Journal
JOURNAL OF VIROLOGY
Volume 82, Issue 15, Pages 7716-7720Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.00120-08
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Funding
- NIAID NIH HHS [T32 AI049815, T32 AI49815, AI049781, R01 AI049781] Funding Source: Medline
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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.
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