Persistence of dual-tropic HIV-1 in an individual homozygous for the CCR5Δ32 allele

Paul R. Gorry; Chengsheng Zhang; Sam Wu; Kevin Kunstman; Elizabeth Trachtenberg; John Phair; Steven Wolinsky; Dana Gabuzda

doi:10.1016/S0140-6736(02)08681-6

Persistence of dual-tropic HIV-1 in an individual homozygous for the CCR5Δ32 allele

Paul R. Gorry, Chengsheng Zhang, Sam Wu, Kevin Kunstman, Elizabeth Trachtenberg, John Phair, Steven Wolinsky, Dana Gabuzda^*

^*Corresponding author for this work

Medicine

Research output: Contribution to journal › Article › peer-review

55 Scopus citations

Abstract

Entry of HIV-1 into a cell happens only after viral envelope glycoproteins have bound to CD4 and a chemokine receptor. Generally, macrophage-tropic strains use CCR5, and T cell-line-tropic strains use CXCR4 as coreceptors for virus entry. Dual-tropic viruses can use both CCR5 and CXCR4. About 1% of white people are homozygous for a non-functional CCR5 allele, containing a 32 base pair deletion (CCR5Δ32). We studied the persistence of dual-tropic HIV-1 in an individual homozygous for this deletion. Our results suggest that structural features of the HIV-1 envelope linked to CCR5 tropism could confer a selective advantage in vivo.

Original language	English (US)
Pages (from-to)	1832-1834
Number of pages	3
Journal	Lancet
Volume	359
Issue number	9320
DOIs	https://doi.org/10.1016/S0140-6736(02)08681-6
State	Published - May 25 2002

Funding

We thank J Moore and T Morgan for doing TAK779 and AMD3100 virus inhibition studies; H Wang for doing reverse transcriptase assays; J Sodroski and M Farzan for helpful discussions; S Crowe, K Leder, and S Zayontz for reviewing the manuscript; and J Sodroski, B Etemad-Moghadam, R Doms, S Peiper, and the NIH AIDS Research and Reference Reagent Program for reagents. The work was supported by a grant from the NIH (RO1 NS37277). Further support was received from the Multicenter AIDS Cohort Study (UO1 AI35039) and from the Center for AIDS Research (P30 AI28691 and CA79458). DG is an Elizabeth Glaser Scientist, supported by the Pediatric AIDS Foundation. The sponsors of the study had no role in study design, data collection, data analysis, data interpretation, or writing of the report.

ASJC Scopus subject areas

General Medicine

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1016/S0140-6736(02)08681-6

Cite this

@article{4fd516e4eca8478da454dbd9d2025987,

title = "Persistence of dual-tropic HIV-1 in an individual homozygous for the CCR5Δ32 allele",

abstract = "Entry of HIV-1 into a cell happens only after viral envelope glycoproteins have bound to CD4 and a chemokine receptor. Generally, macrophage-tropic strains use CCR5, and T cell-line-tropic strains use CXCR4 as coreceptors for virus entry. Dual-tropic viruses can use both CCR5 and CXCR4. About 1% of white people are homozygous for a non-functional CCR5 allele, containing a 32 base pair deletion (CCR5Δ32). We studied the persistence of dual-tropic HIV-1 in an individual homozygous for this deletion. Our results suggest that structural features of the HIV-1 envelope linked to CCR5 tropism could confer a selective advantage in vivo.",

author = "Gorry, {Paul R.} and Chengsheng Zhang and Sam Wu and Kevin Kunstman and Elizabeth Trachtenberg and John Phair and Steven Wolinsky and Dana Gabuzda",

note = "Funding Information: We thank J Moore and T Morgan for doing TAK779 and AMD3100 virus inhibition studies; H Wang for doing reverse transcriptase assays; J Sodroski and M Farzan for helpful discussions; S Crowe, K Leder, and S Zayontz for reviewing the manuscript; and J Sodroski, B Etemad-Moghadam, R Doms, S Peiper, and the NIH AIDS Research and Reference Reagent Program for reagents. The work was supported by a grant from the NIH (RO1 NS37277). Further support was received from the Multicenter AIDS Cohort Study (UO1 AI35039) and from the Center for AIDS Research (P30 AI28691 and CA79458). DG is an Elizabeth Glaser Scientist, supported by the Pediatric AIDS Foundation. The sponsors of the study had no role in study design, data collection, data analysis, data interpretation, or writing of the report.",

year = "2002",

month = may,

day = "25",

doi = "10.1016/S0140-6736(02)08681-6",

language = "English (US)",

volume = "359",

pages = "1832--1834",

journal = "Lancet",

issn = "0140-6736",

publisher = "Elsevier Limited",

number = "9320",

}

TY - JOUR

T1 - Persistence of dual-tropic HIV-1 in an individual homozygous for the CCR5Δ32 allele

AU - Gorry, Paul R.

AU - Zhang, Chengsheng

AU - Wu, Sam

AU - Kunstman, Kevin

AU - Trachtenberg, Elizabeth

AU - Phair, John

AU - Wolinsky, Steven

AU - Gabuzda, Dana

N1 - Funding Information: We thank J Moore and T Morgan for doing TAK779 and AMD3100 virus inhibition studies; H Wang for doing reverse transcriptase assays; J Sodroski and M Farzan for helpful discussions; S Crowe, K Leder, and S Zayontz for reviewing the manuscript; and J Sodroski, B Etemad-Moghadam, R Doms, S Peiper, and the NIH AIDS Research and Reference Reagent Program for reagents. The work was supported by a grant from the NIH (RO1 NS37277). Further support was received from the Multicenter AIDS Cohort Study (UO1 AI35039) and from the Center for AIDS Research (P30 AI28691 and CA79458). DG is an Elizabeth Glaser Scientist, supported by the Pediatric AIDS Foundation. The sponsors of the study had no role in study design, data collection, data analysis, data interpretation, or writing of the report.

PY - 2002/5/25

Y1 - 2002/5/25

N2 - Entry of HIV-1 into a cell happens only after viral envelope glycoproteins have bound to CD4 and a chemokine receptor. Generally, macrophage-tropic strains use CCR5, and T cell-line-tropic strains use CXCR4 as coreceptors for virus entry. Dual-tropic viruses can use both CCR5 and CXCR4. About 1% of white people are homozygous for a non-functional CCR5 allele, containing a 32 base pair deletion (CCR5Δ32). We studied the persistence of dual-tropic HIV-1 in an individual homozygous for this deletion. Our results suggest that structural features of the HIV-1 envelope linked to CCR5 tropism could confer a selective advantage in vivo.

AB - Entry of HIV-1 into a cell happens only after viral envelope glycoproteins have bound to CD4 and a chemokine receptor. Generally, macrophage-tropic strains use CCR5, and T cell-line-tropic strains use CXCR4 as coreceptors for virus entry. Dual-tropic viruses can use both CCR5 and CXCR4. About 1% of white people are homozygous for a non-functional CCR5 allele, containing a 32 base pair deletion (CCR5Δ32). We studied the persistence of dual-tropic HIV-1 in an individual homozygous for this deletion. Our results suggest that structural features of the HIV-1 envelope linked to CCR5 tropism could confer a selective advantage in vivo.

UR - http://www.scopus.com/inward/record.url?scp=0037172396&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0037172396&partnerID=8YFLogxK

U2 - 10.1016/S0140-6736(02)08681-6

DO - 10.1016/S0140-6736(02)08681-6

M3 - Article

C2 - 12044382

AN - SCOPUS:0037172396

SN - 0140-6736

VL - 359

SP - 1832

EP - 1834

JO - Lancet

JF - Lancet

IS - 9320

ER -

Persistence of dual-tropic HIV-1 in an individual homozygous for the CCR5Δ32 allele

Abstract

Funding

ASJC Scopus subject areas

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this