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HLA-Bw4 homozygosity is associated with an impaired CD4 T cell recovery after initiation of antiretroviral therapy


Rauch, A; Nolan, D; Furrer, H; McKinnon, E; John, M; Mallal, S; Gaudieri, S; Günthard, H F; Schmid, P; Battegay, M; Hirschel, B; Telenti, A; James, I (2008). HLA-Bw4 homozygosity is associated with an impaired CD4 T cell recovery after initiation of antiretroviral therapy. Clinical Infectious Diseases, 46(12):1921-1925.

Abstract

We assessed the influence of human leukocyte antigen (HLA) alleles HLA-Bw4 and HLA-Bw6 on CD4 T cell recovery after starting successful combination antiretroviral therapy in 265 individuals. The median gains in the CD4 T cell count after 4 years were 258 cells/microL for HLA-Bw4 homozygotes, 321 cells/microL for HLA-Bw4/Bw6 heterozygotes, and 363 cells/microL for HLA-Bw6 homozygotes (P = .01, compared with HLA-Bw4 homozygotes). HLA-Bw4 homozygosity appears to predict an impaired CD4 T cell recovery after initiation of combination antiretroviral therapy.

Abstract

We assessed the influence of human leukocyte antigen (HLA) alleles HLA-Bw4 and HLA-Bw6 on CD4 T cell recovery after starting successful combination antiretroviral therapy in 265 individuals. The median gains in the CD4 T cell count after 4 years were 258 cells/microL for HLA-Bw4 homozygotes, 321 cells/microL for HLA-Bw4/Bw6 heterozygotes, and 363 cells/microL for HLA-Bw6 homozygotes (P = .01, compared with HLA-Bw4 homozygotes). HLA-Bw4 homozygosity appears to predict an impaired CD4 T cell recovery after initiation of combination antiretroviral therapy.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic for Infectious Diseases
Dewey Decimal Classification:610 Medicine & health
Scopus Subject Areas:Health Sciences > Microbiology (medical)
Health Sciences > Infectious Diseases
Language:English
Date:15 June 2008
Deposited On:14 Nov 2008 08:33
Last Modified:24 Jun 2022 12:15
Publisher:University of Chicago Press
ISSN:1058-4838
OA Status:Hybrid
Publisher DOI:https://doi.org/10.1086/588479
PubMed ID:18466093
  • Content: Published Version
  • Language: English
  • Description: Nationallizenz 142-005