Abstract
Restriction factors are implemented in long-term evolutionary "arms races," in which viral antagonists drive the evolution of host proteins, and vice versa. Consequently, restriction factors are remarkably variable, displaying polymorphism within species and divergence between species as a result of positive selection. This paper investigates diversity in the APOBEC3F (A3F) restriction factors of Old World primates in order to determine whether they display evidence of involvement in an evolutionary "arms race." We speculated that genetic variability in A3F could reflect evolutionary conflict with the VIF proteins of primate lentiviruses, which are known to enhance viral replication by binding and degrading host A3 proteins. A3Fs of several Old World primate species were genotyped, and the sequences revealed both intra-spcies diversity and inter-species divergence. Representative rhesus macaque (<em>macaca mulatta</em>) sequences were cloned and tested for sensitivity to VIFs from various simin immunodeficiency viruses (SIVs). Evolution of A3F in the rhesus lineage is not due to selection by SIVs, but may reflect antagonism by another retrovirus.
Highlights
The SIV of a given primate species cannot readily infect a different species without undergoing numerous adaptamay not be effective against the homologous restriction mechanisms of other organisms.11 tions
Part of this adaptation process involves evading host antiviral proteins known as restriction factors
Interaction between APOBEC3 and Vif target cell types such as T-cells, macrophages, and dendritic cells, and they are active in restricting retroviruses as well Soon after the discovery of HIV-1, the viral protein termed as some other viruses that do not replicate via reverse viral infectivity factor (Vif) was found to be necessary for transcription
Summary
Acquired Immune Deficiency Syndrome (AIDS) was first identified as a disease in 1981, as increasing numbers of homosexual men were dying of opportunistic infections after becoming immunocompromised. The causative agent was soon discovered to be a lentivirus, classified as Human Immunodeficiency Virus Type 1 (HIV-1). HIV-1 and its close relative HIV Type 2 (HIV-2) arose in human populations as a result of cross-species transmission events from natural simian hosts of the Simian Immuno-. Viruses have evolved specific proteins to evade the mechanism of a particular restriction factor This virus-host relationship is highly species-specific because of the rapid adaptation process. The SIV of a given primate species cannot readily infect a different species without undergoing numerous adaptamay not be effective against the homologous restriction mechanisms of other organisms. tions Part of this adaptation process involves evading host antiviral proteins known as restriction factors. Interaction between APOBEC3 and Vif target cell types such as T-cells, macrophages, and dendritic cells, and they are active in restricting retroviruses as well Soon after the discovery of HIV-1, the viral protein termed as some other viruses that do not replicate via reverse viral infectivity factor (Vif) was found to be necessary for transcription.. Highly conserved N-terminal motifs are involved with A3G the idea of an evolutionary “arms race” between restriction and A3F binding. factors and their viral antagonists
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