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Difference in quasispecies of the hypervariable region 1 of hepatitis C virus between alcoholic and non‐alcoholic patients
Author(s) -
Takahashi Kou,
Takahashi Toru,
Takahashi Sumio,
Watanabe Koji,
Boku Saihiro,
Matsui Shigeru,
Arai Futoshi,
Asakura Hitoshi
Publication year - 2001
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1046/j.1440-1746.2001.02462.x
Subject(s) - viral quasispecies , hypervariable region , hepatocellular carcinoma , cirrhosis , medicine , alcoholic liver disease , hepatitis c virus , single strand conformation polymorphism , liver disease , virus , virology , hepatitis c , gastroenterology , genotype , polymerase chain reaction , biology , immunology , antibody , genetics , gene
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 × 10 6 ± 5.16 × 10 6 copies/mL vs 9.00 × 10 7 ± 2.75 × 10 8 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.