4.4 Article

Oxidative stress in Nipah virus-infected human small airway epithelial cells

Journal

JOURNAL OF GENERAL VIROLOGY
Volume 96, Issue -, Pages 2961-2970

Publisher

SOC GENERAL MICROBIOLOGY
DOI: 10.1099/jgv.0.000243

Keywords

-

Funding

  1. University of Texas Medical Branch startup funds
  2. National Institutes of Health [1R21AI111042-01, P01AI07924602]
  3. UTMB Center for Tropical Diseases Postdoctoral Fellowship

Ask authors/readers for more resources

Nipah virus (NiV) is a zoonotic emerging pathogen that can cause severe and often fatal respiratory disease in humans. The pathogenesis of NiV infection of the human respiratory tract remains unknown. Reactive oxygen species (ROS) produced by airway epithelial cells in response to viral infections contribute to lung injury by inducing inflammation and oxidative stress; however, the role of ROS in NiV-induced respiratory disease is unknown. To investigate whether NiV induces oxidative stress in human respiratory epithelial cells, we used oxidative stress markers and monitored antioxidant gene expression. We also used ROS scavengers to assess their role in immune response modulation. Oxidative stress was confirmed in infected cells and correlated with the reduction in antioxidant enzyme gene expression. Infected cells treated by ROS scavengers resulted in a significant decrease of the (F-2)-8-isoprostane marker, inflammatory responses and virus replication. In conclusion, ROS are induced during NiV infection in human respiratory epithelium and contribute to the inflammatory response. Understanding how oxidative stress contributes to NiV pathogenesis is crucial for therapeutic development.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.4
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available