Difference in quasispecies of the hypervariable region 1 of hepatitis C virus between alcoholic and non‐alcoholic patients

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Abstract
Background: Habitual alcohol intake is known to aggravate the clinical outcome of hepatitis C virus (HCV)-related chronic liver diseases and to increase the risk of hepatocellular carcinoma. Methods: To investigate the possible mechanism of these effects by alcohol, we examined 31 cases of HCV-related chronic liver diseases of which 17 cases were drinking just before admission and the remaining 14 cases were non-drinkers. The studied cases included 18 patients with chronic hepatitis, six with liver cirrhosis and seven with hepatocellular carcinoma. The quasispecies of the hypervariable region 1 of the HCV genome were analyzed by using polymerase chain reaction–single strand conformation polymorphism (PCR-SSCP). Hepatitis C virus viral load was quantitated by using multicyclic PCR after reverse transcription of the 5′ non-coding region of the genome. Results: The mean PCR-SSCP band number that reflected the quasispecies complexity in hypervariable region 1 was more significantly increased in alcoholics than in non-alcoholics (5.5 ± 1.4 vs 3.9 ± 1.1, P < 0.01). The significant increase in alcoholics remained, even if the cases were restricted to males (P < 0.01), to HCV genotype 1b (P < 0.05) or to chronic hepatitis (P < 0.05). The HCV viral load was not statistically different between alcoholic and non-alcoholic HCV-related chronic liver diseases (5.02 × 106± 5.16 × 106 copies/mL vs 9.00 × 107± 2.75 × 108 copies/mL, P = 0.28). Mutation events seemed to occur randomly when amino acid sequences of hypervariable region 1 were compared between four drinkers and four non-drinkers. Conclusions: The enhanced quasispecies complexity in hypervariable region 1 of HCV in alcoholics may be the main cause of more progressive HCV-related chronic liver diseases, and may provide the disease the resistance against any therapeutic modalities including interferon.