Proliferation of cells with HIV integrated into cancer genes contributes to persistent infection

Author:

Wagner Thor A.12,McLaughlin Sherry12,Garg Kavita3,Cheung Charles Y. K.3,Larsen Brendan B.2,Styrchak Sheila1,Huang Hannah C.1,Edlefsen Paul T.23,Mullins James I.2,Frenkel Lisa M.12

Affiliation:

1. Seattle Children’s Research Institute, 1900 9th Avenue, Seattle, WA 98101, USA.

2. University of Washington, Seattle, WA, USA.

3. Fred Hutchinson Cancer Research Center, Seattle, WA, USA.

Abstract

A not-so-random integration for HIV Even in the face of a cocktail of antiretroviral drugs, HIV manages to hang on. It does so by integrating its own genome into those of host cells, where it persists in a latent state. To better understand this process, Wagner et al. determined the sites where HIV integrated into three HIV-infected patients treated with antiretroviral drugs for more than a decade. They found an over-representation of sites where HIV integrated into genes associated with cancer and cell proliferation. Also, multiple cells in the same individual harbored the same integration sites. This suggests that integration into specific genes may drive cell proliferation and viral persistence. Science , this issue p. 570

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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