Special Challenges of Rearing Infant Macaques Infected with Lentivirus (SIV, HIV, SHIV)
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Simian immunodeficiency virus
Feline immunodeficiency virus
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markdownabstract__Abstract__
Three years after the identification of HIV-1 as the causative agent of an
acquired immunodeficiency syndrome (AIDS) in humans in 1983, another member
of the Lentiviridae family was discovered in a cattery in Petaluma, California.
Originally named feline T-lymphotropic lentivirus, the virus was finally named feline
immunodeficiency virus (FIV). Within the Lentiviridae family, FIV is placed between
the primate lentiviruses HIV and SIV on the one hand and the ungulate viruses Visna
virus, CAEV, EIAV and BIV on the other hand, on the basis of genome structure
and organisation (Figures 1A and 2). Although FIV is phylogenetically more distant
from HIV-1 than the primate lentiviruses it shares many structural and biochemical
characteristics with HIV and given the close resemblance of the pathogeneses of
infections with both viruses in their respective hosts, FIV infection of the domestic
cat (Felis catus) has established itself, in the two decades that have past since its
identification, as an excellent small animal model for lentiviral infections in general
and lentivirus vaccine development in particular.
Feline immunodeficiency virus
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FIV is a significant pathogen in the cat and is, in addition, the smallest available natural model for the study of lentivirus infections. Although divergent at the amino acid level, the cat lentivirus has an abundance of structural and pathophysiological commonalities with HIV and thus serves well as a model for development of intervention strategies relevant to infection in both cats and man. The following review highlights both the strengths and shortcomings of the FIV/cat model, particular as regards development of antiviral drugs.
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Sparger, E. Elizabeth; Luciw, Paul A.; Elder, John H.; Yamamoto, Janet K.; Lowenstine, Linda J.; Pedersen, Niels C. Author Information
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Feline immunodeficiency virus (FIV) is a lentivirus of domestic cats that causes a spectrum of diseases remarkably similar to AIDS in HIV-infected humans. As part of this spectrum, both HIV-1 and FIV induce neurologic disorders. Because astrocytes are essential in maintaining the homeostasis of the central nervous system, we analyzed FIV for the ability to infect feline astrocytes. Through immunocytochemistry and reverse transcriptase activity, it was demonstrated that two molecular clones of FIV (FIV-34TF10 and FIV-PPR) produce a chronic low level productive infection of feline astrocyte cultures. To investigate the consequences of this infection, selected astrocyte functions were examined. Infection with FIV-34TF10 significantly decreased the ability of astrocytes to scavenge extracellular glutamate (with a peak inhibition of 74%). The effects of the infection did not appear to be a result of toxicity but rather were more selective in nature because the glucose uptake function of the infected astrocyte cultures was not altered. Our data demonstrate that FIV productively infected, at a low level, feline astrocyte cultures, and as a consequence of this infection, an important astroglial function was altered. These findings suggest that a chronic low grade infection of astrocytes may impair the ability of these cells to maintain homeostasis of the central nervous system that, in turn, may contribute to a neurodegenerative disease process that is often associated with lentivirus infections.
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Because HIV-1 does not infect most nonhuman primates, animal modeling of human HIV infection and AIDS has primarily consisted of experimentally infecting macaques with related simian immunodeficiency viruses (SIVMAC). However, the usefulness of such models is limited by the substantial divergence between SIVMAC and HIV-1. We derived an HIV-1‐based virus that includes only small portions of SIVMAC yet replicates robustly in both transformed and primary rhesus macaque T cells. Derivation of simian-tropic HIV-1 (stHIV-1) has important implications for understanding primate lentivirus zoonosis and should allow the development of improved animal models for studies of AIDS and the evaluation of vaccines and treatments.
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Acquired immunodeficiency in non-human primates has been associated with two types of retroviruses: (i) Simian Retrovirus (SRV), a type D virus and (ii) a lentivirus, Simian Immunodeficiency Virus (SIV). Both types represent a serious health threat to animals living in different primate research centres, zoos, medical institutions and in private homes. The sera of 175 monkeys belonging to different species were tested for the presence of antibodies against type D retroviruses and SIV. The Mason-Pfizer monkey virus, the prototype of D retroviruses, and Simian Immunodeficiency Virus, designated SIVmac251, were used. None of the sera tested proved to be positive for the presence of type D retroviruses and only one serum of an African green monkey was positive for the presence of antibodies to SIV.
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