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Feline Immunodeficiency Virus (view source)
Revision as of 11:51, 27 August 2010
, 11:51, 27 August 2010→Pathogenesis
==Pathogenesis==
==Pathogenesis==
The pathogenicity of FIV is strain dependent, and can vary widely. For all strains, feline lymphocytes and macrophages are the preferred cells for virus replication, and so FIV disrupts the function of the immune system. FIV gains entry to the cell via feline CD134, a surface molecule, and uses various chemokine receptors as secondary receptors,sup>fmc</sup>. In acute infection, the virus spreads from the site of entry to the lymphoid tissues and thymus, where it first infects T-lymphocytes and the macrophages. Although both CD4+ and CD8+ cells can be infected by FIV and lysed in culture, the virus appears to preferentially destroy CD4+ cells. This intially results in a change in the ratio of CD4+ to CD8+ cells, from roughly 2:1 to less than 1:1<sup>fmc</sup>. After several months of infection, an absolute reduction in CD4+ isa appreciable.
Hosts remain asymptomatic following FIV infection until cell-mediated immunity is disrupted by a decrease in the production of Th1 cytokines. In the advanced stages of infection, humoral immunity is also adversely affected. Although clinical signs are primarily due to changes related to T-cell populations, macrophages are the main reservoir of FIV in infected cats<sup>fmc</sup>. These cells are capable of transporting virus to the tissues of the body, and also suffer impairment of function, such as an increase in the production of TNF. Microglia and astrocytes in the brain, and megakaryocytes in the bone marrow, can become infected with FIV, and co-infection with feline leukaemia virus can increase the expression of FIV in many tissues, including the kidneys, liver and brain.
==Signalment==
==Signalment==