CCR5/Δccr5 heterozygosity: A selective pressure for the syncytium- Inducing human immunodeficiency virus type 1 phenotype

Richard T. D'Aquila*, Lorraine Sutton, Anu Savara, Michael D. Hughes, Victoria A. Johnson

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

26 Scopus citations

Abstract

Mechanisms underlying the delay in dominance of syncytium-inducing (SI) phenotype HIV-1 (human immunodeficiency virus type 1) in vivo are unknown. Both random mutational events and selective pressures operative only late in the disease process have been suggested to underlie the shift from CCR5 to alternative coreceptor usage. Among the moderately advanced patients who entered AIDS Clinical Trials Group protocol 241, SI vital phenotype was more common among CCR5/Δccr5 heterozygotes (7/7, 100%) than among CCR5/CCR5 homozygotes (29/88, 33%; P < .001, Fisher's exact test). Other characteristics did not differ at study entry by CCR5 genotype, including median CD4 cell counts, plasma RNA levels, and infectious HIV-I titers in circulating cells. These data indicate that CCR5/Δccr5 heterozygosity, which decreases cell-surface levels of CCR5 available to serve as an HIV-1 entry coreceptor, is a selective pressure for evolution of T cell line-tropic viruses that use an alternative coreceptor.

Original languageEnglish (US)
Pages (from-to)1549-1553
Number of pages5
JournalJournal of Infectious Diseases
Volume177
Issue number6
DOIs
StatePublished - 1998

ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases

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