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The immunomodulating V and W proteins of Nipah virus determine disease course

Benjamin A. Satterfield, Robert W. Cross, Karla A. Fenton, Krystle N. Agans, Christopher F. Basler, Thomas W. Geisbert () and Chad E. Mire
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Benjamin A. Satterfield: Galveston National Laboratory, University of Texas Medical Branch
Robert W. Cross: Galveston National Laboratory, University of Texas Medical Branch
Karla A. Fenton: Galveston National Laboratory, University of Texas Medical Branch
Krystle N. Agans: Galveston National Laboratory, 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
Chad E. Mire: Galveston National Laboratory, University of Texas Medical Branch

Nature Communications, 2015, vol. 6, issue 1, 1-15

Abstract: 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.

Date: 2015
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms8483

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DOI: 10.1038/ncomms8483

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