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      Emerging Viruses in the Felidae: Shifting Paradigms

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          Abstract

          The domestic cat is afflicted with multiple viruses that serve as powerful models for human disease including cancers, SARS and HIV/AIDS. Cat viruses that cause these diseases have been studied for decades revealing detailed insight concerning transmission, virulence, origins and pathogenesis. Here we review recent genetic advances that have questioned traditional wisdom regarding the origins of virulent Feline infectious peritonitis (FIP) diseases, the pathogenic potential of Feline Immunodeficiency Virus (FIV) in wild non-domestic Felidae species, and the restriction of Feline Leukemia Virus (FeLV) mediated immune impairment to domestic cats rather than other Felidae species. The most recent interpretations indicate important new evolutionary conclusions implicating these deadly infectious agents in domestic and non-domestic felids.

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          Isolation of a T-lymphotropic virus from domestic cats with an immunodeficiency-like syndrome.

          Hector Ho, J Yamamoto, M Wiktor … (1987)
          A highly T-lymphotropic virus was isolated from cats in a cattery in which all the animals were seronegative for feline leukemia virus. A number of cats in one pen had died and several had an immunodeficiency-like syndrome. Only 1 of 18 normal cats in the cattery showed serologic evidence of infection with this new virus, whereas 10 of 25 cats with signs of ill health were seropositive for the virus. Tentatively designated feline T-lymphotropic lentivirus, this new feline retrovirus appears to be antigenically distinct from human immunodeficiency virus. There is no evidence for cat-to-human transmission of the agent. Kittens experimentally infected by way of blood or plasma from naturally infected animals developed generalized lymphadenopathy several weeks later, became transiently febrile and leukopenic, and continued to show a generalized lymphadenopathy 5 months after infection.
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            Increased mortality and AIDS-like immunopathology in wild chimpanzees infected with SIVcpz.

            Brandon F Keele, James Holland Jones, Karen A. Terio … (2009)
            African primates are naturally infected with over 40 different simian immunodeficiency viruses (SIVs), two of which have crossed the species barrier and generated human immunodeficiency virus types 1 and 2 (HIV-1 and HIV-2). Unlike the human viruses, however, SIVs do not generally cause acquired immunodeficiency syndrome (AIDS) in their natural hosts. Here we show that SIVcpz, the immediate precursor of HIV-1, is pathogenic in free-ranging chimpanzees. By following 94 members of two habituated chimpanzee communities in Gombe National Park, Tanzania, for over 9 years, we found a 10- to 16-fold higher age-corrected death hazard for SIVcpz-infected (n = 17) compared to uninfected (n = 77) chimpanzees. We also found that SIVcpz-infected females were less likely to give birth and had a higher infant mortality rate than uninfected females. Immunohistochemistry and in situ hybridization of post-mortem spleen and lymph node samples from three infected and two uninfected chimpanzees revealed significant CD4(+) T-cell depletion in all infected individuals, with evidence of high viral replication and extensive follicular dendritic cell virus trapping in one of them. One female, who died within 3 years of acquiring SIVcpz, had histopathological findings consistent with end-stage AIDS. These results indicate that SIVcpz, like HIV-1, is associated with progressive CD4(+) T-cell loss, lymphatic tissue destruction and premature death. These findings challenge the prevailing view that all natural SIV infections are non-pathogenic and suggest that SIVcpz has a substantial negative impact on the health, reproduction and lifespan of chimpanzees in the wild.
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              Global distribution of measles genotypes and measles molecular epidemiology.

              Paul Rota, Kevin Brown, Annette Mankertz … (2011)
              A critical component of laboratory surveillance for measles is the genetic characterization of circulating wild-type viruses. The World Health Organization (WHO) Measles and Rubella Laboratory Network (LabNet), provides for standardized testing in 183 countries and supports genetic characterization of currently circulating strains of measles viruses. The goal of this report is to describe the lessons learned from nearly 20 years of virologic surveillance for measles, to describe the global databases for measles sequences, and to provide regional updates about measles genotypes detected by recent surveillance activities. Virologic surveillance for measles is now well established in all of the WHO regions, and most countries have conducted at least some baseline surveillance. The WHO Global Genotype Database contains >7000 genotype reports, and the Measles Nucleotide Surveillance (MeaNS) contains >4000 entries. This sequence information has proven to be extremely useful for tracking global transmission patterns and for documenting the interruption of transmission in some countries. The future challenges will be to develop quality control programs for molecular methods and to continue to expand virologic surveillance activities in all regions. Published by Oxford University Press on behalf of the Infectious Diseases Society of America 2011.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Viruses
                Journal ID (iso-abbrev): Viruses
                Journal ID (publisher-id): viruses
                Title: Viruses
                Publisher: MDPI
                ISSN (Electronic): 1999-4915
                Publication date (Electronic): 07 February 2012
                Publication date Collection: February 2012
                Volume: 4
                Issue: 2
                Pages: 236-257
                Affiliations
                [1 ]Laboratory of Genomic Diversity, National Cancer Institute-Frederick, Frederick, MD 21702, USA; Email: warjohns@ 123456mail.nih.gov (W.E.J.); slatterj@ 123456mail.nih.gov (J.P.-S.)
                [2 ]SAIC-Frederick, Inc., National Cancer Institute-Frederick, Frederick, MD 21702, USA; Email: troyerj@ 123456mail.nih.gov (J.L.T.); Melody.Roelke-Parker@ 123456nih.gov (M.E.R.)
                [3 ]Banfield Pet Hospital, 800 NE Tillamook Street, Portland, OR 97213, USA; Email: Meredith.Brown@ 123456banfield.net
                [4 ]CIMAR, University of Porto, Rua dos Bragas, 177, Porto 4050-123, Portugal; Email: aantunes@ 123456ciimar.up.pt
                Author notes
                [†]

                Present Address: Theodosius Dobzhansky Center for Genome Bioinformatics, St. Petersburg University, St. Petersburg, 190000, Russia.

                [* ]Author to whom correspondence should be addressed; Email: lgdchief@ 123456gmail.com ; Tel.: +1-240-446-1021; Fax: +1-301-662-1413.
                Article
                Publisher ID: viruses-04-00236
                DOI: 10.3390/v4020236
                PMC ID: 3315214
                PubMed ID: 22470834
                SO-VID: 788037c8-83fd-45b8-8ce9-3584e3e6db0f
                Copyright © © 2012 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                Date received : 01 December 2011
                Date revision received : 21 December 2011
                Date accepted : 11 January 2012
                Categories
                Subject: Review

                ScienceOpen disciplines: Microbiology & Virology
                Keywords: fiv,felv,felidae,fcov
                Data availability:
                ScienceOpen disciplines: Microbiology & Virology
                Keywords: fiv, felv, felidae, fcov

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