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The Disassociation of A3G-Related HIV-1 cDNA G-to-A Hypermutation to Viral Infectivity
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The Disassociation of A3G-Related HIV-1 cDNA G-to-A Hypermutation to Viral Infectivity
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Journal Article
The Disassociation of A3G-Related HIV-1 cDNA G-to-A Hypermutation to Viral Infectivity
2024
Overview
APOBEC3G (A3G) restricts HIV-1 replication primarily by reducing viral cDNA and inducing G-to-A hypermutations in viral cDNA. HIV-1 encodes virion infectivity factor (Vif) to counteract A3G primarily by excluding A3G viral encapsidation. Even though the Vif-induced exclusion is robust, studies suggest that A3G is still detectable in the virion. The impact of encapsidated A3G in the HIV-1 replication is unclear. Using a highly sensitive next-generation sequencing (NGS)-based G-to-A hypermutation detecting assay, we found that wild-type HIV-1 produced from A3G-expressing T-cells induced higher G-to-A hypermutation frequency in viral cDNA than HIV-1 from non-A3G-expressing T-cells. Interestingly, although the virus produced from A3G-expressing T-cells induced higher hypermutation frequency, there was no significant difference in viral infectivity, revealing a disassociation of cDNA G-to-A hypermutation to viral infectivity. We also measured G-to-A hypermutation in the viral RNA genome. Surprisingly, our data showed that hypermutation frequency in the viral RNA genome was significantly lower than in the integrated DNA, suggesting a mechanism exists to preferentially select intact genomic RNA for viral packing. This study revealed a new insight into the mechanism of HIV-1 counteracting A3G antiviral function and might lay a foundation for new antiviral strategies.
Publisher
MDPI AG
Subject
Acquired immune deficiency syndrome
/ AIDS
/ Analysis
/ APOBEC-3G Deaminase - genetics
/ APOBEC-3G Deaminase - metabolism
/ APOBEC3G
/ DNA
/ DNA, Complementary - genetics
/ Ethylenediaminetetraacetic acid
/ genome
/ Genomes
/ Genomics
/ High-Throughput Nucleotide Sequencing
/ HIV
/ Human immunodeficiency virus
/ Humans
/ Mutation
/ Plasmids
/ Proteins
/ RNA
/ T cells
/ vif Gene Products, Human Immunodeficiency Virus - genetics
/ vif Gene Products, Human Immunodeficiency Virus - metabolism
/ virion
/ Virions
/ Virus Replication - genetics
/ Viruses
