Journal of Microbiology

Research Support, Non-U.S. Gov't

Antiviral Activities of Flavonoids Isolated from the Bark of Rhus verniciflua Stokes against Fish Pathogenic Viruses In Vitro: So Young Kang , Ji-Young Kang , Myung-Joo Oh; J. Microbiol. 2012;50(2):293-300. Published online April 27, 2012; DOI: https://doi.org/10.1007/s12275-012-2068-7

Abstract: An 80% methanolic extract of Rhus verniciflua Stokes bark showed significant anti-viral activity against fish pathogenic infectious hematopoietic necrosis virus (IHNV) and viral hemorrhagic septicemia virus (VHSV) in a cell-based assay measuring virus-induced cytopathic effect (CPE). Activity-guided fractionation and isolation for the 80% methanolic extract of R. verniciflua yielded the most active ethyl acetate fraction, and methyl gallate (1) and four flavonoids: fustin (2), fisetin (3), butin (4) and sulfuretin (5). Among them, fisetin (3) exhibited high antiviral activities against both IHNV and VHSV showing EC50 values of 27.1 and 33.3 μM with selective indices (SI = CC50/EC50) more than 15, respectively. Fustin (2) and sulfuretin (5) displayed significant antiviral activities showing EC50 values of 91.2– 197.3 μM against IHNV and VHSV. In addition, the antiviral activity of fisetin against IHNV and VHSV occurred up to 5 hr post-infection and was not associated with direct virucidal effects in a timed addition study using a plaque reduction assay. These results suggested that the bark of R. verniciflua and isolated flavonoids have significant anti-viral activity against IHNV and VHSV, and also have potential to be used as anti-viral therapeutics against fish viral diseases.

Calcium in infectious hematopoietic necrosis virus (IHNY) infected fish cell lines: Kim, Nam Shik , Heo, Gnag Joon , Lee, Chang Hee; J. Microbiol. 1996;34(3):263-269.

Abstract: Infection of fish cells with IHNV resulted in gradual increase in cytosolic free Ca^2+ concentration ([Ca^2+]) in CHSE, gradual decrease in [Ca^2+] in FHM, and no significant change in RTG cells. The degree of [Ca^2+] increase or decrease was dependent on the amount of infectious virus, and these [Ca^2+] variations were maximal at 16 hours after virus infection (p.i.) in both cell lines. When the fish cells were infected with inactivated IHNV, evident variation in [Ca^2+] was not observed. Thus, infectivity of IHNV appears to correlate with changes in [Ca^2+] in virus-infected cells. These IHNV-induced [Ca^2+] changes were partially blocked by cycloheximide, but not affected by cordycepin. It seems to be that virus-induced Ca^2+ variations were more related with protein synthesis than RNA synthesis. Various Ca^2+ related drugs were used in search for the mechanisms of the [Ca^2+], changes following IHNV infection of CHSE cells. Decreasing extracellular Ca^2+ concentration or blocking Ca^2+ influx from extracellular media inhibited the IHNV-induced increase in [Ca^2+], in CHSE cells. Similar results were obtained with intracellular Ca^2+ sources are important in IHNV-induced [Ca^2+] increase in CHSE cells.

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