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AIDS Res Hum Retroviruses. 2016 Jan;32(1):44-9. doi: 10.1089/aid.2015.0120. Epub 2015 Sep 18.

HLA Class I Alleles Associated with Mortality in Thai Military Recruits with HIV-1 CRF01_AE Infection.

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1 Infectious Diseases Division, Massachusetts General Hospital, Boston, Massachusetts and Ragon Institute of Massachusetts General Hospital , MIT and Harvard, Cambridge, Massachusetts.
2 Harvard School of Public Health , Boston, Massachusetts.
3 Department of Military and Community Medicine, Phramongkutklao College of Medicine , Bangkok, Thailand .
4 Research Division, Armed Forces Research Institute of Medical Sciences (AFRIMS)-Royal Thai Army , Bangkok, Thailand .
5 International Vaccine Institute, Seoul, Republic of Korea.
6 Henry M. Jackson Foundation for the Advancement of Military Medicine , Bethesda, Maryland.
7 Department of Transfusion Medicine, Faculty of Medicine, Siriraj Hospital , Bangkok, Thailand .
8 Armed Forces Research Institute of Medical Sciences, Bangkok, Thailand and Military Malaria Research Program, Walter Reed Army Institute of Research , Silver Spring, Maryland.
9 Department of Epidemiology, Bloomberg School of Public Health, Johns Hopkins University , Baltimore, Maryland.


In HIV-1-infected patients, variation at the HLA class I locus is associated with disease progression, but few studies have assessed the influence of HLA alleles on HIV-1 CRF01_AE infection, which is dominant in Thailand. We hypothesized that alleles predicted to confer more effective immune responses, such as HLA-B*46, would protect against disease progression. HLA typing was performed on HIV-1 incident cases surviving until 1998-1999 and HIV-1-negative matched controls from Thai army cohorts enrolled between 1991 and 1995. We assessed associations between class I alleles and disease progression subsequent to HLA typing. Ninety-nine HIV-1-incident cases were followed for a median of 3.7 years after HLA typing; during this time, 58 participants died. Two alleles were associated with mortality: HLA B*51 was protective (3-year survival B*51(pos) vs. B*51(neg): 75% vs. 52%; p = 0.034) whereas Cw*04 was deleterious (3-year survival Cw*04(pos) vs. Cw*04(neg): 39% vs. 60%; p = 0.027). HLA-B*46 was not associated with disease progression. Alleles present at different frequencies in HIV-1-incident compared with HIV-1-negative men included HLA-A*02:03, B*35, B*15, and C*08. 1. In conclusion in this Thai army cohort, HLA-B*51 was associated with lower mortality, confirming that this allele, which is protective in clade B HIV-1 infection, has a similar effect on HIV CRF01_AE infection. The deleterious effect of HLA-Cw*04 must be interpreted with caution because it may be in linkage disequilibrium with disease-susceptible HLA-B alleles. We did not find that HLA-B*46 was protective. These findings may inform vaccine development for areas of the world in which HIV-1 CRF01_AE infection is prevalent.

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