StressCovidV1, PubMed, Corpus, bibRecord, 000423

Acute Lung Injury Results from Innate Sensing of Viruses by an ER Stress Pathway.

Identifieur interne : 000423 ( PubMed/Corpus ); précédent : 000422; suivant : 000424

Acute Lung Injury Results from Innate Sensing of Viruses by an ER Stress Pathway.

Auteurs : Eike R. Hrincius ; Swantje Liedmann ; David Finkelstein ; Peter Vogel ; Shane Gansebom ; Amali E. Samarasinghe ; Dahui You ; Stephania A. Cormier ; Jonathan A. Mccullers

Source :

Cell reports [ 2211-1247 ] ; 2015.

RBID : pubmed:26051937

English descriptors

Abstract

Incursions of new pathogenic viruses into humans from animal reservoirs are occurring with alarming frequency. The molecular underpinnings of immune recognition, host responses, and pathogenesis in this setting are poorly understood. We studied pandemic influenza viruses to determine the mechanism by which increasing glycosylation during evolution of surface proteins facilitates diminished pathogenicity in adapted viruses. ER stress during infection with poorly glycosylated pandemic strains activated the unfolded protein response, leading to inflammation, acute lung injury, and mortality. Seasonal strains or viruses engineered to mimic adapted viruses displaying excess glycans on the hemagglutinin did not cause ER stress, allowing preservation of the lungs and survival. We propose that ER stress resulting from recognition of non-adapted viruses is utilized to discriminate "non-self" at the level of protein processing and to activate immune responses, with unintended consequences on pathogenesis. Understanding this mechanism should improve strategies for treating acute lung injury from zoonotic viral infections.

DOI: 10.1016/j.celrep.2015.05.012
PubMed: 26051937

Links to Exploration step

pubmed:26051937

Le document en format XML

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<front><div type="abstract" xml:lang="en">Incursions of new pathogenic viruses into humans from animal reservoirs are occurring with alarming frequency. The molecular underpinnings of immune recognition, host responses, and pathogenesis in this setting are poorly understood. We studied pandemic influenza viruses to determine the mechanism by which increasing glycosylation during evolution of surface proteins facilitates diminished pathogenicity in adapted viruses. ER stress during infection with poorly glycosylated pandemic strains activated the unfolded protein response, leading to inflammation, acute lung injury, and mortality. Seasonal strains or viruses engineered to mimic adapted viruses displaying excess glycans on the hemagglutinin did not cause ER stress, allowing preservation of the lungs and survival. We propose that ER stress resulting from recognition of non-adapted viruses is utilized to discriminate "non-self" at the level of protein processing and to activate immune responses, with unintended consequences on pathogenesis. Understanding this mechanism should improve strategies for treating acute lung injury from zoonotic viral infections. </div>
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Acute Lung Injury Results from Innate Sensing of Viruses by an ER Stress Pathway.

Acute Lung Injury Results from Innate Sensing of Viruses by an ER Stress Pathway.

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