Inhibitory effects on HAV IRES-mediated translation and replication by a combination of amantadine and interferon-alpha View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2010-12

AUTHORS

Lingli Yang, Tomoko Kiyohara, Tatsuo Kanda, Fumio Imazeki, Keiichi Fujiwara, Verena Gauss-Müller, Koji Ishii, Takaji Wakita, Osamu Yokosuka

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. More... »

PAGES

212

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/1743-422x-7-212

DOI

http://dx.doi.org/10.1186/1743-422x-7-212

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1020394263

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/20815893


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