Virus-Directed Damage Control

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Science  11 Mar 2005:
Vol. 307, Issue 5715, pp. 1535
DOI: 10.1126/science.307.5715.1535d

Viruses are successful pathogens because of the many and varied ways they usurp host proteins for their own gain.

Uracil DNA glycosylase (UNG2) is part of the base-excision repair (BER) machinery that helps preserve the integrity of cellular DNA. UNG2 is packaged into the virions of human immunodeficiency virus (HIV) type 1, but the enzyme's role in this context is unclear. Priet et al. now show that the virion-associated UNG2 is essential to the viral life cycle. UNG2 counteracts the misincorporation of uracil into viral DNA, an event that could be deleterious to the virus. Intriguingly, in experiments exploring the effect of HIV on host BER, Aukrust et al. find that CD4+ T cells from HIV-infected patients exhibit a decline in DNA glycosylase activity and are impaired in their capacity to repair cellular DNA damage. Both abnormalities were ameliorated by antiretroviral drugs.

Whether or not these effects on BER are mechanistically linked, it's clear that in both scenarios the advantage goes to the virus. — PAK

Mol. Cell 17, 479 (2005); Blood 10.1182/blood-2004-11-4272 (2005)

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