Effect of DNA repair protein Rad18 on viral infection

Aliza G. Lloyd, Satoshi Tateishi, Paul D. Bieniasz, Mark A. Muesing, Masaru Yamaizumi, Lubbertus C.F. Mulder

Research output: Contribution to journalArticlepeer-review

31 Scopus citations

Abstract

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. Copyright:

Original languageEnglish
Pages (from-to)368-373
Number of pages6
JournalPLoS Pathogens
Volume2
Issue number5
DOIs
StatePublished - May 2006
Externally publishedYes

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