Lessons from the cat: feline immunodeficiency virus as a tool to develop intervention strategies against human immunodeficiency virus type 1.

Department of Molecular Biology, The Scripps Institute, La Jolla, California 92037, USA.
AIDS Research and Human Retroviruses (Impact Factor: 2.46). 07/1998; 14(9):797-801.
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    • "In domestic cats (Felis catus), FIV infection results in immune pathology, secondary infections , and death. The parallels between human and feline AIDS (FAIDS) have been explored for further understanding of HIV/AIDS transmission, infection, and pathology (Bendinelli et al., 1995; Burkhard and Dean, 2003; Elder et al., 1998, 2010; Henriksen et al., 1995; Stump and VandeWoude, 2007). As with HIV and SIV models, there is considerable variation in transmission, course of infection , and outcome of FIV infections in domestic cats. "
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    ABSTRACT: Feline immunodeficiency virus (FIV) infects domestic cats and at least 20 additional species of non-domestic felids throughout the world. Strains specific to domestic cat (FIV(Fca)) produce AIDS-like disease progression, sequelae and pathology providing an informative model for HIV infection in humans. Less is known about the immunological and pathological influence of FIV in other felid species although multiple distinct strains of FIV circulate in natural populations. As in HIV-1 and HIV-2, multiple diverse cross-species infections may have occurred. In the Serengeti National Park, Tanzania, three divergent subtypes of lion FIV (FIV(Ple)) are endemic, whereby 100% of adult lions are infected with one or more of these strains. Herein, the relative distribution of these subtypes in the population are surveyed and, combined with observed differences in lion mortality due to secondary infections based on FIV(Ple) subtypes, the data suggest that FIV(Ple) subtypes may have different patterns of pathogenicity and transmissibility among wild lion populations.
    Veterinary Immunology and Immunopathology 06/2011; 143(3-4):338-46. DOI:10.1016/j.vetimm.2011.06.013 · 1.75 Impact Factor
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    • "Env varies by up to 30 % amongst FIV subtypes (Hosie & Beatty, 2007) and, thus, the preparation of an immunogen capable of inducing broadly neutralizing antibody responses against such diverse isolates of FIV would be of great value to the development of an FIV vaccine. Further, the development of a vaccine against FIV would have implications extending beyond veterinary medicine; FIV is the only non-primate lentivirus that induces AIDS-like symptoms in its natural host and, as such, is a valuable animal model for both prophylactic and therapeutic studies for HIV (Bendinelli et al., 1995; Elder et al., 1998; Okada et al., 1994). Moreover, cats have the advantage of being easier to breed and have shorter life cycles than other animal models currently used for HIV research (Miller et al., 2000). "
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    ABSTRACT: Neutralizing antibodies (NAbs) play a vital role in vaccine-induced protection against infection with feline immunodeficiency virus (FIV). However, little is known about the appropriate presentation of neutralization epitopes in order to induce NAbs effectively; the majority of the antibodies that are induced are directed against non-neutralizing epitopes. Here, we demonstrate that a subtype B strain of FIV, designated NG4, escapes autologous NAbs, but may be rendered neutralization-sensitive following the insertion of two amino acids, KT, at positions 556-557 in the fifth hypervariable (V5) loop of the envelope glycoprotein. Consistent with the contribution of this motif to virus neutralization, an additional three subtype B strains retaining both residues at the same position were also neutralized by the NG4 serum, and serum from an unrelated cat (TOT1) targeted the same sequence in V5. Moreover, when the V5 loop of subtype B isolate KNG2, an isolate that was moderately resistant to neutralization by NG4 serum, was mutated to incorporate the KT motif, the virus was rendered sensitive to neutralization. These data suggest that, even in a polyclonal serum derived from FIV-infected cats following natural infection, the primary determinant of virus-neutralizing activity may be represented by a single, dominant epitope in V5.
    Journal of General Virology 09/2009; 91(Pt 1):242-9. DOI:10.1099/vir.0.015404-0 · 3.53 Impact Factor
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    • "FIV genome is simpler than that of primate lentiviruses, as the immunodeficiency virus (HIV), being characterised by three (rev, vif, orf2) rather than six accessory genes (Elder and Phillips, 1993; Poeschla et al., 1998). However, FIV is also similar to HIV in many molecular and biochemical properties, thus representing an attractive model for AIDS research (Elder et al., 1998). Indeed, FIV and its natural host, have already provided important insights into different aspects of lentiviral pathogenesis (Burkhard and Dean, 2003; Power et al., 2004). "
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    ABSTRACT: RNA-enveloped viruses bud from infected cells by exploiting the multivesicular body (MVB) pathway. In this context, ubiquitination of structural viral proteins and their direct interaction with cellular factors involved in the MVB biogenesis through short proline rich regions, named late domains (L-domains), are crucial mechanisms. Here we report that, in contrast with the human immunodeficiency virus (HIV), the feline immunodeficiency virus (FIV), a non-primate lentivirus, is strictly dependent for its budding on a "PSAP"-type L-domain, mapping in the carboxy-terminal region of Gag, irrespective of a functional viral protease. Moreover, we provide evidence that FIV egress is related to Gag ubiquitination, that is, linked to the presence of an active L-domain. Finally, although FIV Gag does not contain a PPxY motif, we show that the Nedd4-2s ubiquitin ligase enhances FIV Gag ubiquitination and it is capable to rescue viral mutants lacking a functional L-domain. In conclusion, our data bring to light peculiar aspects of FIV egress, but we also demonstrate that a non-primate lentivirus shares with HIV-1 a novel mechanism of connection to the cellular budding machinery.
    Journal of Cellular Physiology 01/2009; 218(1):175-82. DOI:10.1002/jcp.21587 · 3.87 Impact Factor
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