Highlighted Paper selected by Editor-in-Chief : Inhibition Mechanisms of Hepatitis C Virus Infection by Caffeic Acid and Tannic Acid

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  • Shirasago Yoshitaka
    Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases
  • Inamori Yoko
    Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases
  • Suzuki Takeru
    Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases Department of Chemistry, Faculty of Science, Tokyo University of Science
  • Tanida Isei
    Department of Cell Biology and Neurosciences, Juntendo University Graduate School of Medicine
  • Suzuki Tetsuro
    Department of Infectious Diseases, Hamamatsu University School of Medicine
  • Sugiyama Kazuo
    Gyotoku General Hospital
  • Wakita Takaji
    Department of Virology II, National Institute of Infectious Diseases
  • Hanada Kentaro
    Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases
  • Fukasawa Masayoshi
    Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases

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  • Inhibition Mechanisms of Hepatitis C Virus Infection by Caffeic Acid and Tannic Acid

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<p>Previously, we reported that coffee extract and its constituents, caffeic acid (CA) and p-coumaric acid, inhibit infection by the hepatitis C virus (HCV). In the present report, we identified another coffee-related compound, tannic acid (TA), which also inhibits HCV infection. We systematically evaluated which steps of the viral lifecycle were affected by CA and TA. TA substantially inhibits HCV RNA replication and egression, while CA does not. The infectivity of the HCV pretreated with CA or TA was almost lost. Cellular attachment of HCV particles and their interaction with apolipoprotein E, which is essential for HCV infectivity, were significantly reduced by CA. These results indicate that CA inhibits HCV entry via its direct effect on viral particles and TA inhibits HCV RNA replication and particle egression as well as entry into host cells. Taken together, our findings may provide insights into CA and TA as potential anti-HCV strategies.</p>

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