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Journal of Virology, June 2009, p. 6222-6233, Vol. 83, No. 12
0022-538X/09/$08.00+0 doi:10.1128/JVI.00356-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
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Sanggu Kim,2,5,
Namshin Kim,3,
Samson A. Chow,4,5 and
Jerome A. Zack1,4,5*
Department of Medicine, Division of Hematology-Oncology,1 Department of Microbiology Immunology and Molecular Genetics,2 Molecular Biology Institute,3 Department of Molecular and Medical Pharmacology,4 UCLA AIDS Institute, UCLA School of Medicine, Los Angeles, California 900955
Received 17 February 2009/ Accepted 2 April 2009
Until very recently, quiescent CD4+ T cells were thought to be resistant to human immunodeficiency virus (HIV) infection. Subsequent studies, attempting to fully elucidate the mechanisms of resistance, showed that quiescent cells could become infected by HIV at low efficiency and form a latently infected population. In this study, we set out to identify the sites of viral integration and to assess the efficiency of the overall integration process in quiescent cells. Based on our results, HIV integration in quiescent CD4+ T cells occurs in sites similar to those of their prestimulated counterparts. While site selections are similar, the integration process in quiescent cells is plagued by the formation of high levels of incorrectly processed viral ends and abortive two-long-terminal-repeat circles.
Published ahead of print on 15 April 2009.
Supplemental material for this article may be found at http://jvi.asm.org/.
These authors contributed equally to this study.
Present address: Korean Bioinformatics Center, Korea Research Institute of Bioscience and Technology, Daejeon 305-806, South Korea.
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