Feline immunodeficiency virus: an interesting model for AIDS studies and an important cat pathogen

Abstract

The lentivirus feline immunodeficiency virus (FIV) is a widespread pathogen of the domestic cat that is mainly transmitted through bites, although other means of transmission are also possible. Its prevalence ranges from 1 to 10% in different cat populations throughout the world, thus representing a large reservoir of naturally infected animals. FIV resembles the human immunodeficiency virus (HIV) in many respects. Similarities include the structural features of the virion, the general organization and great variability of the genome, the life cycle in the infected host, and most importantly, the pathogenic potential. Infection is associated with laboratory signs of immunosuppression as well as with a large variety of superinfections, tumors, and neurological manifestations. Our understanding of FIV is steadily improving and is providing important clues to the pathogenesis of immunodeficiency-inducing lentiviruses. The cellular receptor for FIV is different from the feline equivalent of the human CD4 molecule used by HIV; nevertheless, the major hallmark of infection is a progressive loss of CD4+ T lymphocytes as in HIV infection. The mechanisms by which FIV escapes the host's immune responses are being actively investigated. FIV causes lysis of infected T cells and also appears to predispose these cells to apoptosis. Infection of macrophages and other cell types has also been documented. For reasons yet to be understood, antibody-mediated neutralization of fresh FIV isolates is very inefficient both in vitro and in vivo. Vaccination studies have provided some encouraging results, but the difficulties encountered appear to match those met in HIV vaccine development. FIV susceptibility to antiviral agents is similar to that of HIV, thus providing a valuable system for in vivo preclinical evaluation of therapies. It is concluded that in many respects FIV is an ideal model for AIDS studies.

Most Potential Linear B Cell Epitopes of Env Glycoproteins of Feline Immunodeficiency Virus Are Immunogenically Silent in Infected Cats

“…The pentapeptide QNQFF, which is conserved among several FIV isolates, was the minimal sequence required for reactivity.13 Another peptide located close to the carboxyl terminus of the molecule was found to react with 80% of naturally infected cats.13 Other regions are seen by variable proportions of infected cat sera (reviewed in Ref. 2). Because the immunodominant sites of the SU glycoprotein detected by these analyses tend to coincide with variable regions, it has been speculated that this might represent a means of diverting immunologie recognition from conserved segments, which are more likely to exert important viral functions.3…”

Modulating DNA Methylation in Activated CD8+ T Cells Inhibits Regulatory T Cell–Induced Binding of Foxp3 to the CD8+ T Cell IL-2 Promoter

“…By comparison, HIV-infected individuals who do not effectively control virus harbor virus-specific CD8 + T cells with altered functionality leading to disruptions in overall immune homeostasis (1, 4). During chronic HIV/FIV, the virus replicates at low levels contributing to a state of chronic immune activation followed by immune exhaustion (6-9). These findings illustrate the need for a more detailed understanding of CD8 + T cell-mediated response to HIV/FIV infection and to define the direct cause for CD8 + dysfunction.…”

Blood Monocytes Harbor HIV Type 1 Strains with Diversified Phenotypes Including Macrophage‐Specific CCR5 Virus

“…Simian immunodeficiency virus variants isolated from sooty mangabeys and chimpanzees inefficiently infect macrophages in vitro and are considerably impaired in their pathogenicity in vivo [8]. After infection with HIV-1, macrophages release several immunoregulatory and inflammatory factors, including tumor necrosis factor-␣, interleukin (IL)-1, and IL-7, which, in turn, influence viral proliferation and disease associated with HIV-1 infection [9].…”