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 HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Marcus, P. I. Articles by Sekellick, M. J. Search for Related Content PubMed PubMed Citation Articles by Marcus, P. I. Articles by Sekellick, M. J. Agricola Articles by Marcus, P. I. Articles by Sekellick, M. J.

Interferon Action III. The Rate of Primary Transcription of Vesicular Stomatitis Virus is Inhibited by Interferon Action

Microbiology Section, U-44, Biological Sciences Group, University of Connecticut, Storrs, Connecticut 06268, U.S.A.

Transcription of vesicular stomatitis virus (VSV) in Vero cells was confined to the synthesis of parentally-derived mRNA (primary transcription) by the use of cycloheximide and/or a ts mutant, G41(IV), at a non-permissive temperature (40 °C). More transcripts accumulated in the presence of cycloheximide than in its absence. This so-called ‘cycloheximide effect’ results from higher rates of virus transcription sustained for longer periods of time. The rate of VSV transcription initially increases linearly for 1 to 2 h after infection. Interferon reduces this rate ( fourfold with 50 units/ml interferon) irrespective of the presence or absence of cycloheximide. The VSV mRNA transcripts synthesized in mock- or interferon-treated cells were equal in size and had an equivalent half-life of 17 h at 40 °C. It seems likely that once transcription is initiated in interferon-treated cells, it is completed successfully.

Since interferon reduces the rate of early VSV primary transcript synthesis to below that achieved in the presence of cycloheximide, we conclude that interferon has an effect on transcription beyond that attributable solely to protein synthesis inhibition. We postulate that interferon decreases the probability of initiating virus transcription. Virus mRNA escaping this facet of interferon action may then encounter other facets such as post-transcriptional modification and/or inhibition of translation. However, the mandatory sequence of primary transcription primary translation for negative-strand viruses like VSV dictates that the overall inhibitory effect of interferon on translation would derive in part from this prior inhibition of transcription. Thus, to apply the term ‘primary effect’ to one particular facet of interferon action may not always be meaningful.

Received 10 November 1976; accepted 20 August 1977.

This article has been cited by other articles:

				M. Basu, R. K. Maitra, Y. Xiang, X. Meng, A. K. Banerjee, and S. Bose Inhibition of vesicular stomatitis virus infection in epithelial cells by alpha interferon-induced soluble secreted proteins J. Gen. Virol., September 1, 2006; 87(9): 2653 - 2662. [Abstract] [Full Text] [PDF]

				M. Nishio, M. Tsurudome, M. Ito, M. Kawano, H. Komada, and Y. Ito High Resistance of Human Parainfluenza Type 2 Virus Protein-Expressing Cells to the Antiviral and Anti-Cell Proliferative Activities of Alpha/Beta Interferons: Cysteine-Rich V-Specific Domain Is Required for High Resistance to the Interferons J. Virol., October 1, 2001; 75(19): 9165 - 9176. [Abstract] [Full Text] [PDF]