Abstract
Current human immunodeficiency virus type 1 pandemic is believed to originate from cross-species transmission of simian immunodeficiency virus (SIV) into human population. Such cross-species transmission, however, is not efficient in general, because viral replication is modulated by host cell factors, with the species-specificity of these factors affecting viral tropism. An understanding of those host cell factors that affect viral replication contributes to elucidation of the mechanism for determination of viral tropism. This review will focus an anti-viral effect of ApoB mRNA editing catalytic subunit, tripartite motif protein 5 alpha, and cyclophilins on SIV replication and provide insight into the mechanism of species-specific barriers against viral infection in human cells. It will then present our current understanding of the mechanism that may explain zoonotic transmission of retroviruses.
Highlights
There is significant evidence that the ongoing worldwide acquired immunodeficiency syndrome (AIDS) epidemic was caused by cross-species transmission of simian immunodeficiency viruses (SIVs) into the human population
Viral replication is modulated by host cell factors, with the species-specificity of these factors affecting viral tropism
Two recent studies showed that the cellular protein SAMHD1 is myeloid-lineage cell-specific HIV-1 restriction factor counteracted by Vpx proteins from HIV-2 and SIVsm (Hrecka et al, 2011; Laguette et al, 2011)
Summary
Current human immunodeficiency virus type 1 pandemic is believed to originate from crossspecies transmission of simian immunodeficiency virus (SIV) into human population Such cross-species transmission, is not efficient in general, because viral replication is modulated by host cell factors, with the species-specificity of these factors affecting viral tropism. This review will focus an anti-viral effect of ApoB mRNA editing catalytic subunit, tripartite motif protein 5 alpha, and cyclophilins on SIV replication and provide insight into the mechanism of species-specific barriers against viral infection in human cells. It will present our current understanding of the mechanism that may explain zoonotic transmission of retroviruses
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