Mechanism of antiviral action of quercetin against cardiovirus infection in mice.

Oral treatment with quercetin protected ABD2F1/Jena mice significantly against intraperitoneal encephalomyocarditis, Col, SK, MM, Mengo M,L and MengoM virus infections, but not against intracerebral challenge with MengoM virus. Enhanced resistance to MengoM virus were induced in the genetically different DBA 2/Jena, C57BL/Jena, C57BL/Lati and ABC2F1/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 (less than 1 : 8) in sera of ABD2F1/Jena mice 1-48 h after oral administration of the drug. The virus spread from the site of injection to the lymph nodes and other target organs were impaired. Silica treatment, to suppress macrophage function, did not evidently increase the susceptibility of ABC2F1/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 ABD2F1/Jena mice.