File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Chemokine coreceptor usage by diverse primary isolates of human immunodeficiency virus type 1

TitleChemokine coreceptor usage by diverse primary isolates of human immunodeficiency virus type 1
Authors
Issue Date1998
PublisherAmerican Society for Microbiology. The Journal's web site is located at http://jvi.asm.org/
Citation
Journal 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.
Persistent Identifierhttp://hdl.handle.net/10722/157281
ISSN
2021 Impact Factor: 6.549
2020 SCImago Journal Rankings: 2.617
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhang, Len_US
dc.contributor.authorHe, Ten_US
dc.contributor.authorHuang, Yen_US
dc.contributor.authorChen, Zen_US
dc.contributor.authorGuo, Yen_US
dc.contributor.authorWu, Sen_US
dc.contributor.authorKunstman, KJen_US
dc.contributor.authorBrown, RCen_US
dc.contributor.authorPhair, JPen_US
dc.contributor.authorNeumann, AUen_US
dc.contributor.authorHo, DDen_US
dc.contributor.authorWolinsky, SMen_US
dc.date.accessioned2012-08-08T08:48:37Z-
dc.date.available2012-08-08T08:48:37Z-
dc.date.issued1998en_US
dc.identifier.citationJournal Of Virology, 1998, v. 72 n. 11, p. 9307-9312en_US
dc.identifier.issn0022-538Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/157281-
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.en_US
dc.languageengen_US
dc.publisherAmerican Society for Microbiology. The Journal's web site is located at http://jvi.asm.org/en_US
dc.relation.ispartofJournal of Virologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCell Line, Transformeden_US
dc.subject.meshHiv Infections - Genetics - Virologyen_US
dc.subject.meshHiv Long-Term Survivorsen_US
dc.subject.meshHiv-1 - Isolation & Purification - Pathogenicity - Physiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshMaleen_US
dc.subject.meshPhenotypeen_US
dc.subject.meshReceptors, Ccr1en_US
dc.subject.meshReceptors, Ccr2en_US
dc.subject.meshReceptors, Ccr3en_US
dc.subject.meshReceptors, Ccr5 - Genetics - Physiologyen_US
dc.subject.meshReceptors, Cxcr4 - Genetics - Physiologyen_US
dc.subject.meshReceptors, Chemokine - Genetics - Physiologyen_US
dc.subject.meshReceptors, Cytokine - Genetics - Physiologyen_US
dc.subject.meshSimian Immunodeficiency Virus - Isolation & Purification - Pathogenicity - Physiologyen_US
dc.titleChemokine coreceptor usage by diverse primary isolates of human immunodeficiency virus type 1en_US
dc.typeArticleen_US
dc.identifier.emailChen, Z:zchenai@hkucc.hku.hken_US
dc.identifier.authorityChen, Z=rp00243en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1128/JVI.72.11.9307-9312.1998-
dc.identifier.pmid9765480-
dc.identifier.scopuseid_2-s2.0-0031684753en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031684753&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume72en_US
dc.identifier.issue11en_US
dc.identifier.spage9307en_US
dc.identifier.epage9312en_US
dc.identifier.isiWOS:000076373700099-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridZhang, L=8783285300en_US
dc.identifier.scopusauthoridHe, T=16935084000en_US
dc.identifier.scopusauthoridHuang, Y=7501575029en_US
dc.identifier.scopusauthoridChen, Z=35271180800en_US
dc.identifier.scopusauthoridGuo, Y=8783285700en_US
dc.identifier.scopusauthoridWu, S=7407178315en_US
dc.identifier.scopusauthoridKunstman, KJ=6602679064en_US
dc.identifier.scopusauthoridBrown, RC=8783286000en_US
dc.identifier.scopusauthoridPhair, JP=7101723853en_US
dc.identifier.scopusauthoridNeumann, AU=7201740253en_US
dc.identifier.scopusauthoridHo, DD=7402971998en_US
dc.identifier.scopusauthoridWolinsky, SM=7005510742en_US
dc.identifier.issnl0022-538X-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats