Faculty, Staff and Student Publications
Publication Date
7-14-2023
Journal
The Journal of Infectious Disease
DOI
10.1093/infdis/jiad062
PMID
36912158
PMCID
PMC11009460
PubMedCentral® Posted Date
March 2023
PubMedCentral® Full Text Version
Post-print
Abstract
We analyzed findings in a same-gender couple discordant in their human immunodeficiency virus (HIV) status. The HIV+ partner was homozygous for CCR5 while his receptive HIV- partner was a CCR5Δ32 heterozygote with a C20S missense mutation in his CCR5 allele. The cells from the HIV- partner showed significant resistance to R5 fusion/infection and had no chemotactic response to CCL4 (macrophage inflammatory protein 1β). We demonstrated abundant CCR5-specific RNA in the HIV- partner's cells but no detectable CCR5 protein. CCR5 promoter region cloned from each partner's DNA indicated no significant impact on RNA transcription. The compound effect of CCR5Δ32 and C20S mutation impaired CCR5 coreceptor function and conferred resistance to HIV-1.
Keywords
HIV Infections, Humans, Disease Resistance, HIV-1, Receptors, CCR5, Male, Mutation, Missense, CCR5, CCR5Δ32, HIV/AIDS, heterozygous, homozygous
Published Open-Access
yes
Recommended Citation
Alkhatib, Bashar; Jabari, Mary; Bilasy, Shymaa; et al., "Resistance to Human Immunodeficiency Virus 1 Infection Conferred by a Compound CCR5Δ32 and CCR5 C20S Heterozygote" (2023). Faculty, Staff and Student Publications. 1391.
https://digitalcommons.library.tmc.edu/uthgsbs_docs/1391
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