Resistance-associated polymorphisms in Dutch hepatitis C genotype 1a patients with and without HIV infection

Autores: Lieveld Faydra I, Swaans Niels, Newsum Astrid M, Ho Cynthia KY, Schinkel Janke, Molenkamp Richard, van der Meer Jan TM, et al

Resumen

Background and aim: Resistance-associated variants (RAVs) on the NS3 region of the hepatitis C virus (HCV) may be relevant for antiviral therapy, but data in human immunodeficiency virus (HIV) coinfected patients are scarce. We assessed frequencies ofNS3 RAVs in patients infected with HCV genotype 1a with or without HIV coinfection. Material and methods: HCV NS3 aminoacids 1-181 were sequenced by the Sanger method and analyzed for RAVs. RAVs and their distribution between HCV genotype 1aclade I and II viruses were compared between HIV-infected versus HIV-uninfected patients. Results: 148 samples were available(n = 68 HIV and n = 80 non-HIV). Relative frequency of clade I and clade II was significantly different between HIV (85% and 15%) and non-HIV groups (49% and 51%). Overall, HIV infected patients exhibited significantly lower prevalence of RAVs than HIV-unin-fected patients (62% vs 79%, p = 0.03). However, Q80K prevalence was significantly higher in HIV-infected subjects (50% vs.24%, p = 0.001), whereas prevalence of S122D/G/N/S (2% vs 16%, p = 0.002) and N174G/N/S (10% vs 55%, p < 0.0001) polymorphisms were significantly lower. Q80K was found exclusively in clade I viruses. S122 (3% vs 22%, p=0.001) and N174 (13% vs 75%, p<0.0001) polymorphisms had significantly lower prevalence in clade I than clade II viruses. Conclusions: In the Nether-lands, prevalence of clade I viruses and Q80K was significantly higher in HCV genotype 1a infected patients with HIV coinfection than in those without HIV coinfection. Prevalence of N174 and S122 polymorphisms was significantly higher in clade II than clade Iviruses.

Palabras clave: Hepatitis C virus HIV Genotype 1a Q80K Drug resistance.

2016-10-21   |   265 visitas   |   Evalua este artículo 0 valoraciones

Vol. 15 Núm.5. Septiembre-Octubre 2016 Pags. 696-704 Ann Hepatol 2016; 15(5)