human leukocyte antigens and hiv type 1 viral load in early and chronic infection predominance of evolving relationships人类白细胞抗原和艾滋病毒1型病毒载量在早期和慢性感染的优势演进的关系.pdfVIP

human leukocyte antigens and hiv type 1 viral load in early and chronic infection predominance of evolving relationships人类白细胞抗原和艾滋病毒1型病毒载量在早期和慢性感染的优势演进的关系.pdf

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human leukocyte antigens and hiv type 1 viral load in early and chronic infection predominance of evolving relationships人类白细胞抗原和艾滋病毒1型病毒载量在早期和慢性感染的优势演进的关系

Human Leukocyte Antigens and HIV Type 1 Viral Load in Early and Chronic Infection: Predominance of Evolving Relationships 1 2 2 2 2 3 Jianming Tang *, Rakhi Malhotra , Wei Song , Ilene Brill , Liangyuan Hu , Paul K. Farmer , Joseph 4 4,5 3 1,2 Mulenga , Susan Allen , Eric Hunter , Richard A. Kaslow * 1 Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, United States of America, 2 Department of Epidemiology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America, 3 Vaccine Research Center, Emory University, Atlanta, Georgia, United States of America, 4 Rwanda- Zambia HIV-1 Research Group, Lusaka, Zambia, 5 Department of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia, United States of America Abstract Background: During untreated, chronic HIV-1 infection, plasma viral load (VL) is a relatively stable quantitative trait that has clinical and epidemiological implications. Immunogenetic research has established various human genetic factors, especially human leukocyte antigen (HLA) variants, as independent determinants of VL set-point. Methodology/Principal Findings: To identify and clarify HLA alleles that are associated with either transient or durable immune control of HIV-1 infection, we evaluated the relationships of HLA class I and class II alleles with VL among 563 seroprevalent Zambians (SPs) who were seropositive at enrollment and 221 seroconverters (SCs) who became seropositive during quarterly follow-up visits. After statistical adjustments for non-genetic factors (sex and age), two unfavorable alleles (A*3601 and DRB

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