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A new point mutation (P157S) in the reverse transcriptase of human immunodeficiency virus type 1 confers low-level resistance to (-)-beta-2',3'-dideoxy-3'-thiacytidine. 1999
R A Smith, and
G J Klarmann, and
K M Stray, and
U K von Schwedler, and
R F Schinazi, and
B D Preston, and
T W North
Eccles Institute of Human Genetics, University of Utah, Salt Lake City, Utah 84112, USA.
A P157S mutation in the reverse transcriptase (RT) of human immunodeficiency virus type 1 conferred fivefold resistance to (-)-beta-2',3'-dideoxy-3'-thiacytidine in cell culture. Interestingly, the P157S mutation resulted in increased sensitivity (two- to threefold) to 3'-azido-3'-deoxythymidine (AZT) and to (R)-9-(2-phosphonylmethoxypropyl)adenine (PMPA). A similar increase in susceptibility to AZT and to PMPA was also conferred by the M184V mutation in RT.
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