Abstract
A total of 786 patients failing antiretroviral therapy were examined for the presence of HIV genotypes causing broad cross-resistance to nucleos(t)ide analogues. They were found to be present in 40% of patients. The Q151M complex and 67/69 inserts were also recognized in 3% of patients. Although thymidine-associated mutations, which favour drug removal (pyrophosphorolysis), were involved in the majority of cases, mutations reducing drug binding were relatively infrequent, probably because of their effect on viral fitness.
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