Page 945 - Clinical Small Animal Internal Medicine
P. 945
883
VetBooks.ir
88
Feline Immunodeficiency Virus
Tom Phillips, DVM, MS, PhD, †
College of Veterinary Medicine, Western University of Health Sciences, Pomona, CA, USA, Deceased
Etiology/Pathophysiology detectable for up to six weeks post infection. Generally,
FIV induces a strong but only partially effective immune
Feline immunodeficiency virus (FIV) is a member of the response. However, there are reports of detectable levels
Lentivirus genus in the Retroviridae virus family. As of FIV DNA in cats without a detectable antibody
such, it is an enveloped virus, has an icosahedral capsid, response. Generally, antibodies to FIV are detected by two
and a genome composed of two (nearly identical) linear, weeks post infection, and most cats develop antibody by
positive sense, single‐stranded RNA molecules. 60 days post infection, although it may be delayed further
Much has been learned about FIV since it was first in some cats. Over the next few weeks after antibody
described in 1987, particularly in regard to its applica development, the virus levels in the blood are gradually
tion as a model to study the closely related lentivirus reduced to undetectable quantities and become clinically
human immunodeficiency virus (HIV). In particular, latent. However, the virus is not truly latent, as it contin
FIV and HIV share remarkable structure and sequence ues to replicate at low levels. During this clinical latent
organization, utilize parallel modes of receptor‐medi phase, the virus infection gradually is eroding normal
ated entry, and result in a similar spectrum of immuno immune function of the infected cat. FIV causes the
deficiency‐related diseases due to analogous modes of T helper cell numbers to decrease with an inversion of the
immune dysfunction. CD4:CD8 ratio. The effect of FIV on feline lymphocyte
The disease course for FIV is variable, likely dependent numbers is likely due to several mechanisms operating
upon the route of infection, strain of virus, age of the ani simultaneously: virus‐induced lysis of infected cells, virus
mal at time of infection, and the robustness of the suppression of the ability of bone marrow and other lym
immune response generated to the virus. Transmission phoid tissues to produce new lymphocytes, immune‐
is primarily through the bite of an infected cat, though mediated lysis of infected cells, and apoptosis. The ability
sexual transmission has been shown to occur in experi of lymphocytes from FIV‐infected cats to proliferate in
mentally infected cats. Infection by blood transfusion response to both B and T cell mitogens is impaired, as is
may also potentially occur. Initially, FIV is transported by the expression of lymphocyte cell surface receptors that
tissue macrophages to lymphoid tissues, where it repli are important in control and proliferation of the immune
cates in lymph nodes, thymus, spleen, bone marrow, response, such as cytokine receptors and MHC class II
brain, lung, gastrointestinal tract, and kidney. FIV gains antigens.
entrance into the cell primarily through receptor media The pathophysiology of FIV neurologic dysfunction is
tion. The main cellular receptors for FIV are the not completely understood as it occurs in the apparent
chemokine receptor, CXCR4, and CD134, a receptor absence of virus replication in neurons, with minimal
expressed by T lymphocytes and activated macrophages. inflammatory lesions in infected cat brains, and only low
Other mechanisms of virus entry may also be important, levels of replication in astrocyte and microglia cells.
such as the use of other receptors and antibody‐medi Infected astrocytes have impaired glutamate uptake
ated entry through FC receptors. function, which may lead to an increased susceptibility
Experimentally, virus is detected in the blood of animals of glutamate toxicity, oxidative stress, and ultimately
usually by two weeks post infection, and remains easily neuron loss. Additionally, FIV envelope protein is toxic
Clinical Small Animal Internal Medicine Volume II, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical