Mechanism of antiviral action of quercetin against cardiovirus infection in mice

Abstract

Oral treatment with quercetin protected ABD2F 1/Jena mice significantly against intraperitoneal encephalomyocarditis, Col. SK, MM, Mengo M,L and Mengo M virus infections, but not against intracerebral challenge with Mengo M virus. Enhanced resistance to Mengo M virus were induced in the genetically different DBA 2/Jena, C57BL6/Jena, C57BL/Lati and ABD2F 1/Jena mice. C57BL6/Jena nu/nu mice were also protected, indicating that the thymus was non-essential to the protective effects of quercetin. In AB/Jena and Lati:CFLP mice the drug failed to be effective. Quercetin was not virucidal and did not interfere with Mengo virus replication in L cells. Interferon was not detected (< 1 : 8) in sera of ABD2F 1/Jena mice 1–48 h after oral administration of the drug. The virus spread from the site of injection to the local lymph nodes and other target organs were impaired. Silica treatment, to suppress macrophage function, did not evidently increase the susceptibility of ABD2F 1/Jena mice to Mengo virus. However, this treatment abolished the antiviral activity of quercetin, indicating the requirement for macrophages for quercetin to be effective. Virus replication could not be demonstrated in cultures of adherent peritoneal macrophages from either untreated or quercetin-treated ABD2F 1/Jena mice.