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Effect of Endogenous Interferon and Actinomycin D on Growth of Japanese Encephalitis Virus in Chick Embryo Cells
Author(s) -
Yamazaki Shudo
Publication year - 1968
Publication title -
japanese journal of microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0021-5139
DOI - 10.1111/j.1348-0421.1968.tb00381.x
Subject(s) - titer , interferon , embryo , strain (injury) , virus , infectivity , virology , biology , endogeny , dactinomycin , inhibitory postsynaptic potential , microbiology and biotechnology , protein biosynthesis , biochemistry , neuroscience , anatomy , cycloheximide
An attenuated virus strain (V423) showed lower multiplication in chick embryo (CE) cells than the original virus strain (Hotta) from which the V423 strain was derived. Both strains induced some amounts of interferon before their infectivity reached a maximum titer. Thirty‐two units of interferon were detected between 24 and 48 hr after infection. While no significant difference was seen in the interferon production between the V423 and Hotta strains, the V423 strain was shown to be much more sensitive to interferon. The lower growth of the V423 strain, therefore, may be explained at least partially by the inhibitory effect of endogenous interferon. This hypothesis was further supported by evidence that actinomycin D (0.2 μg/ml) enhanced the virus growth, presumably as a result of inhibiting interferon formation. This enhancement, however, was revealed only after more than 24 hr postinfection. Within the first 24 hr some slight decrease in the virus growth was observed in actinomycin D‐treated cells. This inhibitory effect of actinomycin D showed a dose response in a confirmatory experiment with different concentrations of the antibiotic.