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Journal of Virology, August 2008, p. 7716-7720, Vol. 82, No. 15
0022-538X/08/$08.00+0     doi:10.1128/JVI.00120-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Compensatory Role of Human Immunodeficiency Virus Central Polypurine Tract Sequence in Kinetically Disrupted Reverse Transcription{triangledown}

Mark Skasko1 and Baek Kim1,2*

Department of Microbiology and Immunology,1 Department of Oncology, School of Medicine, University of Rochester, 601 Elmwood Avenue, Box 672, Rochester, New York 146422

Received 17 January 2008/ Accepted 12 May 2008

We tested whether the additional positive-strand DNA synthesis initiation of human immunodeficiency virus type 1 (HIV-1) from the central polypurine tract (cPPT) facilitates efficient completion of kinetically disturbed proviral DNA synthesis induced by dysfunctional reverse transcriptase (RT) mutants or limited cellular deoxynucleoside triphosphate (dNTP) pools. Indeed, the cPPT enabled the HIV-1 vectors harboring RT mutants with reduced dNTP binding affinity to transduce human lung fibroblasts (HLFs), without which these mutant vectors normally fail to transduce. The cPPT showed little effect on wild-type HIV-1 vector transduction in HLF, whereas it significantly enhanced vector transduction in HLFs engineered to contain reduced dNTP pools, suggesting a novel compensatory role for cPPT in viruses harboring kinetically impaired RT.

* Corresponding author. Mailing address: 601 Elmwood Avenue, Box 672, Department of Microbiology and Immunology, University of Rochester Medical Center, Rochester, NY 14642. Phone: (585) 275-6916. Fax: (585) 473-9573. E mail: baek_kim{at}urmc.rochester.edu

{triangledown} Published ahead of print on 21 May 2008.

Journal of Virology, August 2008, p. 7716-7720, Vol. 82, No. 15
0022-538X/08/$08.00+0     doi:10.1128/JVI.00120-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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