Mutations in the central polypurine tract of HIV-1 result in delayed replication.
The reverse transcription of HIV-1 generates a linear genomic DNA with a single-stranded gap. The gap is believed to be the result of plus-strand priming from a second, centrally located, polypurine tract (PPT). A mutant containing four amino-acid-neutral purine-to-pyrimidine changes within the central PPT did not replicate as fast as wild-type virus. Another mutant with the entire 15-bp PPT deleted was replication-deficient. The results indicate that plus-strand priming at the central PPT is important for viral replication, possibly by ensuring efficient DNA synthesis.
Hungnes
O
O
Department of Virology, National Institute of Public Health, Oslo, Norway.
Tjøtta
E
E
Grinde
B
B
D001483:Base Sequence; D004279:DNA, Viral / Q000235:genetics*; D015497:HIV-1 / Q000235:genetics*; D007700:Kinetics; D008969:Molecular Sequence Data; D016297:Mutagenesis, Site-Directed; D009154:Mutation; D011687:Purines / Q000378:metabolism*; D014779:Virus Replication / Q000235:genetics*
D004279:DNA, Viral; D011687:Purines