Although Macrophage-Tropic Simian/Human Immunodeficiency Viruses Can Exhibit a Range of Pathogenic Phenotypes, a Majority of Isolates Induce No Clinical Disease in Immunocompetent Macaques

Igarashi, Tatsuhiko; Donau, Olivia K.; Imamichi, Hiromi; Nishimura, Yoshiaki; Theodore, Theodore S.; Iyengar, Ranjini; Erb, Christopher T.; Buckler-White, Alicia; Buckler, Charles E.; Martin, Malcolm A.

doi:10.1128/jvi.00517-07

Cited by 4 publications

(3 citation statements)

References 42 publications

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“…The findings with chimeric FIVs may have parallels with previous work involving HIV/simian immunodeficiency virus (SHIV) chimeras (14,17,20,21,30). In these studies, initial SHIVs replicated ex vivo and in macaques but were not highly pathogenic on primary passage (20,21,30).…”

Section: Vol 82 2008 Clade A/c Chimeric Fivs and Infection Kineticssupporting

confidence: 74%

Replication Properties of Clade A/C Chimeric Feline Immunodeficiency Viruses and Evaluation of Infection Kinetics in the Domestic Cat

Rozieres

Thompson

Sundström

et al. 2008

J Virol

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Section: Vol 82 2008 Clade A/c Chimeric Fivs and Infection Kineticssupporting

confidence: 74%

Replication Properties of Clade A/C Chimeric Feline Immunodeficiency Viruses and Evaluation of Infection Kinetics in the Domestic Cat

Rozieres

Thompson

Sundström

et al. 2008

J Virol

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“…An additional factor contributing to immune control of macrophage infection may be direct antiviral activity of CD4 ϩ T cells that is uniquely active in suppressing virus in macrophages [31,32]. Of note, macaque infection with highly M-tropic SHIV in the absence of immune suppression generally does not cause disease and results instead in rapid disappearance of plasma viremia and induction of neutralizing antibodies [33].…”

Section: Macrophage Lineage Cells and Hiv-1 Infection In Vivomentioning

confidence: 99%

HIV-1 envelope–receptor interactions required for macrophage infection and implications for current HIV-1 cure strategies

Gorry

Francella

Lewin

et al. 2013

Journal of Leukocyte Biology

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Myeloid cells residing in the CNS and lymphoid tissues are targets for productive HIV-1 replication, and their infection contributes to the pathological manifestations of HIV-1 infection. The Envs can adopt altered configurations to overcome entry restrictions in macrophages via a more efficient and/or altered mechanism of engagement with cellular receptors. This review highlights evidence supporting an important role for macrophages in HIV-1 pathogenesis and persistence, which need to be considered for strategies aimed at achieving a functional or sterilizing cure. We also highlight that the molecular mechanisms underlying HIV-1 tropism for macrophages are complex, involving enhanced and/or altered interactions with CD4, CCR5, and/or CXCR4, and that the nature of these interactions may depend on the anatomical location of the virus.

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“…The construction and characterization of the SHIV DH12R-Clone 7 (SHIV DH12R-CL-7 ), SHIV DH12R-CL-8 , and SIV mac239 molecular clones and their use to generate virus stocks have been described previously (18,46,52). The origin and preparation of the tissue culture-derived SHIV AD8#2 have been previously reported (34).…”

Section: Methodsmentioning

confidence: 99%

Recombination-Mediated Changes in Coreceptor Usage Confer an Augmented Pathogenic Phenotype in a Nonhuman Primate Model of HIV-1-Induced AIDS

Nishimura

Shingai

Lee

et al. 2011

J Virol

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Evolution of the env gene in transmitted R5-tropic human immunodeficiency virus type 1 (HIV-1) strains is the most widely accepted mechanism driving coreceptor switching. In some infected individuals, however, a shift in coreceptor utilization can occur as a result of the reemergence of a cotransmitted, but rapidly controlled, X4 virus. The latter possibility was studied by dually infecting rhesus macaques with X4 and R5 chimeric simian simian/human immunodeficiency viruses (SHIVs) and monitoring the replication status of each virus using specific primer pairs. In one of the infected monkeys, both SHIVs were potently suppressed by week 12 postinoculation, but a burst of viremia at week 51 was accompanied by an unrelenting loss of total CD4؉ T cells and the development of clinical disease. PCR analyses of plasma viral RNA indicated an env gene segment containing the V3 region from the inoculated X4 SHIV had been transferred into the genetic background of the input R5 SHIV by intergenomic recombination, creating an X4 virus with novel replicative, serological, and pathogenic properties. These results indicate that the effects of retrovirus recombination in vivo can be functionally profound and may even occur when one of the recombination participants is undetectable in the circulation as cell-free virus.

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Although Macrophage-Tropic Simian/Human Immunodeficiency Viruses Can Exhibit a Range of Pathogenic Phenotypes, a Majority of Isolates Induce No Clinical Disease in Immunocompetent Macaques

Cited by 4 publications

References 42 publications

Replication Properties of Clade A/C Chimeric Feline Immunodeficiency Viruses and Evaluation of Infection Kinetics in the Domestic Cat

Replication Properties of Clade A/C Chimeric Feline Immunodeficiency Viruses and Evaluation of Infection Kinetics in the Domestic Cat

HIV-1 envelope–receptor interactions required for macrophage infection and implications for current HIV-1 cure strategies

Recombination-Mediated Changes in Coreceptor Usage Confer an Augmented Pathogenic Phenotype in a Nonhuman Primate Model of HIV-1-Induced AIDS

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