HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Mécs, E. Articles by Fantes, K. H. Search for Related Content PubMed PubMed Citation Articles by Mécs, E. Articles by Fantes, K. H. Agricola Articles by Mécs, E. Articles by Fantes, K. H.

The Effect of Interferon on the Synthesis of RNA in Chick Cells Infected with Semliki Forest Virus

National Institute for Medical Research, Mill Hill, London N.W.7

K. H. Fantes

Glaxo Laboratories Limited, Sefton Park, Stoke Poges, Bucks.

When cells were pretreated with amounts of interferon which caused a 92 to 99% reduction in virus production, the yields of infectious RNA were inhibited by 67 to 81%, while the rate of incorporation of [³H]adenosine into total virus specific RNA was inhibited by only 48 to 65%. Sucrose gradient analysis of the virus specific RNA synthesized in untreated infected cells showed it to consist of (i) 45 S infectious RNA which is probably the RNA of the mature virus, (ii) 26 S ribonuclease-sensitive RNA, possessing not more than 3% of the infectivity of 45 S RNA, whose function is not known, but which is the major component early in infection, and (iii) 20 S ribonuclease-resistant RNA, which is probably a double-stranded replicative form. The inhibition by interferon of the synthetic rates of these three RNA species was not uniform. 45 S RNA showed the same sensitivity to interferon as did infectious RNA. The synthesis of 20 S ribonuclease-resistant RNA and of 26 S ribonuclease-sensitive RNA were relatively resistant to interferon action.

^* Visiting worker on leave from the Microbiological Institute, Medical School, Szeged, Hungary. In receipt of a research fellowship from the Wellcome Trust.

Received 16 July 1966; accepted 15 September 1966.