Author
Listed:
- Benjamin A. Satterfield
(Galveston National Laboratory, University of Texas Medical Branch
University of Texas Medical Branch)
- Robert W. Cross
(Galveston National Laboratory, University of Texas Medical Branch
University of Texas Medical Branch)
- Karla A. Fenton
(Galveston National Laboratory, University of Texas Medical Branch
University of Texas Medical Branch)
- Krystle N. Agans
(Galveston National Laboratory, University of Texas Medical Branch
University of Texas Medical Branch)
- Christopher F. Basler
(Icahn School of Medicine at Mount Sinai)
- Thomas W. Geisbert
(Galveston National Laboratory, University of Texas Medical Branch
University of Texas Medical Branch)
- Chad E. Mire
(Galveston National Laboratory, University of Texas Medical Branch
University of Texas Medical Branch)
Abstract
The viral determinants that contribute to Nipah virus (NiV)-mediated disease are poorly understood compared with other paramyxoviruses. Here we use recombinant NiVs (rNiVs) to examine the contributions of the NiV V and W proteins to NiV pathogenesis in a ferret model. We show that a V-deficient rNiV is susceptible to the innate immune response in vitro and behaves as a replicating non-lethal virus in vivo. Remarkably, rNiV lacking W expression results in a delayed and altered disease course with decreased respiratory disease and increased terminal neurological disease associated with altered in vitro inflammatory cytokine production. This study confirms the V protein as the major determinant of pathogenesis, also being the first in vivo study to show that the W protein modulates the inflammatory host immune response in a manner that determines the disease course.
Suggested Citation
Benjamin A. Satterfield & Robert W. Cross & Karla A. Fenton & Krystle N. Agans & Christopher F. Basler & Thomas W. Geisbert & Chad E. Mire, 2015.
"The immunomodulating V and W proteins of Nipah virus determine disease course,"
Nature Communications, Nature, vol. 6(1), pages 1-15, November.
Handle:
RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms8483
DOI: 10.1038/ncomms8483
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