T-lymphocyte profiles in FIV-infected wild lions and pumas reveal CD4 depletion

Laboratory of Genomic Diversity, Basic Research Program, SAIC Frederick, National Cancer Institute, Frederick, Maryland 21702, USA.
Journal of wildlife diseases (Impact Factor: 1.31). 05/2006; 42(2):234-48. DOI: 10.7589/0090-3558-42.2.234
Source: PubMed

ABSTRACT Feline immunodeficiency virus (FIV) is a lentivirus related to human immunodeficiency virus (HIV) that causes feline AIDS in the domestic cat (Felis catus). Serological surveys indicate that at least 25 other species of cat possess antibodies that cross-react with domestic cat FIV. Most infected nondomestic cat species are without major symptoms of disease. Long-term studies of FIV genome variation and pathogenesis reveal patterns consistent with coadaptation of virus and host in free-ranging FIV-Ple-infected African lions (Panthera leo) and FIV-Pco-infected pumas (Puma concolor) populations. This report examined correlates of immunodeficiency in wild and captive lions and pumas by quantifying CD5(+), CD4(+), and CD8(+) T-cell subsets. Free-ranging FIV-Ple-infected lions had immunofluorescence flow cytometry (IFC) profiles marked by a dramatic decline in CD4(+) subsets, a reduction of the CD4(+)/CD8(+) ratio, reduction of CD8(+)beta(high) cells, and expansion of the CD8(+)beta(low) subset relative to uninfected lions. An overall significant depletion in CD5(+) T-cells in seropositive lions was linked with a compensatory increase in total CD5(-) lymphocytes. The IFC profiles were altered significantly in 50% of the seropositive individuals examined. The FIV-Pco-infected pumas had a more generalized response of lymphopenia expressed as a significant decline in total lymphocytes, CD5(+) T-cells, and CD5(-) lymphocytes as well as a significant reduction in CD4(+) T-cells. Like lions, seropositive pumas had a significant decline in CD8(+)beta(high) cells but differed by not having compensatory expansion of CD8(+)beta(low) cells relative to controls. Results from FIV-infected lions and pumas parallel human and Asian monkey CD4(+) diminution in HIV and SIV infection, respectively, and suggest there may be unrecognized immunological consequences of FIV infection in these two species of large cats.

Download full-text


Available from: Scott B Citino, Jul 17, 2015
  • Source
    • "FIV antibodies are reasonable because FIV is not uncommon in mountain lions . Chronic infection is asymptomatic in this host in Montana , Washington , Texas , and Florida in the United States ( Evermann et al . 1997 , Biek and Poss 2002 , Biek et al . 2006 , Miller et al . 2006 ) , or in Brazilian felids ( Filoni et al . 2006 ) and African lions ( Roelke et al . 2006 ) . Seroprevalence of antibody to FCV was high in bobcats ( Table 2 ) in California , USA , in rural zones where they potentially came into contact with domestic cats ( Riley et al . 2004 ) . Members of the cat family are the only known definitive hosts for T . gondii ( Aiello 1998 ) . After being shed in feces , the sporulated oocysts "
    [Show abstract] [Hide abstract]
    ABSTRACT: An understanding of the prevalence of diseases in free-ranging populations of felids is limited, and there is even less known about the overall health and diseases of wild felids that inhabit or utilize urban areas. We collected serum samples from 9 radiocollared mountain lions (Puma concolor) in the mountains surrounding Tucson, Arizona, USA, from August 2005 to August 2008. We tested serum samples for evidence of exposure to 10 feline viruses: Feline Calicivirus (FCV), Feline Herpesvirus, Feline Enteric Coronavirus, Feline Syncytial Virus–Feline Foamy Virus, Feline Infectious Peritonitis, Feline Immunodeficiency Virus, Feline Panleukopenia Virus (FPLV), Feline Leukemia Virus, Canine Distemper Virus (CDV), and Toxoplasma gondii. The highest prevalences of exposure were: T. gondii (8/9), FPLV (7/9), and FCV (6/9). One male was seropositive for CDV, T. gondii, and FPLV. Mountain lions inhabiting smaller fragmented landscapes and urban areas have more contact with other felids and domesticated animals. Frequent contact among mountain lions, other felids, and domesticated animals can lead to higher risk of exposure and facilitate the spread of the disease from animal to animal. © 2012 The Wildlife Society.
    Wildlife Society Bulletin 09/2012; 36(3):615-620. DOI:10.1002/wsb.155 · 1.27 Impact Factor
  • Source
    • "Authors speculated that this animal suffered from FIV-associated lymphoma similar to that described in the domestic cat (Poli et al., 1995). Roelke et al. (2006) evaluated associations between FIV infection in lions (FIV positive, n = 47, median age = 7.3 years) and disease. Significant lymphoid depletion was documented, as well as a variety of immunodeficiency related syndromes. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Retroviral induced neoplasms have been key to understanding oncogenesis and are important etiologic agents associated with cancer formation. Cats infected with feline immunodeficiency virus (FIV), the feline analogue to human immunodeficiency virus (HIV), are reported to be at increased incidence of neoplasia. This review highlights reported risk factors and tumor cell phenotypes associated with neoplasias arising in FIV-infected animals, differences in oncogenic disease in natural versus experimental FIV infections, and similarities between FIV- and HIV-related malignancies. The most common type of FIV-associated neoplasm reported in the literature is lymphoma, specifically of B-cell origin, with experimentally infected cats developing neoplastic lesions at an earlier age than their naturally infected cohorts. The mechanism of FIV-induced lymphoma has not been completely ascertained, though the majority of published studies addressing this issue suggest oncogenesis arises via indirect mechanisms. HIV-infected individuals have increased risk of neoplasia, specifically B cell lymphoma, in comparison with uninfected individuals. Additional similarities between FIV- and HIV-associated neoplasms include the presence of extranodal lymphoma, a synergism with other oncogenic viruses, and an apparent indirect mechanism of induced oncogenesis. This literature supports study of FIV-associated neoplasms to further characterize this lentiviral-neoplasia association for the benefit of both human and animal disease, and to advance our general knowledge of mechanisms for viral-induced oncogenesis.
    Veterinary Immunology and Immunopathology 06/2011; 143(3-4):227-34. DOI:10.1016/j.vetimm.2011.06.016 · 1.75 Impact Factor
  • Source
    • "The previously accepted paradigm, based on lion and puma studies, was that these viruses were less pathogenic, (Carpenter et al., 1996). However, there is evidence indicating immune suppression may still occur, as recent reports show CD4+ depletion in both wild and captive pumas and lions (Bull et al., 2003; Roelke et al., 2006). Further, a recent study of over 60 lions from Botswana showed that relative to uninfected lions, FIV Ple -infected lions displayed a significant elevation in clinical health conditions such as lymphadenopathy, gingivitis, tongue papillomas, dehydration, and poor coat condition that were attributed to chronic FIV infection (Roelke et al., 2009). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Feline immunodeficiency virus (FIV), a feline lentivirus related to HIV, causes immune dysfunction in domestic and wild cats. The Pallas' cat is the only species from Asia known to harbor a species-specific strain of FIV designated FIV(Oma) in natural populations. Here, a 25% seroprevalence of FIV is reported from 28 wild Mongolian Pallas' cats sampled from 2000 to 2008. Phylogenetic analysis of proviral RT-Pol from eight FIV(Oma) isolates from Mongolia, Russia, China and Kazakhstan reveals a unique monophyletic lineage of the virus within the Pallas' cat population, most closely related to the African cheetah and leopard FIV strains. Histopathological examination of lymph node and spleen from infected and uninfected Pallas' cats suggests that FIV(Oma) causes immune depletion in its' native host.
    Veterinary Immunology and Immunopathology 10/2009; 134(1-2):90-5. DOI:10.1016/j.vetimm.2009.10.014 · 1.75 Impact Factor
Show more