Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
, 351 (1), 101-11

Sendai Virus Defective-Interfering Genomes and the Activation of Interferon-Beta

Affiliations

Sendai Virus Defective-Interfering Genomes and the Activation of Interferon-Beta

Laura Strahle et al. Virology.

Abstract

The ability of some Sendai virus stocks to strongly activate IFNbeta has long been known to be associated with defective-interfering (DI) genomes. We have compared SeV stocks containing various copyback and internal deletion DI genomes (and those containing only nondefective (ND) genomes) for their ability to activate reporter genes driven by the IFNbeta promoter. We found that this property was primarily due to the presence of copyback DI genomes and correlated with their ability to self-anneal and form dsRNA. The level of IFNbeta activation was found to be proportional to that of DI genome replication and to the ratio of DI to ND genomes during infection. Over-expression of the viral V and C proteins was as effective in blocking the copyback DI-induced activation of the IFNbeta promoter as it was in reducing poly-I/C-induced activation, providing evidence that these DI infections activate IFNbeta via dsRNA. Infection with an SeV stock that is highly contaminated with copyback DI genomes is thus a very particular way of potently activating IFNbeta, presumably by providing plentiful dsRNA under conditions of reduced expression of viral products which block the host antiviral response.

Similar articles

See all similar articles

Cited by 94 PubMed Central articles

See all "Cited by" articles

Publication types

Substances

LinkOut - more resources

Feedback