J Gen Virol Email Content Delivery
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Gen Virol 31 (1976), 397-416; DOI 10.1099/0022-1317-31-3-397
© 1976 Society for General Microbiology
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bruton, C. J.
Right arrow Articles by Kennedy, S. I. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bruton, C. J.
Right arrow Articles by Kennedy, S. I. T.
Agricola
Right arrow Articles by Bruton, C. J.
Right arrow Articles by Kennedy, S. I. T.

Defective-Interfering Particles of Semliki Forest Virus: Intracellular Events During Interference

Celia J. Bruton, A. Porter and S. I. T. Kennedy

Department of Biological Sciences, University of Warwick, Coventry CV4 7AL, England

Purified defective-interfering (DI) particles of Semliki Forest virus are unable to carry out any of the steps in virus multiplication except uncoating. Cells co-infected with DI particles and standard virus contain several virus-specified RNA species (DI particle-specific species) absent from cells infected with standard virus alone. Moreover, synthesis of all the virus-specified components distinctive of standard virus-infected cells is reduced. The DI particle-specific RNA species comprise two poly A-containing single-stranded RNAs (DIss1 and DIss2), identical to those found in purified DI particles, two double-stranded RNAs (RFs) and a new size class of replicative intermediate (RI).

Hybridization experiments showed that the nucleotide sequences of DIss1 and DIss2 (i) are present in the 42S genome of standard virus but absent from the 26S RNA — the RNA from standard virus-infected cells which encodes the structural proteins of the virion (Clegg & Kennedy, 1975a) and (ii) are complementary to the negative strands of the DI particle-specific RFs and RI. Oligonucleotide fingerprinting revealed extensive nucleotide sequence homology between DIss1 and DIss2. Analysis of the mRNA complement of standard virus-infected, co-infected and uninfected cells strongly indicated that neither DIss1 nor DIss2 can serve as a functional messenger RNA.

From these studies we propose a mechanism for the multiplication of and interference by DI particles of Semliki Forest virus.

Received 10 November 1975; accepted 30 January 1976.




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
INT J SYST EVOL MICROBIOL MICROBIOLOGY J GEN VIROL
J MED MICROBIOL ALL SGM JOURNALS
Copyright © 1976 by the Society for General Microbiology.