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 , 1993; Saag , 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 , 1990; Fitzgibbon , 1992; Japour , 1991; Land , 1990; Larder , 1989; McLeod , 1992; Richman , 1990; Rooke , 1989; St. Clair , 1991). Genetic characterization of these mutant strains has revealed that specific mutations in the RT coding region are responsible for the observed resistance (Fitzgibbon , 1992; Kellam , 1992; Larder & Kemp, 1989; Richman , 1993; Saag , 1993; St. Clair , 1991).


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