About: Tissue-specific tolerance in fatal Covid-19

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An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Tissue-specific tolerance in fatal Covid-19
Creator	Armstrong, Stuart Hiscox, Julian Dorward, David Hartley, Catherine Penrice-Randal, Rebekah Bchir, M Sc, M Dhaliwal, Kevin Harrison, David Al Qsous, Wael Bouhaidar, Ralph Campbell, Victoria Duguid, Alasdair Eb, Chris Elshani, Mustafa Gachanja, Naomi Kenneth, J Lucas, Christopher Mbchb, Russell Mbe, Anderson Md, Philippe Millar, Tracey Oc Bellamy, Christopher Prost, Sandrine Randle, Nadine Rgn, Lerpiniere Sc, Potey Smith Md, Colin Tagliavini, Giulia Um, In Wallace, William
Source	MedRxiv
abstract	Successful host defence against a pathogen can involve resistance or tolerance, with implications for prioritising either antimicrobial or immunomodulatory therapeutic approaches. Hyper-inflammation occurs in Covid-19 and is associated with worse outcomes. The efficacy of dexamethasone in preventing mortality in critical Covid-19 suggests that inflammation has a causal role in death. Whether this deleterious inflammation 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 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 was identified in the lung, along with an influx of macrophages/monocytes into the parenchyma. In addition, stereotyped abnormal reticulo-endothelial responses (reactive plasmacytosis 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 cell responses.
has issue date	2020-07-04(xsd:dateTime)
bibo:doi	10.1101/2020.07.02.20145003
has license	medrxiv
sha1sum (hex)	91c35e5b90d488530c9d1e3a29c235037e1fe9c0
schema:url	https://doi.org/10.1101/2020.07.02.20145003
resource representing a document's title	Tissue-specific tolerance in fatal Covid-19
resource representing a document's body	covid:91c35e5b90d488530c9d1e3a29c235037e1fe9c0#body_text
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