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 HIV-1, in vitro experiments have shown that its tropism may be narrow and limit...
Main Authors: | , , |
---|---|
Format: | Article |
Language: | English |
Published: |
Frontiers Media S.A.
2013-06-01
|
Series: | Frontiers in Microbiology |
Subjects: | |
Online Access: | http://journal.frontiersin.org/Journal/10.3389/fmicb.2013.00176/full |
id |
doaj-7705d448b3ed473480f6706622fca8b1 |
---|---|
record_format |
Article |
spelling |
doaj-7705d448b3ed473480f6706622fca8b12020-11-24T20:45:53ZengFrontiers Media S.A.Frontiers in Microbiology1664-302X2013-06-01410.3389/fmicb.2013.0017654719Macaques as model hosts for studies of HIV-1 infectionAnisha eMisra0Rajesh eThippeshappa1Jason T Kimata2Baylor College of MedicineBaylor College of MedicineBaylor College of MedicineIncreasing 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 HIV-1, in vitro experiments have shown that its tropism may be narrow and limited to humans and chimpanzees because its replication in other nonhuman primate species is hindered by factors such as TRIM5α, APOBEC3G, 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 SIV 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.http://journal.frontiersin.org/Journal/10.3389/fmicb.2013.00176/fullHIV-1aidsSIVmacaque modelsinnate restriction |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Anisha eMisra Rajesh eThippeshappa Jason T Kimata |
spellingShingle |
Anisha eMisra Rajesh eThippeshappa Jason T Kimata Macaques as model hosts for studies of HIV-1 infection Frontiers in Microbiology HIV-1 aids SIV macaque models innate restriction |
author_facet |
Anisha eMisra Rajesh eThippeshappa Jason T Kimata |
author_sort |
Anisha eMisra |
title |
Macaques as model hosts for studies of HIV-1 infection |
title_short |
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_sort |
macaques as model hosts for studies of hiv-1 infection |
publisher |
Frontiers Media S.A. |
series |
Frontiers in Microbiology |
issn |
1664-302X |
publishDate |
2013-06-01 |
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 HIV-1, in vitro experiments have shown that its tropism may be narrow and limited to humans and chimpanzees because its replication in other nonhuman primate species is hindered by factors such as TRIM5α, APOBEC3G, 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 SIV 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. |
topic |
HIV-1 aids SIV macaque models innate restriction |
url |
http://journal.frontiersin.org/Journal/10.3389/fmicb.2013.00176/full |
work_keys_str_mv |
AT anishaemisra macaquesasmodelhostsforstudiesofhiv1infection AT rajeshethippeshappa macaquesasmodelhostsforstudiesofhiv1infection AT jasontkimata macaquesasmodelhostsforstudiesofhiv1infection |
_version_ |
1716813756332244992 |