We aimed to evaluate the frequency and associated factors of baseline NS5A resistance-associated substitutions (RASs) in patients coinfected with human immunodeficiency virus (HIV) and hepatitis C virus (HCV) monoinfection with genotype 1b (GT1b) or genotype 1a (GT1a). Moreover, we performed a phylogenetic analysis to evaluate the pattern of clustering among samples of patients with RASs. Fifty-five patients were infected with GT1a, of whom 44 (80%) were HIV-infected patients. RAS prevalence in GT1a was 14% (6/44) and distributed as follows: 5 (11%) harbored M28V and 1 (2%) A92T. Twenty-four patients were infected with HCV GT1b, of whom only 5 (21%) were HIV coinfected; RASs were found in 17/24 (71%) patients, as follows: Y93H+F37L+Q54H (1/24), Y93H+F37L (1/24), P58S (1/24), L31F+F37L (1/24), F37L+H/Q54H (3/24), and F37L (10/24). Only GT1b was significantly associated with RASs (adjusted odds ratio 16.37; 95% confidence interval 2.74-97.48;  = 0.002) in the multivariate analysis. A cluster of sequences from HIV/HCV GT1a patients was found; however, we did not find phylogenetic relationships among sequences with NS5A RASs. In our population of HCV-infected patients, the frequency of NS5A RASs at baseline was somewhat similar to the previously reported worldwide rate. HCV GT1b showed the most significant association with harboring of NS5A RASs. Of note, despite there being clusters among sequences of HIV-coinfected patients, NS5A RASs were not transmitted.
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