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Mechanism of enhancement of newcastle disease virus growth in cultured cells by co-infecting hog cholera virus

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Summary

The mechanism of the enhanced replication of Newcastle disease (ND) virus in swine testicle (ST) cells infected with hog cholera (HC) virus (END phenomenon) was studied. Two mechanisms appeared to operate, one being the suppression of interferon production by the coinfecting HC virus and the other a still undefined mechanism not related to interferon. The first mechanism was suggested by the facts that interferon production by ND virus was inhibited by prior infection with HC virus, and that ND virus growth was suppressed by exogenous interferon in both HC infected and uninfected ST cell cultures. The reason for the inhibition of interferon production is unknown; it is neither due to a decreased ND virus adsorption to ST cells nor due to the production of some factor blocking the interferon production. The possibility of an additional mechanism emerged when the effects of 20-methylcholanthrene and actinomycin D were examined. These substances suppressed the interferon induction by ND virus but increased the viral growth only slightly, while in HC infected cells actinomycin D reduced ND virus replication to a marked extent. It thus seems that the second mechanism, which is not related to interferon and which is sensitive to actinomycin D, may be more important than the suppression of interferon production in END phenomenon. Poly I∶C treatment, which could confer on uninfected cells resistance to ND and WEE viruses without inducing detectable amounts of interferon, did not affect the growth of these viruses in HC infected cells. This phenomenon presumably shares a common mechanism with the END phenomenon.

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  1. Masanori Toba

    Present address: Institute of Medical Science, University of Tokyo, Tokyo, Japan

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  1. Institute of Medical Science, University of Tokyo, Tokyo, Japan

    Minoru Matumoto

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  1. Masanori Toba
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  2. Minoru Matumoto
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Toba, M., Matumoto, M. Mechanism of enhancement of newcastle disease virus growth in cultured cells by co-infecting hog cholera virus. Archiv f Virusforschung 34, 310–322 (1971). https://doi.org/10.1007/BF01242977

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  • DOI: https://doi.org/10.1007/BF01242977

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