About: Suppressed anti-inflammatory heat shock response in high-risk COVID-19 patients: lessons from basic research (inclusive bats), light on conceivable therapies

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About: Suppressed anti-inflammatory heat shock response in high-risk COVID-19 patients: lessons from basic research (inclusive bats), light on conceivable therapies Goto Sponge NotDistinct Permalink

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Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Suppressed anti-inflammatory heat shock response in high-risk COVID-19 patients: lessons from basic research (inclusive bats), light on conceivable therapies
Creator	Antonio, Alberto Gomes Heck, Thiago Homem De Bittencourt, Paulo Ludwig, Mirna Nunes Frizzo, Matias
source	Medline; PMC
abstract	The major risk factors to fatal outcome in COVID-19 patients, i.e., elderliness and pre-existing metabolic and cardiovascular diseases (CVD), share in common the characteristic of being chronic degenerative diseases of inflammatory nature associated with defective heat shock response (HSR). The molecular components of the HSR, the principal metabolic pathway leading to the physiological resolution of inflammation, is an anti-inflammatory biochemical pathway that involves molecular chaperones of the heat shock protein (HSP) family during homeostasis-threatening stressful situations (e.g., thermal, oxidative and metabolic stresses). The entry of SARS coronaviruses in target cells, on the other hand, aggravates the already-jeopardized HSR of this specific group of patients. In addition, cellular counterattack against virus involves interferon (IFN)-mediated inflammatory responses. Therefore, individuals with impaired HSR cannot resolve virus-induced inflammatory burst physiologically, being susceptible to exacerbated forms of inflammation, which leads to a fatal “cytokine storm”. Interestingly, some species of bats that are natural reservoirs of zoonotic viruses, including SARS-CoV-2, possess an IFN-based antiviral inflammatory response perpetually activated but do not show any sign of disease or cytokine storm. This is possible because bats present a constitutive HSR that is by far (hundreds of times) more intense and rapid than that of human, being associated with a high core temperature. Similarly in humans, fever is a physiological inducer of HSR while antipyretics, which block the initial phase of inflammation, impair the resolution phase of inflammation through the HSR. These findings offer a rationale for the reevaluation of patient care and fever reduction in SARS, including COVID-19.
has issue date	2020-08-04(xsd:dateTime)
bibo:doi	10.1042/cs20200596
bibo:pmid	32749472
has license	cc-by-nc-nd
sha1sum (hex)	546c93dcaa693d06be28c08f67488259d8e7ed39
schema:url	https://doi.org/10.1042/cs20200596
resource representing a document's title	Suppressed anti-inflammatory heat shock response in high-risk COVID-19 patients: lessons from basic research (inclusive bats), light on conceivable therapies
has PubMed Central identifier	PMC7403894
has PubMed identifier	32749472
schema:publication	Clin Sci (Lond)
resource representing a document's body	covid:546c93dcaa693d06be28c08f67488259d8e7ed39#body_text
is schema:about of	named entity 'COVID-19' named entity 'bat' named entity 'SARS-CoV-2 virus' named entity 'genome sequence' named entity 'heat shock response' named entity 'immune responses' named entity 'senescent cells' named entity 'causal role' named entity 'host cell' named entity 'COVID' named entity 'tissue repair' named entity 'SARS' named entity 'senescence' named entity 'China' named entity 'leucine-rich repeat' named entity 'nitric oxide' named entity 'SARS-CoV-2' named entity 'cardiomyocytes' named entity 'all-cause mortality' named entity 'lymph nodes' named entity 'IL-1β' named entity 'JNK2' named entity 'long-lasting' named entity 'polymorphonuclear cells' named entity 'monocytes' named entity 'HSF1' named entity 'virus' named entity 'IFN' named entity 'SASP' named entity 'common colds' named entity 'SARS' named entity 'virus' named entity 'COVID-19' named entity 'HSP70' named entity 'antipyretics' named entity 'cardiovascular' named entity 'mitogen' named entity 'inflammation' named entity 'cell types' named entity 'GSK-3β' named entity 'HSR' named entity 'inflammation' named entity 'GSH' named entity 'hyperthermia' named entity 'comorbidities' named entity 'sepsis' named entity 'cytokine storm' named entity 'HSR' named entity 'heart failure' named entity 'electric blanket' named entity 'inflammatory conditions' named entity 'HSR' named entity 'COVID' named entity 'HSP70' named entity 'HSP70' named entity 'SARS-CoV-2' named entity 'virus infections' named entity 'obesity' named entity 'HSP70' named entity 'physical activity' named entity 'inflammatory response' named entity 'HSR' named entity 'inducer' named entity 'SARS-CoV-2' named entity 'Collins & Co.' named entity '2003 outbreak' named entity 'heat shock' named entity 'antiviral' named entity 'transcription factors' named entity 'SASP' named entity 'transcription' named entity 'ACE2' named entity 'lungs' named entity 'heat shock response' named entity 'JNK1' named entity 'protein chaperones' named entity 'ARDS'

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