About: ADE and hyperinflammation in SARS-CoV2 infection- Comparison with dengue hemorrhagic fever and feline infectious peritonitis

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About: ADE and hyperinflammation in SARS-CoV2 infection- Comparison with dengue hemorrhagic fever and feline infectious peritonitis Goto Sponge NotDistinct Permalink

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	ADE and hyperinflammation in SARS-CoV2 infection- Comparison with dengue hemorrhagic fever and feline infectious peritonitis
Creator	Ihsan, Awais Ca, Subburaj Chamard, Hugues Cloutier, Maryse Ilangumaran, Ilangumaran, Subburaj Nandi, Madhuparna Ramanathan, Sheela Ramanathan@usherbrooke, Sheela Ullah Ihsan, Awais
Source	Elsevier; PMC
abstract	The COVID-19 pandemic has rapidly spread around the world with significant morbidity and mortality in a subset of patients including the elderly. The poorer outcomes are associated with ‘cytokine storm-like’ immune responses, otherwise referred to as ‘hyperinflammation’. While most of the infected individuals show minimal or no symptoms and recover spontaneously, a small proportion of the patients exhibit severe symptoms characterized by extreme dyspnea and low oxygen tissue levels, with extensive damage to the lungs referred to as acute respiratory distress symptom (ARDS). The consensus is that the hyperinflammatory response of the host is akin to the cytokine storm observed during sepsis and is the major cause of death. Uncertainties remain on the factors that lead to hyperinflammatory response in some but not all individuals. Hyperinflammation is a common feature in different viral infections such as dengue where existing low-titer antibodies to the virus enhances the infection in immune cells through a process called antibody-dependent enhancement or ADE. ADE has been reported following vaccination or secondary infections with other corona, Ebola and dengue virus. Detailed analysis has shown that antibodies to any viral epitope can induce ADE when present in sub-optimal titers or is of low affinity. In this review we will discuss ADE in the context of dengue and coronavirus infections including Covid-19.
has issue date	2020-08-20(xsd:dateTime)
bibo:doi	10.1016/j.cyto.2020.155256
has license	no-cc
sha1sum (hex)	1fbd26421691eaae2a50a1b4df305b4455995cdf
schema:url	https://doi.org/10.1016/j.cyto.2020.155256
resource representing a document's title	ADE and hyperinflammation in SARS-CoV2 infection- Comparison with dengue hemorrhagic fever and feline infectious peritonitis
has PubMed Central identifier	PMC7439999
schema:publication	Cytokine
resource representing a document's body	covid:1fbd26421691eaae2a50a1b4df305b4455995cdf#body_text
is schema:about of	named entity 'Allard' named entity 'Review article' named entity 'DOI' named entity 'HTTPS' named entity 'asymptomatic' named entity 'immune response' named entity 'murine models' named entity 'antibodies' named entity 'sensitizing' named entity 'SARS-CoV' named entity 'Complement-mediated' named entity 'immune complexes' named entity 'inflammatory mediators' named entity 'monocytes' named entity 'bronchoalveolar lavage fluid' named entity 'IL-6' named entity 'life span' named entity 'SARS' named entity 'ZIKV' named entity 'infection' named entity 'vaccination' named entity 'Covid' named entity 'viral titers' named entity 'pro-inflammatory' named entity 'titer' named entity 'proinflammatory cytokines' named entity 'macrophages' named entity 'IL-3' named entity 'nonhuman primates' named entity 'vaccinia virus' named entity 'neutralizing antibodies' named entity 'pediatric' named entity 'ARDS' named entity 'DENV' named entity 'seronegative' named entity 'FcγR' named entity 'vaccination' named entity 'cytokines' named entity 'zika' named entity 'TNFα' named entity 'neutralizing antibodies' named entity 'TNFα' named entity 'CCL2' named entity 'hematopoietic cells' named entity 'dengue' named entity 'upper respiratory tract' named entity 'SARS-CoV2' named entity 'lung' named entity 'IL-1β' named entity 'spike protein' named entity 'ADE' named entity 'long-lasting' named entity 'SARS-CoV' named entity 'immune response' named entity 'inflammatory cytokines' named entity 'monomeric' named entity 'viral load' named entity 'receptor' named entity 'titer' named entity 'endothelial' named entity 'alveolar macrophages' named entity 'viral genome' named entity 'pneumocytes' named entity 'FIP' named entity 'ADE' named entity 'IL-8' named entity 'SARS-CoV' named entity 'IL-1' named entity 'gastrointestinal tracts' named entity 'proinflammatory cytokines' named entity 'Dengue virus' named entity 'SARS' named entity 'viruses' named entity 'older patients'

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