1887

Abstract

Interferon (IFN) restricts a wide variety of viruses. To do so it elicits many antiviral pathways. For example, subclones of the same cell line with a reduced antiviral spectrum are thought to lack one or more antiviral pathways. Our line of L cells exhibits two distinct antiviral activities. The first delays the yield of both wild-type mengovirus ( ) and an IFN-sensitive mutant (-1). The second specifically inhibits -1 virus yields 100-fold. From these cells, a subclone was isolated which had lost the second antiviral activity (i.e. in these cells -1 virus acts like virus). To see whether other cardioviruses are sensitive to these activities, two additional strains [m-mengovirus and encephalomyocarditis-R (EMC-R) virus] were tested in our subclones. Like virus, m-mengovirus yields were delayed by IFN in both subclones; EMC-R virus behaved like -1 virus in both cell lines. When actinomycin D was added at the time of infection, -1 virus was phenotypically reversed to virus, but EMC-R virus was still inhibited. The 2-5A synthetase/RNase L pathway is expressed in both clones. Therefore, at least three antiviral activities against cardioviruses can be distinguished in IFN-treated L cells, and two of them appear not to involve the 2-5A synthetase/RNase L pathway.

Loading

Article metrics loading...

/content/journal/jgv/10.1099/0022-1317-73-9-2299
1992-09-01
2019-11-13
Loading full text...

Full text loading...

http://instance.metastore.ingenta.com/content/journal/jgv/10.1099/0022-1317-73-9-2299
Loading

Most Cited This Month

This is a required field
Please enter a valid email address
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error