FELINE IMMUNODEFICIENCY VIRUS PATHOGENESIS
Pathogenesis of FIV is not fully understood.
Virus is isolated from blood, lymphoid organs, saliva and cerebrospinal
fluid, grown in vitro in
lymphocytes, macrophages and astrocytes.
Some strains of FIV can also grow in other cell types, for example
in some feline fibroblast cell lines.
Cats can be experimentally infected by subcutaneous, intramuscular,
intraperitoneal or intravenous inoculation.
After experimental inoculation of kittens with high doses of FIV,
virus can be isolated from lymphocytes at 1 week, and antibody detected after
about 3 weeks, but time to viraemia and seroconversion is much longer if inoculated
with smaller doses of virus.
Lymphadenopathy is usually seen after 4-6 weeks experimentally,
but severity depends on the dose and strain of virus, and on the age of cats
Acute lymphadenopathy may be accompanied by mild pyrexia and leucopenia,
including lymphopenia and neutropenia.
The lymphadenopathy usually disappears after 2-3 months.
Cats then generally remain healthy for several years. Severe, chronic
disease seen in the field has not been consistently reproduced experimentally.
Field studies suggest clinically asymptomatic infection may last at least 3-5
Not yet known what triggers the onset of terminal AIDS-like disease
Deficiencies in some immune functions can be detected within a
few months of infection and more profound immune dysfunction gradually develops
Decreased numbers of circulating CD4 cells and ratios of CD4:CD8
Reduced in vitro
proliferation responses to some mitogens and in
vivo responses to some antigens can be detected within the first
10 months after infection.
FIV causes a transient decreased expression of CD4 antigen and
syncytium formation in CD4 cell cultures.
Persistent infection causes a progressive decreased expression
of major histocompatibility complex type II antigens (MHCII).
Theories of how feline AIDS
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