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First published online June 20, 2006

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HSV-1 takes ATRIP to VICE city

Viruses have developed many ways to manipulate the DNA replication and repair machinery of their hosts to help them survive and replicate. Now, Dianna Wilkinson and Sandra Weller report that, during lytic infection, herpes simplex virus type 1 (HSV-1) disrupts the ATR-dependent DNA damage response (see p. 2695). ATR – ATM (ataxia telangiectasia-mutated) and Rad3-related kinase – is one of several kinases that activate cell-cycle checkpoints and DNA repair in response to genotoxic stress. It is recruited to sites of DNA damage by its binding partner ATRIP. This recognizes single-stranded DNA bound to hyperphosphorylated replication protein A (P-RPA). Wilkinson and Weller use immunofluorescence to show that HSV-1 infection uncouples ATRIP from ATR and sequesters ATRIP and P-RPA in unique virus-induced nuclear domains (VICE domains). The HSV-1 immediate early protein ICP0 is sufficient to cause this redistribution. Thus, explain the authors, HSV-1 disarms the ATR signalling pathway that would otherwise respond to HSV-1-induced genotoxic stress and interfere with the progression of the viral infection.

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Related articles in JCS:

Herpes simplex virus type I disrupts the ATR-dependent DNA-damage response during lytic infection

Dianna E. Wilkinson and Sandra K. Weller
JCS 2006 119: 2695-2703. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?