TY - JOUR
T1 - The influence of human leukocyte antigen-types on disease progression among HIV-2 infected patients in Guinea-Bissau
AU - Thomsen, Ditte
AU - Erikstrup, Christian
AU - Jespersen, Sanne
AU - Medina, Candida
AU - Té, David da Silva
AU - Correira, Faustino Gomes
AU - Christiansen, Mette
AU - Wejse, Christian
AU - Krarup, Henrik
AU - Møller, Bjarne Kuno
AU - Hønge, Bo Langhoff
AU - Bissau HIV Cohort study group
PY - 2018/3/27
Y1 - 2018/3/27
N2 - Objectives: HIV-2 is endemic in West Africa and is characterized by lower transmissibility because of lower viral load, and HIV-2-infected persons usually have a slower progression to AIDS. The mechanisms behind the slower disease progression are unknown. The main objective was to identify specific HLA class I and II alleles that may influence the disease progression of HIV-2 infection. Design: Cohort follow-up study. Methods: We used high-resolution HLA typing of DNA from 437 antiretroviral naive HIV-2-infected patients from the Bissau HIV Cohort, Guinea-Bissau, to identify HLA alleles with an influence on HIV-2 disease progression. The effect of HLA-type on viral load and CD4 + cell count was assessed initially by ranksum-test and t-test, followed by adjusted logistic regression and multivariable linear regression analysis, respectively. Results: Three alleles (HLA-B ∗ 58:01, HLA-DPB1 ∗ 10:01 and HLA-DRB1 ∗ 11:01) were associated with lower possibility of detectable baseline plasma viral load (P = 0.002, P = 0.044 and P = 0.033, respectively), and no alleles were associated with higher possibility of detectable plasma viral load. HLA-DPB1 ∗ 10:01 and HLA-DRB1 ∗ 11:01 were in linkage disequilibrium (P = 0.047). Patients with heterozygous HLA types in all their HLA class I loci or in one or two loci were not more likely to have undetectable viral load compared with patients that were homozygous in all their class I loci after adjusting for sex and CD4 + cell count (P = 0.93 and P = 0.88, respectively). Conclusion: The three alleles HLA-B ∗ 58:01, HLA-DPB1 ∗ 10:01 and HLA-DRB1 ∗ 11:01 may protect against HIV-2 disease progression towards AIDS.
AB - Objectives: HIV-2 is endemic in West Africa and is characterized by lower transmissibility because of lower viral load, and HIV-2-infected persons usually have a slower progression to AIDS. The mechanisms behind the slower disease progression are unknown. The main objective was to identify specific HLA class I and II alleles that may influence the disease progression of HIV-2 infection. Design: Cohort follow-up study. Methods: We used high-resolution HLA typing of DNA from 437 antiretroviral naive HIV-2-infected patients from the Bissau HIV Cohort, Guinea-Bissau, to identify HLA alleles with an influence on HIV-2 disease progression. The effect of HLA-type on viral load and CD4 + cell count was assessed initially by ranksum-test and t-test, followed by adjusted logistic regression and multivariable linear regression analysis, respectively. Results: Three alleles (HLA-B ∗ 58:01, HLA-DPB1 ∗ 10:01 and HLA-DRB1 ∗ 11:01) were associated with lower possibility of detectable baseline plasma viral load (P = 0.002, P = 0.044 and P = 0.033, respectively), and no alleles were associated with higher possibility of detectable plasma viral load. HLA-DPB1 ∗ 10:01 and HLA-DRB1 ∗ 11:01 were in linkage disequilibrium (P = 0.047). Patients with heterozygous HLA types in all their HLA class I loci or in one or two loci were not more likely to have undetectable viral load compared with patients that were homozygous in all their class I loci after adjusting for sex and CD4 + cell count (P = 0.93 and P = 0.88, respectively). Conclusion: The three alleles HLA-B ∗ 58:01, HLA-DPB1 ∗ 10:01 and HLA-DRB1 ∗ 11:01 may protect against HIV-2 disease progression towards AIDS.
KW - Journal Article
KW - Guinea-Bissau
KW - HIV-2
KW - viral load
KW - human leukocyte antigens
KW - West Africa
KW - CD4 + cell counts
UR - http://www.scopus.com/inward/record.url?scp=85044190946&partnerID=8YFLogxK
U2 - 10.1097/QAD.0000000000001758
DO - 10.1097/QAD.0000000000001758
M3 - Journal article
C2 - 29369163
SN - 0269-9370
VL - 32
SP - 721
EP - 728
JO - AIDS
JF - AIDS
IS - 6
ER -