Pathology
The virus gains entry to the host’s cells through the interaction of the envelope glycoproteins (from the glycoprotein env) of the virus and the target cells’ surface receptors. First the SU glycoprotein binds to CD134, a receptor on the host cell. This initial binding changes the shape of the SU protein to one that facilitates interaction between SU and the chemokine receptor CXCR4. This interaction causes the viral and cellular membranes to fuse, allowing the transfer of the viral RNA into the cytoplasm where it is reverse transcribed and integrated into the cellular genome through non-homologous recombination. Once integrated into the host cell’s genome, the virus can lay dormant in the asymptotic stage for extended periods of time without being detected by the immune system or can cause lysis of the cell. (4,5)
CD134 is predominately found on activated T cells and binds to OX40 ligand causing T-cell stimulation, proliferation, activation, and apoptosis (3). This leads to a significant drop in cells which have critical roles in the immune system. Low levels of CD4+ and other affected immune system cells cause the cat to be susceptible to opportunistic diseases once the disease progresses to feline acquired immune deficiency syndrome (FAIDS).
Read more about this topic: Feline Immunodeficiency Virus
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—Bronislaw Geremek (b. 1932)