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Published on: August 31, 2014
CCL3L gene copy number and survival in an HIV-1 infected Zimbabwean population
Margit Hørup Larsen1, Lise Wegner Thørner, Rutendo Zinyama
1Department of Clinical Immunology, Copenhagen University Hospital, Denmark. margit.h.larsen@rh.regionh.dk
Insights
Copy number variation (CNV) in the C-C motif chemokine ligand 3-like (CCL3L) gene was not associated with HIV status, disease progression, or survival in a Zimbabwean cohort. This study found no link between CCL3L CNV and HIV pathogenesis.
Area of Science:
- Immunology
- Genetics
- Virology
Background:
- The C-C motif chemokine ligand 3-like (CCL3L) protein inhibits HIV entry by binding to CCR5.
- Copy number variation (CNV) in CCL3L has been inconsistently linked to HIV susceptibility and AIDS progression.
Purpose of the Study:
- To investigate the association between CCL3L CNV and HIV status, progression (CD4 T-cell count, viral load), and survival in a Zimbabwean population.
- To explore the effect of CCL3L CNV on CCL3 protein concentration.
Main Methods:
- A treatment-naïve cohort of 153 HIV-infected and 159 HIV-uninfected individuals was followed for up to 4.3 years.
- CCL3L CNV was quantified using duplex real-time polymerase chain reaction.
Main Results:
- No significant association was found between CCL3L CNV strata and HIV status (P=0.7).
- CCL3L CNV did not correlate with CD4 T-cell counts (P=0.9), viral load (P=0.9), or CCL3 protein levels (P=1.0).
- Survival among HIV-infected individuals did not differ based on CCL3L copy number.
Conclusions:
- CCL3L CNV does not appear to influence HIV status, disease progression, or survival in this Zimbabwean cohort.
- The findings suggest CCL3L CNV is not a significant factor in HIV pathogenesis within this population.
Abstract:
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-naïve 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.
