The highly active antiretroviral treatment (HAART) has allowed people living with HIV to live longer with a better quality of life. However, toxicity and the emergence of drug resistance arise from HAART use. Therefore, new antiretroviral therapy is needed since no cure or vaccine is available against HIV. Virus-host interaction has been proven to be important in the last decade. Host factors such as the C-C chemokine receptor type 5 (CCR5), a receptor used by HIV to penetrate host cells, have led to the discovery of the Maraviroc, which is an antiretroviral medication used in the United States. In contrast, other factors like C-X-C Motif Chemokine Receptor 4 (CXCR4) and the Apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3G (APOBEC3G), a potent host defense factor against HIV, is under investigation. APOBEC3G antiviral activity remains a possible therapeutic target against HIV. This systematic review aimed to synthesize the available evidence on the role of APOBEC3G polymorphisms and their expression on HIV infection disease progression in Africa. We used Web of Science, PubMed, Embase, and Google Scholar and searched for relevant publications in French or English reporting on APOBEC3G polymorphisms association with HIV infection in African populations from January 2009 to May 2023. The PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-analyzes) was used to process for reporting systematic review. Fifteen studies were included, of which seven were on APOBEC3G polymorphisms and eight were on APOBEC3G expression. Among the APOBEC3G polymorphisms, the most studied was H186R or rs8177832. The average of the minor allele frequency of H186R of APOBEC3G available for the studies included in this study was 0.29 with a 95% CI (0.172; 0.401) and varied from 0.108 reported in Uganda to 0.47 recorded from Burkina Faso. The polymorphism H186R was not associated with HIV status in Southern Africa. However, the referent allele of H186R was protective against HIV infection in Western Central Africa, while in West Africa, it was the minor allele (G) of H186R which was protective against HIV. This review warrants a need to increase research on APOBEC3G, from its variants to its hypermutations on the continent with an essential variety of HIV-1 subtypes, to impact the research on A3G-based anti-HIV strategies.
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