Rabies virus

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This article is about the virus. For the disease, see Rabies. For other uses, see Rabies
(disambiguation).

Rabies

Virus classification

Group: Group V ((-)ssRNA)

Order: Mononegavirales

Family: Rhabdoviridae

Genus: Lyssavirus

Species: Rabies

TEM micrograph with numerous rabies virions (small dark-grey rod-like particles) and Negri
bodies (the larger pathognomonic cellular inclusions of rabies infection)

The rabies virus is neurotrophic virus that causes fatal disease in human and animals. Rabies
transmission can occur through the saliva of animals.
The rabies virus has a cylindrical morphology and is the type species of the Lyssavirus genus of
the Rhabdoviridae family. These viruses are enveloped and have a single stranded RNA genome
with negative-sense. The genetic information is packaged as a ribonucleoprotein complex in
which RNA is tightly bound by the viral nucleoprotein. The RNA genome of the virus encodes
five genes whose order is highly conserved. These genes code for nucleoprotein (N),
phosphoprotein (P), matrix protein (M), glycoprotein (G) and the viral RNA polymerase (L).[1]

All transcription and replication events take place in the cytoplasm inside a specialized “virus
factory“, the Negri body (named after Adelchi Negri[2]). These are 2–10 µm in diameter and are
typical for a rabies infection and thus have been used as definite histological proof of such
infection.[3]

Contents
[hide]

 1 Classification
 2 Structure
 3 Genome
 4 Life cycle
 5 Infection
 6 References

[edit] Classification
The rabies virus is a member of the Lyssavirus genus. This genus of RNA viruses also includes
the Aravan virus, Australian bat lyssavirus, Duvenhage virus, European bat lyssavirus 1,
European bat lyssavirus 2, Irkut virus, Khujand virus, Lagos bat virus, Mokola virus and the
West Caucasian bat virus. Together with the Vesiculovirus and others they form the
Rhabdoviridae family.

[edit] Structure
Lyssaviruses have helical symmetry, so their infectious particles are approximately cylindrical in
shape. They are characterized by an extremely broad host spectrum ranging from plants to
insects and mammals; human-infecting viruses more commonly have cubic symmetry and take
shapes approximating regular polyhedra.

The virus has a bulletlike shape with a length of about 180 nm and a cross-sectional diameter of
about 75 nm. One end is rounded or conical and the other end is planar or concave. The
lipoprotein envelope carries knob-like spikes composed of Glycoprotein G. Spikes do not cover
the planar end of the virion (virus particle). Beneath the envelope is the membrane or matrix (M)
protein layer which may be invaginated at the planar end. The core of the virion consists of
helically arranged ribonucleoprotein.

[edit] Genome
The genome is unsegmented linear single stranded RNA with negative-sense. The genetic
information is packaged as a ribonucleoprotein complex (RNP) in which RNA is tightly bound
by the viral nucleoprotein. The RNA genome of the virus encodes five genes, namely the genes
for nucleoprotein (N), phosphoprotein (P), matrix protein (M), glycoprotein (G) and the viral
RNA polymerase (L). The order 3'-N-P-M-G-L-5' of these genes is highly conserved.[1]

[edit] Life cycle

Viral life cycle

 Life cycle
 Entry
 Replication
 Shedding
 Latency

After receptor binding, rabies virus enters its host cells through the endosomal transport
pathway. Inside the endosome, the low pH value induces the membrane fusion process, thus
enabling the viral genome to reach the cytosol. Both processes, receptor binding and membrane
fusion, are catalyzed by the glycoprotein G which plays a critical role in pathogenesis (mutant
virus without G proteins cannot propagate).[1]

The next step after entry is the transcription of the viral genome by the P-L polymerase (P is an
essential cofactor for the L polymerase) in order to make new viral protein. The viral polymerase
can only recognize ribonucleoprotein and cannot use free RNA as template. Transcription is
regulated by cis-acting sequences on the virus genome and by protein M which is not only
essential for virus budding but also regulates the fraction of mRNA production to replication.
Later in infection, the activity of the polymerase switches to replication in order to produce full-
length positive-strand RNA copies. These complementary RNAs are used as templates to make
new negative-strand RNA genomes. They are packaged together with protein N to form
ribonucleoprotein which then can form new viruses.[3]
[edit] Infection
From the wound of entry, the rabies virus travels quickly along the neural pathways to the central
nervous system (CNS). The retrograde axonal transport of the rabies virus to the CNS is the key
step of pathogenesis during natural infection. The exact molecular mechanism of this transport is
unknown although binding of the P protein from rabies virus to the dynein light chain protein
DYNLL1 has been shown[4]. P also acts as an interferon antagonist, thus decreasing the immune
response of the host.

From the CNS, the virus further spreads to other organs. The salivary glands located in the
tissues of the mouth and cheeks receive high concentrations of the virus, thus allowing for it to
be further transmitted. Fatality can occur within anywhere from two days to five years from the
time of initial infection.[5]

[edit] References
1. ^ a b c Finke S, Conzelmann KK (August 2005). "Replication strategies of rabies virus". Virus
Res. 111 (2): 120–31. doi:10.1016/j.virusres.2005.04.004. PMID 15885837.
2. ^ synd/2491 at Who Named It?
3. ^ a b Albertini AA, Schoehn G, Weissenhorn W, Ruigrok RW (January 2008). "Structural aspects
of rabies virus replication". Cell. Mol. Life Sci. 65 (2): 282–94. doi:10.1007/s00018-007-7298-1.
PMID 17938861.
4. ^ Raux H, Flamand A, Blondel D (November 2000). "Interaction of the rabies virus P protein
with the LC8 dynein light chain". J. Virol. 74 (21): 10212–6. doi:10.1128/JVI.74.21.10212-
10216.2000. PMID 11024151. PMC 102061. http://jvi.asm.org/cgi/pmidlookup?
view=long&pmid=11024151.
5. ^ "Rabies". University of Northern British Columbia.
http://www.unbc.ca/nlui/wildlife_diseases_bc/rabies.htm. Retrieved 2008-10-10.
Viral life cycle
From Wikipedia, the free encyclopedia
Jump to: navigation, search
Viral life cycle

 Life cycle
 Entry
 Replication
 Shedding
 Latency

Viruses are similar to living organisms, however there are differences. One of the ways a virus
can be seen as living is that a virus needs to replicate and create progeny. However, unlike other
organisms, a virus cannot survive on its own. It is only active when replicating within a host,
using a hosts' resources and food. Once inside a host, a virus's sole purpose is to make as many
copies of itself, and infect other host cells; everything it does is to benefit its fitness and increase
the number of its offspring.

Contents
[hide]

 1 Overview
 2 Exposure of host
 3 Viral Entry
 4 Viral replication
 5 Viral shedding
 6 Viral latency
 7 References

[edit] Overview
As stated above, the viral life cycle is dependent on a host cell. A virus is unable to replicate on
its own or use "raw" materials on which to survive. Hence a virus will remain dormant until it is
able to infect the next host, activate and replicate. Some viruses can live in an open environment
for a short time, in some cases, only a few hours. Therefore, viruses use the most efficient
method to locate a host, create progeny, and spread to other hosts[1].

[edit] Exposure of host

Usually viral infection occurs when a virus enters the host, either:

 through a physical breach (a cut in the skin)

 direct inoculation (e.g.mosquito bite[2])
 direct infection of the surface itself (inhalation of the virus into trachea[3])

It is usually only after a virus enters a host that it can gain access to possible susceptible cells.

[edit] Viral Entry

Main article: Viral entry

In order for the virus to reproduce and thereby establish infection, it must enter cells of the host
organism and use those cells' materials. In order to enter the cells, proteins found on the surface
of the virus interact with proteins of the cell. Attachment, or adsorption, occurs between the viral
particle and the host cell membrane. A hole forms in the cell membrane, then the virus particle or
its genetic contents are released into the host cell, where viral reproduction may commence.

[edit] Viral replication

Main article: Viral replication

Next, a virus must take control of the host cell's replication mechanisms. It is at this stage a
distinction between susceptibility and permissibility of a host cell is made. Permissibility
determines the outcome of the infection. After control is established and the environment is set
for the virus to begin making copies of itself, replication occurs quickly.

[edit] Viral shedding

Main article: Viral shedding

After a virus has made many copies of itself, it usually has exhausted the cell of its resources.
The host cell is now no longer useful to the virus, therefore the cell often dies and the newly
produced viruses must find a new host. The process by which virus progeny are released to find
new hosts, is called shedding. This is the final stage in the viral life cycle.
[edit] Viral latency
Main article: Viral latency

Some viruses can "hide" within another cell, either to evade the host cell defenses or immune
system, or simply because it is not in the best interest of the virus to continually replicate. This
hiding is deemed latency. During this time, the virus will not produce any progeny, it will remain
inactive until external stimuli (such as light or stress) prompts it into activation.

[edit] References
1. ^ N.J. Dimmock et al. "Introduction to Modern Virology, 6th edition." Blackwell Publishing,
2007.
2. ^ Bureau for Public Health Division of Surveillance and Disease Control. "Take precautions
against mosquitos, dead birds to prevent West Nile, encephalitis viruses." W V Med J. 2005 Mar-
Apr;101(2):90.
3. ^ Quan FS, Compans RW, Nguyen HH, Kang SM. "Induction of Heterosubtypic Immunity to
Influenza Virus by Intranasal Immunization." J Virol. 2007 Nov 21