2011
DOI: 10.1101/cshperspect.a007153
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Nonpathogenic Simian Immunodeficiency Virus Infections

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Cited by 62 publications
(51 citation statements)
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“…In addition, it identifies another striking similarity between VNPs and naturally SIVsmm-infected SMs, who also experience a non-pathogenic, immunologically benign infection despite chronic virus replication [20]. Our observation that T CM and T SCM in VNPs harbor less HIV DNA as opposed to PPs is also consistent with another recent report suggesting that VNPs tend to have lower T cell activation than progressors in peripheral blood, yet higher T cell activation in the rectal mucosa, where a much higher proportion of CD4+ T cell have an effector phenotype [18].…”
Section: Discussionmentioning
confidence: 90%
“…In addition, it identifies another striking similarity between VNPs and naturally SIVsmm-infected SMs, who also experience a non-pathogenic, immunologically benign infection despite chronic virus replication [20]. Our observation that T CM and T SCM in VNPs harbor less HIV DNA as opposed to PPs is also consistent with another recent report suggesting that VNPs tend to have lower T cell activation than progressors in peripheral blood, yet higher T cell activation in the rectal mucosa, where a much higher proportion of CD4+ T cell have an effector phenotype [18].…”
Section: Discussionmentioning
confidence: 90%
“…Thus, our understanding of the evolutionary history of primate lentiviruses is still incomplete. To date, serological evidence of SIV infection has been reported for over 40 primate species, and molecular data have been obtained for most of these (also see Klatt et al 2011). The latter studies have shown that the great majority of primate species harbor a single "type" or "strain" of SIV.…”
Section: Primate Lentivirusesmentioning
confidence: 98%
“…Nonhuman primates (NHP), whether naturally or experimentally infected with simian immunodeficiency viruses (SIVs), display phenotypic variation on multiple levels, including differences in relative susceptibility to infection, variability in both acute and long-term viral replication levels, differing rates of disease progression, and differences in degree of pathogenesis (see Klatt et al 2011;Lifson and Haigwood 2011). NHP populations, including both wild populations and captive-bred colonies, comprise genetically variable, outbred individuals, and it is reasonable to assume that variation in virological phenotypes reflects, in part, host genetic variation.…”
Section: Primate Geneticsmentioning
confidence: 99%