Effect of DNA Repair Protein Rad18 on Viral Infection

PLoS Pathogens

Satoshi Tateishi¹  Masaru Yamaizumi¹  Mark A Muesing²  Aliza G Lloyd²  Paul D Bieniasz²  Lubbertus C. F Mulder² 

[1] Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan;The Aaron Diamond AIDS Research Center, The Rockefeller University, New York, New York, United States of America

关键词: HIV-1;    DNA repair;    Vector-borne diseases;    Adenoviruses;    Reverse transcription;    Flow cytometry;    Green fluorescent protein;    Viral transmission;    infection;   

DOI  :  10.1371/journal.ppat.0020040

学科分类：生物科学（综合）

来源: Public Library of Science

【 摘 要 】

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.

【 授权许可】

CC BY