J Gen Virol Try Microbiology Online
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Gen Virol 73 (1992), 389-396; DOI 10.1099/0022-1317-73-2-389
© 1992 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 HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Patel, A. H.
Right arrow Articles by Elliott, R. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Patel, A. H.
Right arrow Articles by Elliott, R. M.
Agricola
Right arrow Articles by Patel, A. H.
Right arrow Articles by Elliott, R. M.

Characterization of Bunyamwera virus defective interfering particles

Arvind H. Patel1,2, and Richard M. Elliott2

1 Medical Research Council Virology Unit
and2 Institute of Virology, University of Glasgow, Church Street, Glasgow G11 5JR, U.K.

In an attempt to isolate conditional lethal amber nonsense mutants of Bunyamwera virus, five variants were found which produced small plaques on BHK and mouse L cells. Characterization of these variants by Northern blotting showed that they synthesized defective (subgenomic) RNAs derived from the L RNA segment. No subgenomic M or S segment RNAs were detected. The defective L RNAs were shown to be packaged into virus particles, and four of five preparations caused interference with the multiplication of standard virus. When defective-containing preparations were mixed with standard virus and grown in doubly infected cells a reduction in titre of standard virus of up to 400-fold was observed. Hence these preparations most probably contained defective interfering (DI) particles. Novel DI-specific polypeptides were synthesized in DI virus-infected cells. These novel proteins could be precipitated by antisera raised against either the N or C terminus, or both, of the L protein. Nucleotide sequence analysis of cloned cDNA to prominent DI RNAs in three different defective virus preparations revealed that the DI RNA in each case had suffered a single internal deletion of the L segment while retaining the 5'- and 3'-terminal sequences. The extent of the deletion ranged between 72% and 77% of the L RNA segment. Our results suggest that these DI particles may have arisen during the attempted isolation of Bunyamwera virus amber mutants on mouse L cells, since defective/subgenomic RNAs derived from the L and M segments were readily generated in mouse L cells but not in BHK cells, following infection with wild-type virus.

Received 10 September 1991; accepted 29 October 1991.


This article has been cited by other articles:


Home page
J. Virol.Home page
A. K. Overby, R. F. Pettersson, and E. P. A. Neve
The Glycoprotein Cytoplasmic Tail of Uukuniemi Virus (Bunyaviridae) Interacts with Ribonucleoproteins and Is Critical for Genome Packaging
J. Virol., April 1, 2007; 81(7): 3198 - 3205.
[Abstract] [Full Text] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
A. Bridgen and R. M. Elliott
Rescue of a segmented negative-strand RNA virus entirely from cloned complementary DNAs
PNAS, December 24, 1996; 93(26): 15400 - 15404.
[Abstract] [Full Text] [PDF]




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 © 1992 by the Society for General Microbiology.