- Abstract:
-
Treatment of wild-type human immunodeficiency virus [HIV-1(IIIB)]-infected cell cultures with the thiocarboxanilide UC-781 under low selective pressure (i.e., 0.01 microg/ml) resulted in the emergence of V106A RT mutant virus. On increasing drug concentrations (stepwise up to 30 microg/ml) the virus retained the V106A RT mutation but acquired the novel F227L mutation in the RT genome in addition to the L100I, K1O1I, and Y181C mutations. This multiple-mutant virus proved highly resistant to vi...
Expand abstract - Publication status:
- Published
- Publisher copy:
- 10.1089/aid.1998.14.255
-
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- Journal:
- AIDS research and human retroviruses
- Volume:
- 14
- Issue:
- 3
- Pages:
- 255-260
- Publication date:
- 1998-02-05
- DOI:
- EISSN:
-
1931-8405
- ISSN:
-
0889-2229
- URN:
-
uuid:91a72474-f00d-4ebd-9e4b-94d2238e8583
- Source identifiers:
-
26720
- Local pid:
- pubs:26720
- Copyright date:
- 1998
Journal article
A novel mutation (F227L) arises in the reverse transcriptase of human immunodeficiency virus type 1 on dose-escalating treatment of HIV type 1-infected cell cultures with the nonnucleoside reverse transcriptase inhibitor thiocarboxanilide UC-781.
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