Abstract
ObjectivesGenetic polymorphism of viral receptors is relevant to risks of HIV-1 infection, while it is still under debated whether the polymorphism of SDF1, a unique ligand for HIV-1 coreceptor CXCR4, is associated with HIV susceptibility and AIDS disease progression. Therefore, we provided an updated quantitative assessment by meta-analysis from 16 case-control and 7 cohort studies.MethodsArticles reporting the relationship between SDF1 polymorphism and HIV susceptibility or AIDS progression were retrieved from PubMed, Embase and Ovid electronic databases up to Apr 2017. Data were pooled by odds ratios (ORs) for HIV-1 infection with 95% confidence intervals (CIs) and summary relative hazards (RHs) for AIDS progression with 95% CIs using 1987 Center for Disease Control (CDC) case definition of AIDS (CDC87) and 1993 Center for Disease Control (CDC) case definition of AIDS (CDC93) and death as endpoints.ResultsAs a result, 16 studies regarding susceptibility to HIV-1 infection with 2803 HIV-infected patients and 3697 healthy individuals and 7 studies regarding disease progression with 4239 subjects were included in the meta-analysis. For risks of infection, no evidences indicated SDF1 polymorphism was associated with the risk of HIV-1 infection in all genetic models (recessive model: OR = 0.94, 95% Cl: 0.75–1.17; homozygous model: OR = 0.89, 95% Cl: 0.70–1.15; heterozygous model: OR = 1.06, 95% Cl: 0.83–1.35; allele model: OR = 0.95, 95% Cl: 0.79–1.13), Furthermore, we failed to find an delayed AIDS progression except in some specific cohorts including MACS cohorts (RH = 0.38, 95% Cl: 0.17–0.59 for time to AIDS; RH = 0.27, 95% Cl: 0.07–0.46 for time to death at the study entry).ConclusionsOverall, no significant association was found between SDF1 polymorphism and HIV susceptibility. A protective effect of SDF1 on AIDS progression and death was seen especially in two studies based on the same cohorts. In conclusion, SDF1 polymorphism exerts a moderate protective effect against AIDS disease deterioration in some specific populations.
Highlights
Viral entry of human immunodeficiency viruses (HIV) required CD4 molecule and one member of CC or CXC chemokine-receptor families as co-receptors on cell membrane of lymphocytes
No evidences indicated SDF1 polymorphism was associated with the risk of HIV-1 infection in all genetic models, we failed to find an delayed AIDS progression except in some specific cohorts including MACS cohorts (RH = 0.38, 95% Cl: 0.17–0.59 for time to AIDS; relative hazards (RHs) = 0.27, 95% Cl: 0.07–0.46 for time to death at the study entry)
No significant association was found between SDF1 polymorphism and HIV susceptibility
Summary
Viral entry of human immunodeficiency viruses (HIV) required CD4 molecule and one member of CC or CXC chemokine-receptor families as co-receptors on cell membrane of lymphocytes. Genetic polymorphism of chemokines or chemokine-receptors was reported to be relevant to risks of human immunodeficiency viruses infection and disease progression. A guanine to adenine mutation at nucleotide position 801 in the 3’ untranslated region (UTR) of SDF1 (abbreviated as SDF13’A) was reported to confer resistance to HIV infection [1, 2] and delay disease progression in homozygous individuals. The authors proposed that SDF1-3’A mutation resulted in higher production of plasma SDF1 level, thereby preventing X4-tropic HIV viruses from binding to CXCR4 receptor [3]. No significant association between SDF1-3’A and HIV infection [7,8,9,10] or AIDS progression was found in other researches. We evaluated the association of SDF1 polymorphism with HIV susceptibility and AIDS disease progression by 16 case-control studies and 7 cohort studies. It is the first time to evaluate the association of SDF1 polymorphism and AIDS progression based on different sources of research subjects
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