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               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
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