RIG-I activation inhibits ebolavirus replication

Christina F. Spiropoulou, Priya Ranjan, Melissa B. Pearce, Tara K. Sealy, César G. Albariño, Shivaprakash Gangappa, Takashi Fujita, Pierre E. Rollin, Stuart T. Nichol, Thomas Ksiazek, Suryaprakash Sambhara

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

Hemorrhagic fever viruses are associated with rapidly progressing severe disease with high case fatality, making them of public health and biothreat importance. Effective antivirals are not available for most of the members of this diverse group of viruses. A broad spectrum strategy for antiviral development would be very advantageous. Perhaps the most challenging target would be the highly immunosuppressive filoviruses, ebolavirus and marburgvirus, associated with aerosol infectivity and case fatalities in the 80-90% range. Here we report that activation of evolutionarily conserved cytosolic viral nucleic acid sensor, RIG-I can cause severe inhibition of ebolavirus replication. These findings indicate that RIG-I-based therapies may provide an attractive approach for antivirals against Ebola hemorrhagic fever, and possibly other HF viruses.

Original languageEnglish (US)
Pages (from-to)11-15
Number of pages5
JournalVirology
Volume392
Issue number1
DOIs
StatePublished - Sep 15 2009
Externally publishedYes

Fingerprint

Ebolavirus
Antiviral Agents
Viruses
Ebola Hemorrhagic Fever
Marburgvirus
Immunosuppressive Agents
Aerosols
Nucleic Acids
Fever
Public Health
Therapeutics

Keywords

  • Ebolavirus
  • RIG-I

ASJC Scopus subject areas

  • Virology

Cite this

Spiropoulou, C. F., Ranjan, P., Pearce, M. B., Sealy, T. K., Albariño, C. G., Gangappa, S., ... Sambhara, S. (2009). RIG-I activation inhibits ebolavirus replication. Virology, 392(1), 11-15. https://doi.org/10.1016/j.virol.2009.06.032

RIG-I activation inhibits ebolavirus replication. / Spiropoulou, Christina F.; Ranjan, Priya; Pearce, Melissa B.; Sealy, Tara K.; Albariño, César G.; Gangappa, Shivaprakash; Fujita, Takashi; Rollin, Pierre E.; Nichol, Stuart T.; Ksiazek, Thomas; Sambhara, Suryaprakash.

In: Virology, Vol. 392, No. 1, 15.09.2009, p. 11-15.

Research output: Contribution to journalArticle

Spiropoulou, CF, Ranjan, P, Pearce, MB, Sealy, TK, Albariño, CG, Gangappa, S, Fujita, T, Rollin, PE, Nichol, ST, Ksiazek, T & Sambhara, S 2009, 'RIG-I activation inhibits ebolavirus replication', Virology, vol. 392, no. 1, pp. 11-15. https://doi.org/10.1016/j.virol.2009.06.032
Spiropoulou CF, Ranjan P, Pearce MB, Sealy TK, Albariño CG, Gangappa S et al. RIG-I activation inhibits ebolavirus replication. Virology. 2009 Sep 15;392(1):11-15. https://doi.org/10.1016/j.virol.2009.06.032
Spiropoulou, Christina F. ; Ranjan, Priya ; Pearce, Melissa B. ; Sealy, Tara K. ; Albariño, César G. ; Gangappa, Shivaprakash ; Fujita, Takashi ; Rollin, Pierre E. ; Nichol, Stuart T. ; Ksiazek, Thomas ; Sambhara, Suryaprakash. / RIG-I activation inhibits ebolavirus replication. In: Virology. 2009 ; Vol. 392, No. 1. pp. 11-15.
@article{f7965fef766c4956b4be8030d171221b,
title = "RIG-I activation inhibits ebolavirus replication",
abstract = "Hemorrhagic fever viruses are associated with rapidly progressing severe disease with high case fatality, making them of public health and biothreat importance. Effective antivirals are not available for most of the members of this diverse group of viruses. A broad spectrum strategy for antiviral development would be very advantageous. Perhaps the most challenging target would be the highly immunosuppressive filoviruses, ebolavirus and marburgvirus, associated with aerosol infectivity and case fatalities in the 80-90{\%} range. Here we report that activation of evolutionarily conserved cytosolic viral nucleic acid sensor, RIG-I can cause severe inhibition of ebolavirus replication. These findings indicate that RIG-I-based therapies may provide an attractive approach for antivirals against Ebola hemorrhagic fever, and possibly other HF viruses.",
keywords = "Ebolavirus, RIG-I",
author = "Spiropoulou, {Christina F.} and Priya Ranjan and Pearce, {Melissa B.} and Sealy, {Tara K.} and Albari{\~n}o, {C{\'e}sar G.} and Shivaprakash Gangappa and Takashi Fujita and Rollin, {Pierre E.} and Nichol, {Stuart T.} and Thomas Ksiazek and Suryaprakash Sambhara",
year = "2009",
month = "9",
day = "15",
doi = "10.1016/j.virol.2009.06.032",
language = "English (US)",
volume = "392",
pages = "11--15",
journal = "Virology",
issn = "0042-6822",
publisher = "Academic Press Inc.",
number = "1",

}

TY - JOUR

T1 - RIG-I activation inhibits ebolavirus replication

AU - Spiropoulou, Christina F.

AU - Ranjan, Priya

AU - Pearce, Melissa B.

AU - Sealy, Tara K.

AU - Albariño, César G.

AU - Gangappa, Shivaprakash

AU - Fujita, Takashi

AU - Rollin, Pierre E.

AU - Nichol, Stuart T.

AU - Ksiazek, Thomas

AU - Sambhara, Suryaprakash

PY - 2009/9/15

Y1 - 2009/9/15

N2 - Hemorrhagic fever viruses are associated with rapidly progressing severe disease with high case fatality, making them of public health and biothreat importance. Effective antivirals are not available for most of the members of this diverse group of viruses. A broad spectrum strategy for antiviral development would be very advantageous. Perhaps the most challenging target would be the highly immunosuppressive filoviruses, ebolavirus and marburgvirus, associated with aerosol infectivity and case fatalities in the 80-90% range. Here we report that activation of evolutionarily conserved cytosolic viral nucleic acid sensor, RIG-I can cause severe inhibition of ebolavirus replication. These findings indicate that RIG-I-based therapies may provide an attractive approach for antivirals against Ebola hemorrhagic fever, and possibly other HF viruses.

AB - Hemorrhagic fever viruses are associated with rapidly progressing severe disease with high case fatality, making them of public health and biothreat importance. Effective antivirals are not available for most of the members of this diverse group of viruses. A broad spectrum strategy for antiviral development would be very advantageous. Perhaps the most challenging target would be the highly immunosuppressive filoviruses, ebolavirus and marburgvirus, associated with aerosol infectivity and case fatalities in the 80-90% range. Here we report that activation of evolutionarily conserved cytosolic viral nucleic acid sensor, RIG-I can cause severe inhibition of ebolavirus replication. These findings indicate that RIG-I-based therapies may provide an attractive approach for antivirals against Ebola hemorrhagic fever, and possibly other HF viruses.

KW - Ebolavirus

KW - RIG-I

UR - http://www.scopus.com/inward/record.url?scp=69249202248&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=69249202248&partnerID=8YFLogxK

U2 - 10.1016/j.virol.2009.06.032

DO - 10.1016/j.virol.2009.06.032

M3 - Article

VL - 392

SP - 11

EP - 15

JO - Virology

JF - Virology

SN - 0042-6822

IS - 1

ER -