Effect of DNA repair protein Rad18 on viral infection.

Host factors belonging to the DNA repair machineries are assumed to aid retroviruses in the obligatory step of integration. Here we describe the effect of DNA repair molecule Rad18, a component of the post-replication repair pathway, on viral infection. Contrary to our expectations, cells lacking Ra...

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Main Authors: Aliza G Lloyd, Satoshi Tateishi, Paul D Bieniasz, Mark A Muesing, Masaru Yamaizumi, Lubbertus C F Mulder
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2006-05-01
Series:PLoS Pathogens
Online Access:https://doi.org/10.1371/journal.ppat.0020040
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author Aliza G Lloyd
Satoshi Tateishi
Paul D Bieniasz
Mark A Muesing
Masaru Yamaizumi
Lubbertus C F Mulder
author_facet Aliza G Lloyd
Satoshi Tateishi
Paul D Bieniasz
Mark A Muesing
Masaru Yamaizumi
Lubbertus C F Mulder
author_sort Aliza G Lloyd
collection DOAJ
description Host factors belonging to the DNA repair machineries are assumed to aid retroviruses in the obligatory step of integration. Here we describe the effect of DNA repair molecule Rad18, a component of the post-replication repair pathway, on viral infection. Contrary to our expectations, cells lacking Rad18 were consistently more permissive to viral transduction as compared to Rad18(+/+) controls. Remarkably, such susceptibility was integration independent, since retroviruses devoid of integration activity also showed enhancement of the initial steps of infection. Moreover, the elevated sensitivity of the Rad18(-/-) cells was also observed with adenovirus. These data indicate that Rad18 suppresses viral infection in a non-specific fashion, probably by targeting incoming DNA. Furthermore, considering data published recently, it appears that the interactions between DNA repair components with incoming viruses, often result in inhibition of the infection rather than cooperation toward its establishment.
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spelling doaj.art-5dcfe56be2894fb7878bd35cd7eee0112022-12-21T20:06:49ZengPublic Library of Science (PLoS)PLoS Pathogens1553-73661553-73742006-05-0125e4010.1371/journal.ppat.0020040Effect of DNA repair protein Rad18 on viral infection.Aliza G LloydSatoshi TateishiPaul D BieniaszMark A MuesingMasaru YamaizumiLubbertus C F MulderHost factors belonging to the DNA repair machineries are assumed to aid retroviruses in the obligatory step of integration. Here we describe the effect of DNA repair molecule Rad18, a component of the post-replication repair pathway, on viral infection. Contrary to our expectations, cells lacking Rad18 were consistently more permissive to viral transduction as compared to Rad18(+/+) controls. Remarkably, such susceptibility was integration independent, since retroviruses devoid of integration activity also showed enhancement of the initial steps of infection. Moreover, the elevated sensitivity of the Rad18(-/-) cells was also observed with adenovirus. These data indicate that Rad18 suppresses viral infection in a non-specific fashion, probably by targeting incoming DNA. Furthermore, considering data published recently, it appears that the interactions between DNA repair components with incoming viruses, often result in inhibition of the infection rather than cooperation toward its establishment.https://doi.org/10.1371/journal.ppat.0020040
spellingShingle Aliza G Lloyd
Satoshi Tateishi
Paul D Bieniasz
Mark A Muesing
Masaru Yamaizumi
Lubbertus C F Mulder
Effect of DNA repair protein Rad18 on viral infection.
PLoS Pathogens
title Effect of DNA repair protein Rad18 on viral infection.
title_full Effect of DNA repair protein Rad18 on viral infection.
title_fullStr Effect of DNA repair protein Rad18 on viral infection.
title_full_unstemmed Effect of DNA repair protein Rad18 on viral infection.
title_short Effect of DNA repair protein Rad18 on viral infection.
title_sort effect of dna repair protein rad18 on viral infection
url https://doi.org/10.1371/journal.ppat.0020040
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