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Macaques as model hosts for studies of HIV-1 infection

Increasing evidence indicates that the host range of primate lentiviruses is in part determined by their ability to counteract innate restriction factors that are effectors of the type 1 interferon (IFN-1) response. For human immunodeficiency virus type 1 (HIV-1), in vitro experiments have shown tha...

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Autores principales: Misra, Anisha, Thippeshappa, Rajesh, Kimata, Jason T.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3695370/
https://www.ncbi.nlm.nih.gov/pubmed/23825473
http://dx.doi.org/10.3389/fmicb.2013.00176
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author Misra, Anisha
Thippeshappa, Rajesh
Kimata, Jason T.
author_facet Misra, Anisha
Thippeshappa, Rajesh
Kimata, Jason T.
author_sort Misra, Anisha
collection PubMed
description Increasing evidence indicates that the host range of primate lentiviruses is in part determined by their ability to counteract innate restriction factors that are effectors of the type 1 interferon (IFN-1) response. For human immunodeficiency virus type 1 (HIV-1), in vitro experiments have shown that its tropism may be narrow and limited to humans and chimpanzees because its replication in other non-human primate species is hindered by factors such as TRIM5α (tripartite motif 5 alpha), APOBEC3G (apolipoprotein B mRNA-editing, enzyme-catalytic, polypeptide-like 3), and tetherin. Based on these data, it has been hypothesized that primate lentiviruses will infect and replicate in a new species if they are able to counteract and evade suppression by the IFN-1 response. Several studies have tested whether engineering HIV-1 recombinants with minimal amounts of simian immunodeficiency virus sequences would enable replication in CD4(+) T cells of non-natural hosts such as Asian macaques and proposed that infection of these macaque species could be used to study transmission and pathogenesis. Indeed, infection of macaques with these viruses revealed that Vif-mediated counteraction of APOBEC3G function is central to cross-species tropism but that other IFN-induced factors may also play important roles in controlling replication. Further studies of these macaque models of infection with HIV-1 derivatives could provide valuable insights into the interaction of lentiviruses and the innate immune response and how lentiviruses adapt and cause disease.
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spelling pubmed-36953702013-07-02 Macaques as model hosts for studies of HIV-1 infection Misra, Anisha Thippeshappa, Rajesh Kimata, Jason T. Front Microbiol Microbiology Increasing evidence indicates that the host range of primate lentiviruses is in part determined by their ability to counteract innate restriction factors that are effectors of the type 1 interferon (IFN-1) response. For human immunodeficiency virus type 1 (HIV-1), in vitro experiments have shown that its tropism may be narrow and limited to humans and chimpanzees because its replication in other non-human primate species is hindered by factors such as TRIM5α (tripartite motif 5 alpha), APOBEC3G (apolipoprotein B mRNA-editing, enzyme-catalytic, polypeptide-like 3), and tetherin. Based on these data, it has been hypothesized that primate lentiviruses will infect and replicate in a new species if they are able to counteract and evade suppression by the IFN-1 response. Several studies have tested whether engineering HIV-1 recombinants with minimal amounts of simian immunodeficiency virus sequences would enable replication in CD4(+) T cells of non-natural hosts such as Asian macaques and proposed that infection of these macaque species could be used to study transmission and pathogenesis. Indeed, infection of macaques with these viruses revealed that Vif-mediated counteraction of APOBEC3G function is central to cross-species tropism but that other IFN-induced factors may also play important roles in controlling replication. Further studies of these macaque models of infection with HIV-1 derivatives could provide valuable insights into the interaction of lentiviruses and the innate immune response and how lentiviruses adapt and cause disease. Frontiers Media S.A. 2013-06-28 /pmc/articles/PMC3695370/ /pubmed/23825473 http://dx.doi.org/10.3389/fmicb.2013.00176 Text en Copyright © Misra, Thippeshappa and Kimata. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.
spellingShingle Microbiology
Misra, Anisha
Thippeshappa, Rajesh
Kimata, Jason T.
Macaques as model hosts for studies of HIV-1 infection
title Macaques as model hosts for studies of HIV-1 infection
title_full Macaques as model hosts for studies of HIV-1 infection
title_fullStr Macaques as model hosts for studies of HIV-1 infection
title_full_unstemmed Macaques as model hosts for studies of HIV-1 infection
title_short Macaques as model hosts for studies of HIV-1 infection
title_sort macaques as model hosts for studies of hiv-1 infection
topic Microbiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3695370/
https://www.ncbi.nlm.nih.gov/pubmed/23825473
http://dx.doi.org/10.3389/fmicb.2013.00176
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