CCL3L gene copy number and survival in an HIV-1 infected Zimbabwean population

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• 作者：Margit Hø ; rup Larsen^a ; ^{margit.h.larsen@rh.regionh.dk} ; Lise Wegner Thø ; rner^a ; Rutendo Zinyama^b ; ^c ; Janne Amstrup^a ; Per Kallestrup^d ; Jan Gerstoft^e ; Exnevia Gomo^c ; Christian Erikstrup^f ; Henrik Ullum^a
• 关键词：CCL3L ; CNV ; HIV survival ; CCL3 protein
• 刊名：Infection ; Genetics and Evolution
• 出版年：2012
• 期刊代码：119_15671348
• 类别：med
• 出版时间：July, 2012
• 卷：12
• 期：5
• 页码：1087-1093
• 文件大小：545 K

摘要

The C-C motif chemokine ligand 3-like (CCL3L) protein is a potent chemoattractant which by binding to C-C chemokine receptor type 5 (CCR5) inhibits human immunodeficiency virus (HIV) entry. Copy number variation (CNV) of the CCL3L has been shown to be associated with HIV susceptibility and progression to AIDS, but these results have been inconsistent. We examined a Zimbabwean study population for an association of CCL3L CNV with HIV status, progression (CD4 T-cells and viral load), and survival. Another aim was to investigate the possible effects of CCL3L CNV on CCL3 protein concentration. A treatment-na茂ve cohort, which included 153 HIV infected and 159 HIV uninfected individuals, was followed for up to 4.3 years. The CNV of the CCL3L was determined by duplex real-time polymerase chain reaction. We found no association between four CCL3L CNV strata and HIV status (P = 0.7), CD4 T-cell count (P = 0.9), viral load (P = 0.9), or CCL3 protein levels (P = 1.0). Survival among the HIV infected individuals did not differ according to CCL3L copy number. In this cohort, CCL3L CNV did not affect HIV status, pathogenesis, or survival.