About: Beyond Anti-viral Effects of Chloroquine/Hydroxychloroquine

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

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Beyond Anti-viral Effects of Chloroquine/Hydroxychloroquine
Creator	Puppo, Francesco Gros, Frédéric Herbeuval, Jean-Philippe Rodero, Mathieu Bekaddour, Nassima Conti, Fabrizio Dieudonné, Yannick Frenger, Quentin Gies, Vincent Guffroy, Aurélien Korganow, Anne-Sophie Gheita, Tamer
Source	Medline; PMC
abstract	As the world is severely affected by COVID-19 pandemic, the use of chloroquine and hydroxychloroquine in prevention or for the treatment of patients is allowed in multiple countries but remained at the center of much controversy in recent days. This review describes the properties of chloroquine and hydroxychloroquine, and highlights not only their anti-viral effects but also their important immune-modulatory properties and their well-known use in autoimmune diseases, including systemic lupus and arthritis. Chloroquine appears to inhibit in vitro SARS virus' replication and to interfere with SARS-CoV2 receptor (ACE2). Chloroquine and hydroxychloroquine impede lysosomal activity and autophagy, leading to a decrease of antigen processing and presentation. They are also known to interfere with endosomal Toll-like receptors signaling and cytosolic sensors of nucleic acids, which result in a decreased cellular activation and thereby a lower type I interferons and inflammatory cytokine secretion. Given the antiviral and anti-inflammatory properties of chloroquine and hydroxychloroquine, there is a rational to use them against SARS-CoV2 infection. However, the anti-interferon properties of these molecules might be detrimental, and impaired host immune responses against the virus. This duality could explain the discrepancy with the recently published studies on CQ/HCQ treatment efficacy in COVID-19 patients. Moreover, although these treatments could be an interesting potential strategy to limit progression toward uncontrolled inflammation, they do not appear per se sufficiently potent to control the whole inflammatory process in COVID-19, and more targeted and/or potent therapies should be required at least in add-on.
has issue date	2020-07-02(xsd:dateTime)
bibo:doi	10.3389/fimmu.2020.01409
bibo:pmid	32714335
has license	cc-by
sha1sum (hex)	585b867d6ce445ca460a8c74e9d81f2d8df79e82
schema:url	https://doi.org/10.3389/fimmu.2020.01409
resource representing a document's title	Beyond Anti-viral Effects of Chloroquine/Hydroxychloroquine
has PubMed Central identifier	PMC7343769
has PubMed identifier	32714335
schema:publication	Front Immunol
resource representing a document's body	covid:585b867d6ce445ca460a8c74e9d81f2d8df79e82#body_text
is schema:about of	named entity 'progression' named entity 'Chloroquine' named entity 'control' named entity 'ACE2' named entity 'potent' named entity 'Hydroxychloroquine' named entity 'KNOWN' named entity 'REPLICATION' named entity 'DECREASE' named entity 'SARS' named entity 'BUT' named entity 'TO CONTROL' named entity 'TREATMENTS' named entity 'ALLOWED' named entity 'INTERFERON ' named entity 'STRATEGY' named entity 'VIRUS' named entity 'USE' named entity 'LIMIT' named entity 'CONTROVERSY' named entity 'ARTHRITIS' named entity 'COVID-19 PANDEMIC' named entity 'lupus' named entity 'patients' named entity 'interfere' named entity 'chloroquine' named entity 'SARS virus' named entity 'remained' named entity 'targeted' named entity 'autoimmune diseases' named entity 'add-on' named entity 'COVID-19' named entity 'treatment of patients' named entity 'Chloroquine' named entity 'endosomal' named entity 'SARS virus' named entity 'Chloroquine' named entity 'Toll-like receptors' named entity 'Hydroxychloroquine' named entity 'Anti-viral' named entity 'mode of action' named entity 'COVID' named entity 'interferons' named entity 'endogenous' named entity 'gene' named entity 'lungs' named entity 'SARS-CoV2' named entity 'STING' named entity 'infection' named entity 'coronavirus' named entity 'intracellular compartments' named entity 'systemic lupus erythematosus' named entity 'autophagosomes' named entity 'cytosolic' named entity 'MAVS' named entity 'MyD88' named entity 'NETosis' named entity 'autoimmune' named entity 'type I interferon' named entity 'TLR7' named entity 'inflammatory cytokine' named entity 'clinical symptoms' named entity 'PPT1' named entity 'STING' named entity 'autoimmune diseases' named entity 'cytokines' named entity 'inflammation' named entity '49, 50' named entity 'inflammation' named entity 'type I interferons'

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