Induction of interferon and interferon signaling pathways by replication of defective interfering particle RNA in cells constitutively expressing vesicular stomatitis virus replication proteins

Debasis Panda, Phat X. Dinh, Lalit K. Beura, Asit K Pattnaik

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

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-β promoter, IFN-stimulated response element (ISRE) promoter, and NF-κB 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.

Original languageEnglish (US)
Pages (from-to)4826-4831
Number of pages6
JournalJournal of virology
Volume84
Issue number9
DOIs
StatePublished - May 1 2010

Fingerprint

Defective Viruses
Vesiculovirus
Vesicular Stomatitis
interferons
Virus Replication
virus replication
Interferons
RNA
Proteins
proteins
promoter regions
cells
HEK293 Cells
Viral Genome
response elements
Response Elements
Viral Proteins
Up-Regulation
genome

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

Cite this

@article{a5354d4a77ad4918a41ff03750feccf3,
title = "Induction of interferon and interferon signaling pathways by replication of defective interfering particle RNA in cells constitutively expressing vesicular stomatitis virus replication proteins",
abstract = "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-β promoter, IFN-stimulated response element (ISRE) promoter, and NF-κB 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.",
author = "Debasis Panda and Dinh, {Phat X.} and Beura, {Lalit K.} and Pattnaik, {Asit K}",
year = "2010",
month = "5",
day = "1",
doi = "10.1128/JVI.02701-09",
language = "English (US)",
volume = "84",
pages = "4826--4831",
journal = "Journal of Virology",
issn = "0022-538X",
publisher = "American Society for Microbiology",
number = "9",

}

TY - JOUR

T1 - Induction of interferon and interferon signaling pathways by replication of defective interfering particle RNA in cells constitutively expressing vesicular stomatitis virus replication proteins

AU - Panda, Debasis

AU - Dinh, Phat X.

AU - Beura, Lalit K.

AU - Pattnaik, Asit K

PY - 2010/5/1

Y1 - 2010/5/1

N2 - 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-β promoter, IFN-stimulated response element (ISRE) promoter, and NF-κB 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.

AB - 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-β promoter, IFN-stimulated response element (ISRE) promoter, and NF-κB 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.

UR - http://www.scopus.com/inward/record.url?scp=77950798666&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77950798666&partnerID=8YFLogxK

U2 - 10.1128/JVI.02701-09

DO - 10.1128/JVI.02701-09

M3 - Article

C2 - 20181705

AN - SCOPUS:77950798666

VL - 84

SP - 4826

EP - 4831

JO - Journal of Virology

JF - Journal of Virology

SN - 0022-538X

IS - 9

ER -