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Virus latency (or viral latency) is the ability of a pathogenic virus to lie dormant within a cell, denoted as the lysogenic part of the viral life cycle. A latent viral infection is a type of persistent viral infection which is distinguished from a chronic viral infection. A latent infection is a phase in certain viruses life cycles in which after initial infection, virus production ceases. However, the virus genome is not fully eradicated. The result of this is that the virus can reactivate and begin producing large amounts of viral progeny without the host being infected by new outside virus, denoted as the lytic part of the viral life cycle stays within the host indefinitely.
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Episomal latency refers to the use of genetic episomes during latency. In this type, viral genes are floating in the cytoplasm or nucleus as distinct objects, both as linear or lariat structures. Episomal latency is more vulnerable to marauding ribozymes or host foreign gene degradation than provirus latency. Examples include the family herpesviridae, exemplified by the Herpes simplex virus which undergoes episomal latency in neuron cells and leaves linear genetic material floating in the cytoplasm.
Advantages include the fact that the virus does not need to enter the nucleus, and hence may avoid ND10 domains from activating interferon via that pathway. Also, episomal latency is far easier to maintain and reactivate than proviral latency.
Proviral latency begin with the virus genome integrates into the host genome, effectively become a provirus. This requires that the viral gene get into the nucleus and insert itself into the host genome, the family of which exemplifies this behavior being the Retroviruses. For example, the Retrovirus, HIV, enters the nucleus and inserts its gene between Long Terminal Repeats using integrase and remains within the hosts own gene.
Advantages include automatic host cell division results in replication of the viruses gene, and the fact that it is near impossible to remove an integrated provirus from an infected cell without killing the cell.
Disadvantages include the need to enter the nucleus (and the need for packaging proteins that will allow for that) and increased difficulty in maintaining the latency.
Both proviral and episomal latency may require maintenance for continued infection and fidelity of viral genes. Latency is generally maintained by viral proteins in order to keep the viral genes from being digested by marauding cellular ribozymes or being found out by the immune system, as well as keeping the gene in good condition. Certain proteins may also inhibit apoptosis or induce cell growth and division to allow more copies of the infected cell to be produced.
Latency can be maintained without the need of proteins and an interesting example of this are the endogenous retroviruses. Generally these types of viruses have been highly evolved with the hosts immune system to be able to survive without the need of any immune system modulating maintenance proteins.
While viral latency exhibits no active viral shedding nor causes any pathologies or symptoms, the virus is still able to reactivate via external activators (i.e. sunlight, stress) to cause an acute infection. In the case of Herpes simplex virus, which generally infects an individual for life, a serotype of the virus reactivates occasionally to cause cold sores. The sores are quickly resolved by the immune system, however may be a minor annoyance from time to time. In the case of varicella zoster virus, after an initial acute infection (chickenpox) the virus lies dormant until reactivated as herpes zoster.
More serious ramifications of a latent infection could be the possibility of transforming the cell, and forcing the cell into uncontrolled cell division. This is a result of the random insertion of the viral genome into the hosts own gene and suppression of host cellular growth factors for the benefit of the virus. A famous event of this actually happening with gene therapy through the use of retroviral vectors is the Necker Hospital in Paris, where 8 young boys received treatment for a genetic disorder, after which 4 developed leukemia.
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Virus_latency". A list of authors is available in Wikipedia.|