Viruses may need to
travel a significant distance to get to target
2. Replication at Portal of Entry
a) Must replicate at that site
3. Dissemination to Principal Target, Replication, Shedding
a) Spread to nearby sites/target site
b) At the target site, you begin to see signs

and symptoms associated with the disease

c) Prodromal symptoms - non-specific,
precedes the attack on target tissue
d) Shedding - how they get out of host,
deeper in the target site is, the more interesting their ways of getting out
e) 50% or more of viral infections are
subclinical - didnt know you had them or have very slight symptoms
(immune system works pretty well)
(1) Inapparent infection - its
there but you don't know its happening
(2) Apparent infection usually most infectious
(3) People who dont look
sick can still be shedding viruses asymptomatically
B. Factors Affecting Pathogenesis
1. Target Accessibility
a) Are there physical barriers between
portal of entry and desired target?
(1) Mucous membranes?
(2) Distance?
(3) Tissues that resist
viruses?
(4) What are the defense
mechanisms of the host?
2. Target Cell Susceptibility
a) How susceptible/welcoming is the host
cell to propagation of the viruses?
(1) Some cells wont
replicate viruses
b) Do they have attachment sites?
c) correct intracellular environment
3. Virus Susceptibility to Defenses
a) Some viruses are good at evading
defenses, some arent
4. Natural selection prefers somewhat less virulent strains
a) not good to kill your host
b) Worst microbial pathogens tend to be
animal pathogens to which we have not well adapted
c) Viruses that kill people reach a dead
end, less virulent viruses can continue replicating and shedding
5. Disease only happens if/when the virus has replicated
sufficiently to damage essential cells which do not grow back very quickly
a) Release of toxic products from infected
tissues as a part of inflammatory response
b) Very often the major signs and
symptoms are manifestations of the immune response
C. Outcomes of Viral Infection
1. Acute Infection:
a) Progeny are produced through multiple
rounds of replication
b) Significant cell death at portal & target
site
c) Millions of progeny are produced over a
short period of time
d) Immune system eventually catches up
and eliminate the virus, or you die

2. Latent Infection
a) Occurs with some DNA virus
b) Progeny viruses are not produced
c) Virus DNA will persist within the host cell
- immortalized by replicating with the host cell
(1) chromosomal bodies
d) At some point, they can be reactivated stress, immune problems
e) Retroviruses - process can lead to more
serious consequences
(1) Malignancy
3. Chronic Infection
a) Progeny will continue to be made
throughout the period of chronic infection in reduced numbers
(1) Originally release
without harm to the host
(2) Takes a long time for
damage to accumulate
(3) Hepatitis B virus
D. Host Cell Pathogenesis
1. direct vs indirect damage
2. How to damage the cell?
a) Not by depriving of nutrients, exposing
to toxins, etc. like bacteria
3. Direct damage
a) The damage is a result of disrupting of
normal host cell pathways
b) Virus replication will steal many
macromolecular components and energy that would be used for making
the cells own processes
(1) The cells resources are
committed to making viruses
(2) Competition for
ribosomes - viruses seem to have dominance
(3) Competition for
promoters
4. Indirect damage
a) When viruses enter the host cell
genome, may induce mutations
b) General inflammatory response of the
host causing damage to cells
E. Tropism
1.
a) Certain viruses will only infect certain
cells
2. Determining Factors
a) Presence of receptor sites needed for
attachment
b) Particular cell transcription factors that
recognize specific viral promoters
(1) Hosts ability to support
replication of the virus
c) Physical barriers - inaccessible tissue,
temperature, pH, enzymes
(1) Rhinovirus - specifically
grow in upper respiratory, grow best in slightly reduced

temperature/pH - wont grow in gut, too warm, too low pH

(2) Rabies - attaches to
acetylcholine receptors & salivary glands
3. Examples by type (?)
F. Infection spread Sequence
1. Portal of Entry (POE)
a) routes
(1) airborne, droplets,
direct contact, GI tract (fecaloral), contact with lesions,
blood and body fluids, insect viruses, fomites
b) endogenous vs exogenous virus
(1) Endogenous - latent
viruses that are living within us
(a) Can be
reactivated to an infectious form like herpes
(b) Variable
s that affect the outcome
(i)
D
ependent on the original virus dose
(a)
N
ot really known how many viruses it
takes to get a disease
(b)
M
ay vary from person to person
depending on their immune system
(c)
U
sually need a bunch to get infected but
some viruses need less (influenza ~ 10)
(ii)
I
nfectivity of the virus
(iii)
V
irulence
(iv)
W
here the location of implementation took place
(2) Exogenous - get them
from somebody else
(a) Most
infectious viruses are acquired this way
c) congenital
2. POE replication and spread
a) Can spread to adjacent cells, local
infection at point of entry
b) Can spread beyond adjacent cells to
further places extracellularly, through lymphatics, through mucous
membranes
c) Establishment at the point of entry may
be followed by continual replication and shedding
3. Dissemination from POE
a) Disseminate

(1) Want to get to a discrete

other location besides the POE
b) viremic vs neural
(1) Viremia - viruses have
entered the blood, cant really do anything in there, nothing to
attach to
(a) Princip
al mode of dissemination by virus
(b) progen
y diffuse Lymphatics blood stream target
organ
(c) If they
get to the target organ they start replicating
(d) If they
kill enough cells, you start to see the typical signs and
symptoms, and shedding starts to take place
(2) Neural - only happens
in a few viruses, rabies, etc.
(a) Virus
spreads through axons and dendrites in the neural
system
(i)
S
hielded from antibodies and immune response,
as well as antivirals
(b) Some
are bizarre - Rabies must go from neural tissue back to
salivary glands where it is shed from the body, must be
transmitted through infected bites
4. Incubation (usually 1-3 days,some longer)
5. Replication in Target organ
6. Shedding
a) Most frequent exits
(1) Respiratory - coughing,
sneezing, talking, etc.
(2) GI tract - feces
7. Congenital Infections
G. Host Defense Factors
1. Innate
a) Inflammation, cytokines, interferons
2. Cell-mediated
a) Most important antiviral factor
b) Lymphocytes are good at attacking virus
infected cells
3. Humoral
4. Antibodies have little role in stopping an acute viral
infection - takes time to generate them
5. Interferons are natural antiviral materials synthesized
by cells that have become infected by viruses
a) May non-specifically inhibit viral
replication
b) May make proteins that inhibit
replication
6. Evasion of Immune Response
a) HIV - Replicates in macrophages and Tlymphocytes, the cells that would kill them

b) May avoid action of T-lymphocytes by

blocking antigen processing
c) May express glycopeptides that interfere
with interferon actions
H. Diagnostic Considerations
1. Virus antigen detection kits
a) ELIZA
b) Lateral flow - immunochromatographic
assay
c) PCR - expensive
(1) Inexpensive PCR kits
are a work in progress
2. Tissue cultivation typically not used anymore
I. Antiviral Treatment - next time, but heres a few things he said
1. Lots of different treatments that all do similar things
2. Do one thing to one virus at one part of its replication
cycle
3. Also drugs that interfere with DNA polymerase, or
attaches to viral DNA to make it not make sense
4/6/15
4. DO NOTHING TO THE INITIAL INVADING
ORGANISMS
5. should not do damage to the host
6. hard to tease apart processes that are only viral vs. only
host because they depend on the host processes
J. Anti viral groups
1. virucides
a) will directly inactivate
b) not really good treatment methods
c) good for surfaces or skin
d) outside/ external use
2. Immunomodulators
a) antibodies from someone else
b) subtle and success is variable
3. Antivirals
a) inhibit portion of replication
(1) virus specific events
(a) to stop
attachment, uncoating, generation of progeny viral DNA
or RNA
(b) most
common target is nucleic acid synthesis via interacting
with DNA polymerase
(c) work
best but often not needed in immunocompetent
(d) do not
work against latent viruses...must be actively replicating
K. Primary Antiviral targets
1. HIV
2. influenza
3. Herpes
4. hep b and c
5. rsv

6. picorna
7. papilloma
a) like you see with bacteria viruses can
become resistant to antiviral agents
(1) viral resistance
increases with use just like bacteria and antibiotics
(a) hypothe
sis of natural resistance that already exsist
(b) spontan
eous mutations can occur during drug exposer
(i)
j
ust by a single mutation this can occur easily
L. Risk factors
1. high virus load that starts replicating right away
2. infection over a long period of time with rapid replication
3. high intrinsic mutation rate
4. antiviral target that can be easily mutated by virus
without being detrimental
5. exposed to prolonged or repeated antiviral treatment
6. immunocompromised patient
a) due to prolonged and repeated
treatment
M. Anti-influenza drugs (shows influenza replication cycle)
1. Amantadine / Rimantidine
a) block uncoating
(1) the infecting RNA is not
released from coating...thats all it does...just stops it!!!
(a) aside:
not used very much
b) first group
2. Oseltamivir (Tamiflu) or zanamivir
a) neuraminidase inhibitors
(1) needs neuraminidase to
get out
(a) cant
get out
(i)
m
ust use within 48 hours early not once roaring
sick
(ii)
s
hortens fever and reduces risk of death with
hospitalized patients
N. Anti-retroviral agents
1. Used with HIV
2. replication cycle stopping points /GROUPS
a) attachment/ binding AND fusion
(1) binding via??
(2) fusion via GP 41
b) Reverse transcription
(1) reverse transcriptase
inhibitors
(a) NRTI/Nt
RTI

(i)
a
nalogs that competitively inhibit reverse
transcriptase with other nucleosides
(b) NNRTI
non nucleoside RTI
(i)
n
on competitive...inhibit the RT directly
c) integration
(1) must become a part of
the host chromosome via integrase
(a) integras
e inhibitors
(i)
p
revent insertion into host genome
(a)
r
altegravir
d) Maturation
(1) cleavage carried out by
a protease must work right to have proper surface proteins
(a) inhibit
the protease that have bad surface proteins that cant
attach.
O. Nucleoside analogs
1. inhibit viral DNA polymerase
2. block viral progeny DNA change as chain terminators
a) acyclovir group
(1) deoxy guanosine /
guanosine analogs
(a) produc
e triphosphate that inhibits DNA ploymerase
(b) or acts
a chain terminator
(i)
f
or herpese 1 and 2
(ii)
v
ericella zoster
(iii)
c
mv
b) Adefovir
(1) adenosine analog
metabolized to a di phosphate
(a) competi
tive inhibitor of RT (BONUS)
(i)
u
sed with HEP B
(a)
n
ot as good a vaccine but not a bad

treatment
c) Cidofovir
(1) competitive inhibitor of
DNA polymerase as a di phosphate
d) Ribavirin
(1) it doesnt not work...data
is poor
(2) guanosine analog
(a) different
(i)
i
nhibits formation of RNA
(ii)
c
an cause a lethal mutation in the RNA genome
(a)
v
ery effective against some
(i)
R
SV parimyxo?
e) Foscarnet
(1) noncompetively inhibits
DNA polymerase
(a) HIV no
very effective though
(b) primary
certain herpes type 1 and 2 resistant to acyclovir
f) Docosanol
(1) not directly virucidal
(a) against
herpes?
g) Sofosbuvir
(1) inhibits Hep C RNA
polymerase
(2) gets incorporated into
new HCV RNA
(a) termina
tion of DNA syn
(b) only
active against viruses BIG +
(c) used in
conjuction of alph interferon or ribavirin
(d) 12
week course $84,000 24 week recommended $168,000
P. interferons
1. are a type of cytokine
2. have properties
3. induction by the prescence of viruses
4. they themselves are not anti viral
a) biochemical changes cause antiviral
proerties
b) effector protiens induce virus
resistance.
c) linked to signaling pathways that
upregulate interferon genes

(1) inhibit virus replication

processes
(2) dont use interferon
treatment to the extreme because overstimulation of cytokines is
not good
5. Types
a) I
(1) alpha or Beta
(a) Principl
e antiviral interferons!!!
(2) gamma and lambda
(a) immuno
regulation
(i)
m
VI.
VII.

ediation of immune system

Viral infections in humans
A. we skipped this?
Viral Respiratory Agents
A. common viral agents of resp infections
1. picorna
a) Enteroviruses Uri agents
(1)
b) Rhinoviruses A--> C
(1) non specific URIs upper
resp infections
(a) best
known for this
(2) common cold
(3) differs from enterovirus
via
(a) replicat
e at 33 degrees C upper nasal passages
(b) not
viable in stomach pH
(4) hundreds of serotypes
(5) between march and
october most infections...there is no time that you cant get a cold
(6) transmission
(a) direct
contact to nose or eye
(b) nasal
secretions
(c) contami
nated environmental object
(d) They
are naked viruses so they can hang around a while on
surfaces
(e) mainly
from the person next to you with the common cold
2. corona
a) common cold and have come a lot
further
(1) ssRNA

(2) ENVELOPED
(3) bigger 80- 90 nm 3X the
size
(4) mainly pathogens of
URT of humans and animals
(5) during peak infection
35% of etiological agents (dont know what that means)
(a) 15% of
diagnosed common colds
(b) alpha
and beta are the common ones
(i)
b
eta= SARS and MERS and a few others
(ii)
S
ARS virus
(a)
t
hought to be a recombinant of a
mammalian and avian
(b)
p
otential to be more virulent in a human
host
(i)
m
ore likely to see systemic
spread
(ii)
p
neas? pneumona and death
(c)
n
ot easily transmitted from person to
person but rather animals
(d)
P
CR tests
(iii)
M
ERS
(a)
2
012 thought is originated in egyptian
tomb bats..and carried by mammals
(b)
m
ost who get MERS have acute resp.
problems
(c)
E
ASILY TRANSMITTED PERSON TO
PERSON
(d)
N

o specific treatment
(i)
b
ut approved the use of rabirovin
but not very effective
3. Enterovirus D68
a) asthma patients have issues because of
URIs
4. coxsackie and echo
a) URI
b) coxsakie A herpengina
(1) ulcers closest to
diagnosis you can get
5. manifestations of common cold
a) can be as early as 12 hours?
b) can last 7-12 days
c) symptoms
(1) nasal dryness (first
things to be noticed) and other nasal stuff...
(2) sore throat sometimes
(3) headache
(4) ear and facial pressure
(5) loss of taste and or
smell
(6) cough so hard they
puke (posttussive vomiting)
(7) hoarseness
(8) fever (not common)
infants and toddlers more common for fever and just runny nose
(a) school
age children, nasal congestion cough runny nose
(i)
a
side: only 1 to 2 percent of colds will progress
into worse secondary bacterial infections
(ii)
v
iruses can cause sinusitis and otitis media more
commonly than bacteria
(iii)
e
xacerbation of asthma
(iv)
v
irus isolation is not done for common colds
(v)
t
reatments ...nasal decongestants
6. Negative sense RNA viruses?
a) paramyxo
(1) RSV
(a) leading
cause Resp. infections in children and
BRONCHIOLITIS!!!!!
(2) treatment is
symptomatic

b) orthomyxovirus
(1) influenza A-->C
(a) 8
DIFFERENT SEGMENTS OF DNA AND THIS CAUSES
THE CONTINUEOUS PROBLEM OF
CHANGE/MUTATION IN INFLUENZA
(i)
t
his is why influenze is still here and not
eradicated
(b)
Mutation
(i)
a
ntigenic DRIFT= small few amino acids
(a)
c
ontinuous mutations
(b)
w
hy we get annual flu shots
(ii)
a
ntigenic SHIFT= abrupt major
(a)
u
sually changes in N or H pieces that
make it a new flu
(i)
H
1N1
(ii)
f
requently pandemics
(iii)
a
nimal genes in there
(iv)
A
LL TYPE A!!!!
(c) peak flu
time Oct to april
(d) complic
ations
(i)
s
econdary bacterial pneumonia PNUEMONIAS
INGENERAL
(e) identify
(i)
v
ia lateral flow
(ii)
A
infects animals...B we care about no animals
too...C we dont care and no animals

(iii)
A
ll SHIFT=A
(f) H5=AVI
AN
(i)
H
5N1 found...some incidence of human infection
and include resp. failure
(ii)
r
equire close contact with poultry...not readily
between humans
(iii)
f
ear that human human transfer will become
possible
(g) swine
H1?
(i)
r
est of virus is human
(ii)
R
EADILY SPREADS BETWEEN HUMANS
(h) Aside:
current 2014- 2015 trivalent
(i)
A
/ California H1N1
(ii)
A
/Texas H3N2
(iii)
B
/ mass H? N? 3 2?
(iv)
q
uad B/ brisbane H?N? 3 2?
(a)
o
nly 23% effective because H3N2 and its
constant small antigenic drifts
(b)
d
oes not mean that it is no good
(c)
B
s are not as variable and H1N1 not as
variable
7. non enveloped dsDNA virus icosahedral
a) Adeno
(1) causes
(a) conjunc
tivitis
(b) cancer

(c) GI
(d) childho
od pneumonias
(2) symptoms
(a) conjunc
tivitis
(i)
p
ink eye
(3) diagnosis
(a) not
persued
(4) treatment
(a) no
approved treatment
b) Parvo
(1) B19 fifth disease
(a) why
fifth
(i)
1
st measels
(ii)
2
nd scarlet fever
(iii)
3
rd rubella
(iv)
4
th disease was probably staph scalded skin
Flatow
(v)
5
th erythema
(vi)
6
th roseola infantium HHV6/7
(b) childho
od erythema
(i)
t
runk and face
(ii)
can happen in pregnant women transfer to fetus
and death of fetus due to premature rupture..and
miscarriage
(iii)
p
regnant women should look out for listeria and
plasmodium...parvo can be bad too
B. Viral gastroenteritis vs. Enterocolitis
1. GE
a) non inflamm infection of stomach small
bowel duodenum of colon

(1) watery violent volume

not being absorbed
(2) maybe toxin
(3) the worry of dehydration
aka cholera
2. EC
a) inflamm infection of distal small intestine
and colon
b) most viral
(1) viruses do attack cells
but white cells respond
c) tend to be systemic
(1) typhoid and listeriosis
3. aside: diarrhea
a) anything that isn't a brick this definition
varies
b) 90% of diarrhea is caused by infectious
agents

c) ????turkey trots?