Once an animal has become infected with FIV the viral particles replicate in T-lymphocytes (CD4+ and CD8+), B-lymphocytes, macrophages and astrocytes (11). This results in an accumulation of virus particles in the lymphoid organs such as the thymus, spleen and lymph nodes. Peak viremia occurs several weeks after the initial infection. Following this peak virus concentration the number of viral particles decreases as the host develops an immune response to the virus.  CD8 + T cell mediated immunity are responsible for viral suppression. The cat now enters the sub clinical phase of disease where it appears healthy but the virus continues to replicate and infect cells. CXCR4 is the receptor on the cell that the virus targets (6). Progression of the disease results in a generalized impairment of the immune system mainly from a decrease in the number of CD4+ cells of T-lymphocytes (11).

 T Cells and Macrophages

Impaired immune function also occurs due to:


-         inability for lymphocytes to proliferate when stimulated by B and T cells

-         impaired priming of T cells by T cell mitogens

-         lymphocytes may have decreased or altered cell surface molecule expression

-         (decreased amplification or control of immune response)

-         altered production of cytokines (increased interferon, tumor necrosis factor, interleukin 4,6,10,12) often resulting in more severe clinical signs during infection (6)

-         Altered function of the neutrophils (11)


The humoral immune response remains functional by responds with polyclonal gammopathy due to B- cell stimulation. (11)


Altered neurological function may not be associated with direct infection but rather abnormal CNS cell metabolism and function making it susceptible to oxidative damage leading to mitochondrial membrane disturbance. Mitochondrial damage impairs the cell from maintaining normal concentration gradients such as intracellular calcium concentrations.(6)

Gross pathologic lesions are not usually present due to primary viral effects but rather, lesions that are present are usually associated with the secondary disease processes. However, kittens infected with FIV can have early thymic depletion or progressive infection the thymus architecture becomes obliterated and minimal function thymic tissue remains.(13)