Effects of APOBEC3G's Cytidine Deaminase Activity on Retroviral Evolution

Mary-Benedicta Obikili

doi:10.52214/cusj.v15i1.7788

Abstract

Apolipoprotein B editing complex (APOBEC3/A3) genes are found in mammalian cells. In primates, there are 7 APOBEC3 genes, namely, 3A, 3B, 3C, 3DE, 3F, 3G, and 3H. Previous research has shown that A3 proteins help to inhibit viral infection via their cytidine deaminase activity. However, it has also been found that A3 proteins could also lead to viral evolution, where viruses such as HIV (Human Immunodeficiency Virus) instead gain beneficial mutations that enable them to overcome the antiviral activity of A3 proteins, gain resistance to certain drugs used for treating viral infections and escape recognition by the immune system. This paper is a review article summarizing the role of A3G on viral infection and evolution, and the potential impact viral evolution could have in treatment of retroviral infections such as HIV.

Highlights

Apolipoprotein B- Editing Complex 3 (APOBEC3/A3) genes encode enzymes that prevent viral infection through their cytidine deaminase activity [1]
APOBEC3 proteins help inhibit viral infection through their cytidine deaminase activity, A3D, A3F, A3G, and A3H may play a role in viral evolution, where viruses such as HIV gain beneficial mutations that enable them to overcome the antiviral activity of A3 proteins
Many studies have shown the effects of the cytidine deaminase activity of the A3 genes on retroviral evolution

Summary

Introduction

Apolipoprotein B- Editing Complex 3 (APOBEC3/A3) genes encode enzymes that prevent viral infection through their cytidine deaminase activity [1]. APOBEC3 proteins help inhibit viral infection through their cytidine deaminase activity, A3D, A3F, A3G, and A3H may play a role in viral evolution, where viruses such as HIV gain beneficial mutations that enable them to overcome the antiviral activity of A3 proteins The cytidine deaminase activity of A3 proteins may lead to retroviral evolution, where the virus gains beneficial mutations that help the virus to counteract A3 antiviral activity [5, 6].

Results

Conclusion