SARS-CoV and IFN: Too Little, Too Late

Eveline Kindler; Volker Thiel

doi:10.1016/j.chom.2016.01.012

SARS-CoV and IFN: Too Little, Too Late

Cell Host Microbe. 2016 Feb 10;19(2):139-41. doi: 10.1016/j.chom.2016.01.012.

Authors

Eveline Kindler¹, Volker Thiel²

Affiliations

¹ Department of Infectious Diseases and Pathobiology, University of Bern, 3012 Bern, Switzerland; Federal Department of Home Affairs, Institute of Virology and Immunology, 3012 Bern and 3147 Mittelhäusern, Switzerland.
² Department of Infectious Diseases and Pathobiology, University of Bern, 3012 Bern, Switzerland; Federal Department of Home Affairs, Institute of Virology and Immunology, 3012 Bern and 3147 Mittelhäusern, Switzerland. Electronic address: [email protected].

Abstract

Dysregulated type I interferon (IFN-I) expression can lead to severe pathology and disease. In this issue of Cell Host & Microbe, Channappanavar et al. (2016) use a SARS-coronavirus animal model to describe how rapid and robust virus replication with delayed IFN-I can lead to lung immunopathology, with fatal outcomes.

Publication types

Research Support, Non-U.S. Gov't
Comment

MeSH terms

Animals
Interferon Type I*
Lung / virology
Severe acute respiratory syndrome-related coronavirus*
Virus Replication

Substances

Interferon Type I