Important note: Information in this article was accurate in June 2001. The state of the art may have changed since the publication date.AIDSWEEKLY Plus; Monday, June 18, 2001
Michael Greer, Senior Medical Writer
NewsRx - HIV patients homozygous for a class of human leukocyte antigen (HLA)-B alleles display natural suppression of viral replication and resistance to AIDS progression, researchers report.
"Certain HLA-B antigens have been associated with lack of progression to AIDS," explained A.E. Goldfeld and colleagues at Boston's Center for Blood Research. "HLA-B alleles can be divided into two mutually exclusive groups based on the expression of the molecular epitopes HLA-Bw4 and HLA-Bw6."
Goldfeld and coworkers showed that carrying a set of HLA-B alleles that express the Bw4, but not the Bw6, epitope is the factor that confers this protection.
Homozygosity for HLA-Bw4 alleles was significantly associated with "profound" suppression of HIV viral load, they said. This condition was also significantly linked to the ability to maintain relatively normal CD4 cell counts and to avoid progression to full-blown AIDS.
The HLA-Bw4 motif binds to a natural killer cell inhibitory receptor, the researchers noted. This differentiates it from HLA-Bw6, which does not act as a ligand for such receptors and may explain its antiviral effects.
The link between HLA-Bw4 homozygosity and protection from AIDS was independent of other genetic factors that might confer resistance ("Control of HIV 1 viremia and protection from AIDS are associated with HLA-Bw4 homozygosity," Proc Natl Acad Sci U S A 2001 Apr 24;98(9):5140-5.
"We conclude that homozygosity for HLA-Bw4-bearing B alleles is associated with a significant advantage [for HIV patients]," Goldfeld and colleagues wrote, "and that the HLA-Bw4 motif is important in AIDS pathogenesis."
The corresponding author for this report is A.E. Goldfeld, Center for Blood Research, 800 Huntington Avenue, Boston, MA 02115, USA.
Key points reported in this study include:
This article was prepared by AIDS Weekly editors from staff and other reports.
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