Corpus overview


Overview

MeSH Disease

Human Phenotype

Transmission

There are no transmission terms in the subcorpus


Seroprevalence
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    Tissue-specific tolerance in fatal Covid-19

    Authors: David A Dorward; Clark D Russell; In Hwa Um; Mustafa Elshani; Stuart D Armstrong; Rebekah Penrice-Randal; Tracey Millar; Chris EB Lerpiniere; Giulia Tagliavini; Catherine S Hartley; Nadine P Randall; Naomi N Gachanja; Philippe MD Potey; Alison M Anderson; Victoria L Campbell; Alasdair J Duguid; Wael Al Qsous; Ralph BouHaidar; J Kenneth Baillie; Kevin Dhaliwal; William A Wallace; Christopher OC Bellamy; Sandrine Prost; Colin Smith; Julian A Hiscox; David J Harrison; Christopher D Lucas; - ICECAP

    doi:10.1101/2020.07.02.20145003 Date: 2020-07-04 Source: medRxiv

    Successful host defence against a pathogen can involve resistance or tolerance, with implications for prioritising either antimicrobial or immunomodulatory therapeutic approaches. Hyper- inflammation MESHD occurs in Covid-19 and is associated with worse outcomes. The efficacy of dexamethasone in preventing mortality in critical Covid-19 suggests that inflammation MESHD has a causal role in death MESHD. Whether this deleterious inflammation MESHD is primarily a direct response to the presence of SARS-CoV-2 requiring enhanced resistance, or an independent immunopathologic process necessitating enhanced tolerance, is unknown. Here we report an aberrant immune response in fatal Covid-19, principally involving the lung and reticuloendothelial system, that is not clearly topologically associated with the virus, indicating tissue-specific tolerance of SARS-CoV-2. We found that inflammation MESHD and organ dysfunction in fatal Covid-19 did not map to the widespread tissue and cellular distribution of SARS-CoV-2 RNA and protein, both between and within tissues. A monocyte/myeloid-rich vasculitis MESHD vasculitis HP was identified in the lung, along with an influx of macrophages/monocytes into the parenchyma. In addition, stereotyped abnormal reticulo-endothelial responses (reactive plasmacytosis HP and iron-laden macrophages) were present and dissociated from the presence of virus in lymphoid tissues. Our results support virus-independent immunopathology being one of the primary mechanisms underlying fatal Covid-19. This supports prioritising pathogen tolerance as a therapeutic strategy in Covid-19, by better understanding non-injurious organ-specific viral tolerance mechanisms and targeting aberrant macrophage and plasma SERO cell responses.

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MeSH Disease
Human Phenotype
Transmission
Seroprevalence


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