Feline Immunodeficiency virus
By: Emily Nutt
Introduction
Approximately 1.5 to 3 percent of all healthy cats in the United States are infected with Feline Immunodeficiency Virus or FIV. Sick cats are even more likely to contract FIV since they have a 15 percent chance of contracting the virus [2]. FIV is a type of lentivirus, a retrovirus that propagates at a slow pace. This slow propogation causes a huge gap of months to years from when the cat becomes infected with the virus and when it begins to show symptoms. A more widely known lentivirus is that of Human Immunodeficiency Virus or HIV. Unlike HIV, FIV infects cats through biting that occurs during fighting. HIV and FIV infect their host T-cells in a similar manor because they are both retroviruses.
All retroviruses use reverse transcriptase to covert their RNA genome into double-stranded DNA, which is then transcribed and translated to create new virions. These types of viruses carry the protein reverse transcriptase in side the viron instead of an early gene being translated to form the protein. In fact the reverse transcriptase is already bound to the viral RNA with a primer attached before the virus infects the host cell [7]. Like all viruses, retroviruses bind a receptor protein on the host cell and fuse with the host membrane. Once the capsid has been uncoated the RNA is converted to double-stranded DNA through the reverse transcriptase. The new DNA copy then enters the nucleus and integrates into the host genome. At first the viral genome is able to replicate slowly only creating a few virions and thus not directly affecting the host. The host cell’s RNA polymerase and ribosomes create virions through transcription and translation of viral genes. The viruses are assembled and then bud out of the host cell to infect new host cells [7]. After sometime the host cell can then generate a large amount of virions, thus causing the host to show symptoms of immunodeficiency. However it is unknown how this process of rapid viral growth occurs and why viruses like FIV can infect the host for months to years without the host showing symptoms.
The structure and process of lentivirus infections characterizes the three stages of FIV infection. The first stage of FIV is during the first two to four months after infection when the infected cat shows signs of short term illness. The infected cat may show symptoms like increased body temperature, and enlarged lymph nodes [1]. This short term illness could be a result of early and sparse virion replication in the host. In the second stage of FIV, the cat appears completely healthy with no signs of illness. However in the third phase of the illness the cat expresses signs of a compromised immunsystem. Signs of immunodeficiency include; weight loss, inappetence, high body temperature, gingivitis, infected lymphnodes, and abnormal cell growth resulting in tumors [1]. The three stages of FIV are similar to that of the stages of HIV, both stages of infection are characterized by the retrovirus lifecycle. The genome of FIV reveals important viral proteins and thus potential vaccine targets, as well as showing how the virus evolved.. The evolution of the virus explains how both domestic cats and exotic or non-domestic cats were initially infected with FIV. The viral evolution also reveals how the virus has mutated to become specialized for each species of cat. Further analysis of the genome of FIV and how it relates to the evolution of the virus is described below.
The Genome of FIV
All lentiviruses are made up of several key genes; gag, pol, env, rev, orfA and vif. Gag and Gag-Pol create the core of the FIV virion. The gag protein is modified post-transcription to create proteins for the viral matrix, capsid, and nucleocapsid. The pol gene produces a protease, reverse transcriptase, integrase and a protease-like protein. The protease-like protein is not found in primate lentiviruses. However it is found in FIV and maybe used to prevent misincorporation of the viral genome. Other evidence suggests that the protease like-protein is needed for efficient growth of infected T lymphocytes [8]. The vif protein is conserved in both HIV and FIV, and plays a role in the latency of FIV infection in cats. The rev protein functions as a stability and transport of unspliced viral RNA molecules to the nucleus of the host cell. Open reading frame A or orf A is induces host cell arrest at the second gap phase of the cell cylce [3]. Only gag and pol are the genes are in the primary viral genome and it is only after splicing that the other viral genes are expressed.
Splicing plays a key role in the expression of env, rev, orfA and vif genes of FIV. The vif and env genes are created through a single splicing of the primary transcript, while the rev gene arises from multiple splicing events. The figure reveals the different splice sites found for the FIV genome. Part (b) shows the different splice donor sites (SD) and the splice acceptor sites (SA) as well as the spliced mRNA produced from the genome [8]. The numbers by the spliced products reveal the kilo bases of each RNA product. The 4.4 kb mRNA contains both the orfA and env open reading frame. The larger mRNA contains the complete orfA gene [8]. There are two 4.4 kilo base mRNAs in the figure both seem to produce env and orf genes, however the 4.4 kilo bases with a longer orfA mRNA contains the whole gene of orfA. The 1.4 kb mRNA contains the three exons of the rev gene. The mRNA with 5.2 kb contains the vif gene in the larger mRNA product. The 1.7 kb mRNA contains pieces of both orfA and orfB, however the exact products these mRNAs produce is uncertain [8]. Splicing of the viral genome allows for FIV to carry a smaller genome that produces many different genes. The gag and pol genes remain quite conserved throughout different FIV strains, however the other genes vary greatly between different feline immunodeficiency viruses. This difference in env, rev, vif and orfA between types of FIV is due to different splice sites on the viral genome.
Genomic Variation of FIV
Relationship of FIV to other Lentiviruses
Include some current research in each topic, with at least one figure showing data.
Conclusion
Overall paper length should be 3,000 words, with at least 3 figures.
References
Edited by student of Joan Slonczewski for BIOL 238 Microbiology, 2009, Kenyon College.
Include some current research in each topic, with at least one figure showing data.
[edit] Conclusion
Overall paper length should be 3,000 words, with at least 3 figures.
[edit] References
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