Induction of interferon and interferon signaling pathways by replication of defective interfering particle RNA in cells constitutively expressing vesicular stomatitis virus replication proteins.
We show here that replication of defective interfering (DI) particle RNA in HEK293 cells stably expressing vesicular stomatitis virus (VSV) replication proteins potently activates interferon (IFN) and IFN signaling pathways through upregulation of IFN-beta promoter, IFN-stimulated response element (ISRE) promoter, and NF-kappaB promoter activities. Replication of DI particle RNA, not mere expression of the viral replication proteins, was found to be critical for induction of IFN and IFN signaling. The stable cells supporting replication of DI RNA described in this report will be useful in further examining the innate immune signaling pathways and the host cell functions in viral genome replication.
Panda
Debasis
D
School of Veterinary Medicine and Biomedical Sciences and the Nebraska Center for Virology, University of Nebraska-Lincoln, Lincoln, Nebraska 68583-0900, USA.
Dinh
Phat X
PX
Beura
Lalit K
LK
Pattnaik
Asit K
AK
D002460:Cell Line; D003673:Defective Viruses / Q000235:genetics* / Q000276:immunology*; D006801:Humans; D016899:Interferon-beta / Q000096:biosynthesis; D007372:Interferons / Q000096:biosynthesis*; D016328:NF-kappa B / Q000096:biosynthesis; D011401:Promoter Regions, Genetic; D012367:RNA, Viral / Q000378:metabolism*; D015398:Signal Transduction; D015533:Transcriptional Activation; D015854:Up-Regulation; D018116:Vesiculovirus / Q000235:genetics* / Q000276:immunology*
D016328:NF-kappa B; D012367:RNA, Viral; D016899:Interferon-beta; D007372:Interferons