Characterization of anti-herpes simplex virus type 1 activity of an alkaloid FK 3000 from Stephania cepharantha.

Accession number;02A0774019
Title;Characterization of anti-herpes simplex virus type 1 activity of an alkaloid FK 3000 from Stephania cepharantha.
Author; OHSAKI M (Toyama Medical And Pharmaceutical Univ., Toyama, Jpn) KUROKAWA M (Toyama Medical And Pharmaceutical Univ., Toyama, Jpn) NAWAWI A (Toyama Medical And Pharmaceutical Univ., Toyama, Jpn) NAKAMURA N (Toyama Medical And Pharmaceutical Univ., Toyama, Jpn) HATTORI M (Toyama Medical And Pharmaceutical Univ., Toyama, Jpn) SHIRAKI K (Toyama Medical And Pharmaceutical Univ., Toyama, Jpn)
Journal Title;Journal of Traditional Medicines
Journal Code:Y0941A
ISSN:1340-6302
VOL.19;NO.4;PAGE.129-136(2002)
Figure&Table&Reference;FIG.6, TBL.1, REF.26
Pub. Country;Japan
Language;English
Abstract;A morphinane alkaloid FK 3000 (6,7-di-O-acetylsinococuline) from the root tubers of Stephania cepharantha showed antiviral activity against acyclovir (ACV)- and phosphonoacetic acid (PAA)-resistant herpes simplex virus type 1 (HSV-1), influenza virus, measles virus, and poliovirus. The anti-HSV action of FK 3000 was assessed in comparison with that of PAA that inhibits the activity of HSV DNA polymerase and HSV DNA synthesis. FK 3000 inhibited the growth of thymidine kinase-deficient and ACV and PAA-resistant HSV-1 strains, as well as wild type HSV strains in Vero cells. This compound, as well as PAA, interfered with the synthesis of late viral proteins but not early viral proteins. The analysis of HSV DNA synthesis by slot blot hybridization showed that FK 3000 inhibited the viral DNA synthesis in a dose-dependent manner. However, the viral RNA was partially synthesized in the presence of FK 3000 (even at a dose that HSV DNA synthesis was inhibited) and PAA, indicating that FK 3000, as well as PAA, allowed early viral RNA synthesis but not viral DNA synthesis. Since partially purified HSV DNA polymerase activity was not inhibited by FK 3000, this compound was suggested to inhibit HSV DNA synthesis by a mechanism different from that of PAA. (author abst.)