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Article: Chemokine coreceptor usage by diverse primary isolates of human immunodeficiency virus type 1
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TitleChemokine coreceptor usage by diverse primary isolates of human immunodeficiency virus type 1
 
AuthorsZhang, L2 3
He, T3
Huang, Y3
Chen, Z3
Guo, Y3
Wu, S
Kunstman, KJ
Brown, RC
Phair, JP
Neumann, AU1
Ho, DD3
Wolinsky, SM
 
Issue Date1998
 
PublisherAmerican Society for Microbiology. The Journal's web site is located at http://jvi.asm.org/
 
CitationJournal Of Virology, 1998, v. 72 n. 11, p. 9307-9312 [How to Cite?]
 
AbstractWe tested chemokine receptor subset usage by diverse, well- characterized primary viruses isolated from peripheral blood by monitoring viral replication with CCR1, CC2b, CCR3, CCR5, and CXCR4 U87MG.CD4 transformed cell lines and STRL33/BONZO/TYMSTR and GPR15/BOB HOS.CD4 transformed cell lines. Primary viruses were isolated from 79 men with confirmed human immunodeficiency virus type 1 (HIV-1) infection from the Chicago component of the Multicenter AIDS Cohort Study at interval time points. Thirty-five additional well-characterized primary viruses representing HIV-1 group M subtypes A, B, C, D, and E and group O and three primary simian immunodeficiency virus (SIV) isolates were also used for these studies. The restricted use of the CCR5 chemokine receptor for viral entry was associated with infection by a virus having a non-syncytium-inducing phenotype and correlated with a reduced rate of disease progression and a prolonged disease-free interval. Conversely, broadening chemokine receptor usage from CCR5 to both CCR5 and CXCR4 was associated with infection by a virus having a syncytium-inducing phenotype and correlated with a faster rate of CD4 T-cell decline and progression of disease. We also observed a greater tendency for infection with a virus having a syncytium-inducing phenotype in men heterozygous for the defective CCR5 Δ32 allele (25%) than in those men homozygous for the wild-type CCR5 allele (6%) (P = 0.03). The propensity for infection with a virus having a syncytium-inducing phenotype provides a partial explanation for the rapid disease progression among some men heterozygous for the defective CCR5 Δ32 allele. Furthermore, we did not identify any primary viruses that used CCR3 as an entry cofactor, despite this CC chemokine receptor being expressed on the cell surface at a level commensurate with or higher than that observed for primary peripheral blood mononuclear cells. Whereas isolates of primary viruses of SIV also used STRL33/BONZO/TYMSTR and GPR15/BOB, no primary isolates of HIV-1 used these particular chemokine receptor-like orphan molecules as entry cofactors, suggesting a limited contribution of these other chemokine receptors to viral evolution. Thus, despite the number of chemokine receptors implicated in viral entry, CCR5 and CXCR4 are likely to be the physiologically relevant chemokine receptors used as entry cofactors in vivo by diverse strains of primary viruses isolated from blood.
 
ISSN0022-538X
2013 Impact Factor: 4.648
 
ISI Accession Number IDWOS:000076373700099
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorZhang, L
 
dc.contributor.authorHe, T
 
dc.contributor.authorHuang, Y
 
dc.contributor.authorChen, Z
 
dc.contributor.authorGuo, Y
 
dc.contributor.authorWu, S
 
dc.contributor.authorKunstman, KJ
 
dc.contributor.authorBrown, RC
 
dc.contributor.authorPhair, JP
 
dc.contributor.authorNeumann, AU
 
dc.contributor.authorHo, DD
 
dc.contributor.authorWolinsky, SM
 
dc.date.accessioned2012-08-08T08:48:37Z
 
dc.date.available2012-08-08T08:48:37Z
 
dc.date.issued1998
 
dc.description.abstractWe tested chemokine receptor subset usage by diverse, well- characterized primary viruses isolated from peripheral blood by monitoring viral replication with CCR1, CC2b, CCR3, CCR5, and CXCR4 U87MG.CD4 transformed cell lines and STRL33/BONZO/TYMSTR and GPR15/BOB HOS.CD4 transformed cell lines. Primary viruses were isolated from 79 men with confirmed human immunodeficiency virus type 1 (HIV-1) infection from the Chicago component of the Multicenter AIDS Cohort Study at interval time points. Thirty-five additional well-characterized primary viruses representing HIV-1 group M subtypes A, B, C, D, and E and group O and three primary simian immunodeficiency virus (SIV) isolates were also used for these studies. The restricted use of the CCR5 chemokine receptor for viral entry was associated with infection by a virus having a non-syncytium-inducing phenotype and correlated with a reduced rate of disease progression and a prolonged disease-free interval. Conversely, broadening chemokine receptor usage from CCR5 to both CCR5 and CXCR4 was associated with infection by a virus having a syncytium-inducing phenotype and correlated with a faster rate of CD4 T-cell decline and progression of disease. We also observed a greater tendency for infection with a virus having a syncytium-inducing phenotype in men heterozygous for the defective CCR5 Δ32 allele (25%) than in those men homozygous for the wild-type CCR5 allele (6%) (P = 0.03). The propensity for infection with a virus having a syncytium-inducing phenotype provides a partial explanation for the rapid disease progression among some men heterozygous for the defective CCR5 Δ32 allele. Furthermore, we did not identify any primary viruses that used CCR3 as an entry cofactor, despite this CC chemokine receptor being expressed on the cell surface at a level commensurate with or higher than that observed for primary peripheral blood mononuclear cells. Whereas isolates of primary viruses of SIV also used STRL33/BONZO/TYMSTR and GPR15/BOB, no primary isolates of HIV-1 used these particular chemokine receptor-like orphan molecules as entry cofactors, suggesting a limited contribution of these other chemokine receptors to viral evolution. Thus, despite the number of chemokine receptors implicated in viral entry, CCR5 and CXCR4 are likely to be the physiologically relevant chemokine receptors used as entry cofactors in vivo by diverse strains of primary viruses isolated from blood.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationJournal Of Virology, 1998, v. 72 n. 11, p. 9307-9312 [How to Cite?]
 
dc.identifier.epage9312
 
dc.identifier.isiWOS:000076373700099
 
dc.identifier.issn0022-538X
2013 Impact Factor: 4.648
 
dc.identifier.issue11
 
dc.identifier.pmid9765480
 
dc.identifier.scopuseid_2-s2.0-0031684753
 
dc.identifier.spage9307
 
dc.identifier.urihttp://hdl.handle.net/10722/157281
 
dc.identifier.volume72
 
dc.languageeng
 
dc.publisherAmerican Society for Microbiology. The Journal's web site is located at http://jvi.asm.org/
 
dc.publisher.placeUnited States
 
dc.relation.ispartofJournal of Virology
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAnimals
 
dc.subject.meshCell Line, Transformed
 
dc.subject.meshHiv Infections - Genetics - Virology
 
dc.subject.meshHiv Long-Term Survivors
 
dc.subject.meshHiv-1 - Isolation & Purification - Pathogenicity - Physiology
 
dc.subject.meshHumans
 
dc.subject.meshMale
 
dc.subject.meshPhenotype
 
dc.subject.meshReceptors, Ccr1
 
dc.subject.meshReceptors, Ccr2
 
dc.subject.meshReceptors, Ccr3
 
dc.subject.meshReceptors, Ccr5 - Genetics - Physiology
 
dc.subject.meshReceptors, Cxcr4 - Genetics - Physiology
 
dc.subject.meshReceptors, Chemokine - Genetics - Physiology
 
dc.subject.meshReceptors, Cytokine - Genetics - Physiology
 
dc.subject.meshSimian Immunodeficiency Virus - Isolation & Purification - Pathogenicity - Physiology
 
dc.titleChemokine coreceptor usage by diverse primary isolates of human immunodeficiency virus type 1
 
dc.typeArticle
 
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Author Affiliations
  1. Bar-Ilan University
  2. Aaron Diamond AIDS Research Center
  3. Rockefeller University