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Antiviral Therapeutic Research Unit, Wellcome Research Laboratories, Langley Court, South Eden Park Road, Beckenham, Kent BR3 3BS, U.K.
Introduction. It has become apparent from recent studies that human immunodeficiency virus type 1 (HIV-1) has an enormous capacity to mutate in order to become resistant to anti-retroviral agents (for a review see Larder, 1993). Monotherapy with nucleoside analogues or non-nucleoside reverse transcriptase (RT) inhibitors (NNRTIs) has, without exception, resulted in the emergence of drug-resistant virus. This may take only a matter of weeks with NNRTIs (Richman et al., 1993; Saag et al., 1993), or months to years in the case of the most studied nucleosides 3'-azido-3'-deoxythymidine (AZT, zidovudine), 2',3'-dideoxyinosine (ddI) and 2',3'-dideoxycytidine (ddC; Boucher et al., 1990; Fitzgibbon et al., 1992; Japour et al., 1991; Land et al., 1990; Larder et al., 1989; McLeod et al., 1992; Richman et al., 1990; Rooke et al., 1989; St. Clair et al., 1991). Genetic characterization of these mutant strains has revealed that specific mutations in the RT coding region are responsible for the observed resistance (Fitzgibbon et al., 1992; Kellam et al., 1992; Larder & Kemp, 1989; Richman et al., 1993; Saag et al., 1993; St. Clair et al., 1991).
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