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Herpes virus hijacks DNA repair process

erbert W. "Skip" Virgin, M.D., Ph.D., Edward Mallinckrodt Professor and head of the Department of Pathology and Immunology, Tarakanova found that murine herpes virus, rather than the host cell, was triggering the DNA damage response. She showed that introducing just one viral protein into cells led to activation of two cellular proteins involved in the damage response, ATM and H2AX.

The viral protein that triggered this inappropriate activation, orf36, is a kinase, a type of protein that chemically modifies other molecules to activate different processes or transmit signals. Genetic comparisons with several human herpes viruses revealed kinases similar to orf36 in the human viruses. Scientists then took a similar kinase from human Epstein-Barr virus and showed that introducing it into cells also activated the DNA damage response.

When the research team genetically disabled orf36 in the murine herpes virus and infected mouse cells with it, the virus no longer activated the DNA damage response. The virus's ability to replicate also dramatically decreased.

Kinases are versatile proteins that sometimes play multiple roles. To ensure that enhanced viral replication wasn't linked to orf36's interactions with other molecules, researchers turned to mice lacking the genes for ATM and H2AX, the damage response proteins activated by infection. When they infected cells from these mice with murine herpes virus, its ability to reproduce was again curtailed. How DNA damage response benefits viral replication is still a mystery and a topic of continuing investigation in the Virgin lab.

"The discovery that induction of the cells' DNA damage response is an intentional viral strategy, rather than a passive cellular response to viral invasion, means that we should look into whether other DNA viruses use a similar approach to enhance their growth," says Virgin.


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Source:Washington University School of Medicine


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