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SIV replication in human cells

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 facto...

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Detalles Bibliográficos
Autores principales: Sakuma, Ryuta, Takeuchi, Hiroaki
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Research Foundation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3366772/
https://www.ncbi.nlm.nih.gov/pubmed/22679440
http://dx.doi.org/10.3389/fmicb.2012.00162
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author Sakuma, Ryuta
Takeuchi, Hiroaki
author_facet Sakuma, Ryuta
Takeuchi, Hiroaki
author_sort Sakuma, Ryuta
collection PubMed
description 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.
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spelling pubmed-33667722012-06-07 SIV replication in human cells Sakuma, Ryuta Takeuchi, Hiroaki Front Microbiol Microbiology 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. Frontiers Research Foundation 2012-04-27 /pmc/articles/PMC3366772/ /pubmed/22679440 http://dx.doi.org/10.3389/fmicb.2012.00162 Text en Copyright © Sakuma and Takeuchi. http://www.frontiersin.org/licenseagreement This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) , which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited.
spellingShingle Microbiology
Sakuma, Ryuta
Takeuchi, Hiroaki
SIV replication in human cells
title SIV replication in human cells
title_full SIV replication in human cells
title_fullStr SIV replication in human cells
title_full_unstemmed SIV replication in human cells
title_short SIV replication in human cells
title_sort siv replication in human cells
topic Microbiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3366772/
https://www.ncbi.nlm.nih.gov/pubmed/22679440
http://dx.doi.org/10.3389/fmicb.2012.00162
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