Abstract
Hepatitis A virus (HAV) causes acute hepatitis and sometimes leads to fulminant hepatitis. Amantadine is a tricyclic symmetric amine that inhibits the replication of many DNA and RNA viruses. Amantadine was reported to suppress HAV replication, and the efficacy of amantadine was exhibited in its inhibition of the internal ribosomal entry site (IRES) activities of HAV. Interferon (IFN) also has an antiviral effect through the induction of IFN stimulated genes (ISG) and the degradation of viral RNA. To explore the mechanism of the suppression of HAV replication, we examined the effects of the combination of amantadine and IFN-alpha on HAV IRES-mediated translation, HAV replicon replication in human hepatoma cell lines, and HAV KRM003 genotype IIIB strain replication in African green monkey kidney cell GL37. IFN-alpha seems to have no additive effect on HAV IRES-mediated translation inhibition by amantadine. However, suppressions of HAV replicon and HAV replication were stronger with the combination than with amantadine alone. In conclusion, amantadine, in combination of IFN-alpha, might have a beneficial effect in some patients with acute hepatitis A.
Highlights
Hepatitis A virus (HAV) causes acute hepatitis and sometimes leads to fulminant hepatitis
Improved sanitation and living standards mean that fewer countries remain highly endemic, but the risk of HAV infection is present in countries lacking HAV immunity or where the endemicity of hepatitis A is low or intermediate [1]
We previously reported that amantadine inhibits hepatitis A virus internal ribosomal entry site (IRES)-mediated translation in human hepatoma cells [2]
Summary
Hepatitis A virus (HAV) causes acute hepatitis and sometimes leads to fulminant hepatitis. We previously reported that amantadine inhibits hepatitis A virus internal ribosomal entry site (IRES)-mediated translation in human hepatoma cells [2]. We evaluated the HAV antiviral activity of amantadine and IFN-alpha.
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