Abstract
The transmission of viruses from animal hosts into humans have led to the emergence of several diseases. Usually these cross-species transmissions are blocked by host restriction factors, which are proteins that can block virus replication at a specific step. In the natural virus host, the restriction factor activity is usually suppressed by a viral antagonist protein, but this is not the case for restriction factors from an unnatural host. However, due to ongoing viral evolution, sometimes the viral antagonist can evolve to suppress restriction factors in a new host, enabling cross-species transmission. Here we examine the classical case of this paradigm by reviewing research on APOBEC3 restriction factors and how they can suppress human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV). APOBEC3 enzymes are single-stranded DNA cytidine deaminases that can induce mutagenesis of proviral DNA by catalyzing the conversion of cytidine to promutagenic uridine on single-stranded viral (−)DNA if they escape the HIV/SIV antagonist protein, Vif. APOBEC3 degradation is induced by Vif through the proteasome pathway. SIV has been transmitted between Old World Monkeys and to hominids. Here we examine the adaptations that enabled such events and the ongoing impact of the APOBEC3-Vif interface on HIV in humans.
Highlights
Spillover of viruses from animal hosts have led to the emergence of several human diseases including COVID-19, severe acute respiratory syndrome (SARS), Nipah, Ebola, influenza and acquired immunodeficiency syndrome (AIDS) [1,2,3,4]
This review examines cross species transmission of the simian immunodeficiency virus (SIV) between primates, with specific focus on the APOBEC3 family of cellular restriction factors that act as single-stranded DNA cytosine deaminases
The A3-mediated restriction is a numbers game and restriction in the presence of a Vif adapted to the specific host A3s is not guaranteed, nearly 30% of nonfunctional but integrated human immunodeficiency virus (HIV)-1 genomes sequenced from HIV-1+ individuals show the characteristic C/G→T/A mutations induced by A3s [99]
Summary
Spillover of viruses from animal hosts have led to the emergence of several human diseases including COVID-19, severe acute respiratory syndrome (SARS), Nipah, Ebola, influenza and acquired immunodeficiency syndrome (AIDS) [1,2,3,4]. To overcome these multiple barriers presented by the host, the virus must make corresponding changes in its genome [6] These cellular restriction factors are always evolving under strong positive selection pressure to acquire adaptations that circumvent suppression by viral pathogens. This positive selection of restriction factors leads to differences in functionality, even in similar species, resulting in the ability of these cellular restriction factors to act as barriers to the cross species transmission of viruses [7] To successfully overcome these barriers and infect a new host, the virus needs to make adaptive changes in its genes that can counteract the new host’s restriction factor. This review examines cross species transmission of the simian immunodeficiency virus (SIV) between primates, with specific focus on the APOBEC3 family of cellular restriction factors that act as single-stranded (ss) DNA cytosine deaminases
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