Temporal effect of HLA-B*57 on viral control during primary HIV-1 infection
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1742-4690-10-139.pdf
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Author(s)
Vaidya, Sagar A
Streeck, Hendrik
Beckwith, Noor
Ghebremichael, Musie
Pereyra, Florencia
Addo, Marylyn M.
Rychert, Jenna
Routy, Jean-Pierre
Jessen, Heiko
Kelleher, Anthony D
Date Issued
November 2013
Journal
Retrovirology
Publisher
BioMed Central Ltd
Citation
Vaidya, Sagar A et al. “Temporal Effect of HLA-B*57 on Viral Control during Primary HIV-1 Infection.” Retrovirology 10.1 (2013): 139.
Version
Final published version
Abstract
Background:
HLA-B alleles are associated with viral control in chronic HIV-1 infection, however, their role in primary HIV-1 disease is unclear. This study sought to determine the role of HLA-B alleles in viral control during the acute phase of HIV-1 infection and establishment of the early viral load set point (VLSP).
Findings:
Individuals identified during primary HIV-1 infection were HLA class I typed and followed longitudinally. Associations between HLA-B alleles and HIV-1 viral replication during acute infection and VLSP were analyzed in untreated subjects. The results showed that neither HLA-B*57 nor HLA-B*27 were significantly associated with viral control during acute HIV-1 infection (Fiebig stage I-IV, n=171). HLA-B*57 was however significantly associated with a subsequent lower VLSP (p<0.001, n=135) with nearly 1 log[subscript 10] less median viral load. Analysis of a known polymorphism at position 97 of HLA-B showed significant associations with both lower initial viral load (p<0.01) and lower VLSP (p<0.05). However, this association was dependent on different amino acids at this position for each endpoint.
Conclusions:
The effect of HLA-B*57 on viral control is more pronounced during the later stages of primary HIV-1 infection, which suggests the underlying mechanism of control occurs at a critical period in the first several months after HIV-1 acquisition. The risk profile of polymorphisms at position 97 of HLA-B are more broadly associated with HIV-1 viral load during primary infection and may serve as a focal point in further studies of HLA-B function.
MIT Department
Koch Institute for Integrative Cancer Research at MIT
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DOI of Published Version
https://doi.org/10.1186/1742-4690-10-139
