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ABSTRACT
BACKGROUND
Direct-acting antivirals (DAAs) against hepatitis C virus (HCV) infection showed the presence of resistant-associated substitutions (RASs). The aim of the present study was to carry out a follow-up of patients with baseline RASs to report the impact of RASs on DAA therapy outcome.
METHODS
In a cohort study, we analyzed NS5A and NS5B RASs among nine thalassemia cases by baseline RASs. In a 2-year follow-up, we analyzed viral markers and biochemical and hematological parameters of the participants and their sustained virologic response (SVR). Statistical analyses were performed using SPSS software version 22.
RESULTS
RASs for HCV subtype 1a included M28V, L31M, and H58P. For subtype 1b: L28M, R30Q, S24F, and C316N. And for subtype 3a: C316S, and S24F. In patients with cirrhosis (n = 5), ALT (p = 0.001) and AST (p = 0.007) levels were significantly reduced after treatment, and creatinine level slightly increased (p = 0.025). However, no significant data was observed in non-cirrhotic patients following the treatment.
CONCLUSION
The present study did not show any adverse effects of DAA therapy among patients with thalassemia suffering from chronic HCV infection with baseline RASs. Furthermore, reduction in ferritin and liver stiffness levels after DAA therapy could show the efficacy of DAA in such patients.
KEYWORDS:
Direct acting antivirals (DAAs), Resistant associated substitutions (RASs), Chronic HCV infection
INTRODUCTION
Globally, 71 million individuals suffer from chronic hepatitis C virus (HCV) infection with genotypes having specific geographical differences.1 HCV lifecycle is associated with intra- and extrahepatocellular complications, such as cirrhosis and hepatocellular carcinoma (HCC).2 However, recently, it has been shown that direct-acting antivirals (DAAs) have extensively been effective and can reduce the disease burden. It has been shown that DAAs results in a sustained virologic response (SVR) in more than 90% of the treated patients.3
Recently, wide range usage of DAAs against HCV has increased the risk of emerging resistant-associated variants (RAVs) and/or resistant associated substitutions (RASs). Although RASs usually lead to single or multiple antiviral drug resistance, their functions have been altered in unknown situations.4-5 Moreover, there is some evidence that elucidates the co-occurrence of RASs, such as C316N in 1b subtype NS5B gene, which has co-occurring mutations, including L159F, A207T, and A218S. This phenomenon could enhance antiviral resistance activity and confer ultimate...