About: Contribution of Fcγ Receptor-Mediated Immunity to the Pathogenesis Caused by the Human Respiratory Syncytial Virus

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About: Contribution of Fcγ Receptor-Mediated Immunity to the Pathogenesis Caused by the Human Respiratory Syncytial Virus 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
title	Contribution of Fcγ Receptor-Mediated Immunity to the Pathogenesis Caused by the Human Respiratory Syncytial Virus
Creator	Escobar-Vera, Jorge Acevedo, Orlando Beals, Tomas Benavente, Felipe Díaz, Fabián Fe, Díaz Fm, Benavente Gaudin, Raphael Gomez, Ricardo González, Escobar-Vera González, Pablo Ja, Soto Kalergis, Alexis Negrotto, Soledad Oa, Acevedo Soto, Jorge Te, Beals Teresa Sanchez-Aparicio, Maria
source	Medline; PMC
abstract	The human Respiratory Syncytial Virus (hRSV) is the leading cause of severe acute lower respiratory tract infections (ALRTIs) in humans at all ages and is the main cause of hospitalization due to pneumonia, asthma, and bronchiolitis in infants. hRSV symptoms mainly develop due to an excessive host immune and inflammatory response in the respiratory tissue. hRSV infection during life is frequent and likely because of non-optimal immunological memory is developed against this virus. Vaccine development against this pathogen has been delayed after the detrimental effects produced in children by vaccination with a formalin-inactivated hRSV preparation (FI-hRSV), which caused enhanced disease upon natural viral infection. Since then, several studies have focused on understanding the mechanisms underlying such disease exacerbation. Along these lines, several studies have suggested that antibodies elicited by immunization with FI-hRSV show low neutralizing capacity and promote the formation of immune complexes containing hRSV (hRSV-ICs), which contribute to hRSV pathogenesis through the engagement of Fc gamma receptors (FcγRs) expressed on the surface of immune cells. Furthermore, a role for FcγRs is supported by studies evaluating the contribution of these molecules to hRSV-induced disease. These studies have shown that FcγRs can modulate viral clearance by the host and the inflammatory response triggered by hRSV infection. In addition, ICs can facilitate viral entry into host cells expressing FcγRs, thus extending hRSV infectivity. In this article, we discuss current knowledge relative to the contribution of hRSV-ICs and FcγRs to the pathogenesis caused by hRSV and their putative role in the exacerbation of the disease caused by this virus after FI-hRSV vaccination. A better understanding FcγRs involvement in the immune response against hRSV will contribute to the development of new prophylactic or therapeutic tools to promote virus clearance with limited inflammatory damage to the airways.
has issue date	2019-03-29(xsd:dateTime)
bibo:doi	10.3389/fcimb.2019.00075
bibo:pmid	30984626
has license	cc-by
sha1sum (hex)	889915a03b21c44b0c3d21f13fb8d04a7cdd0f50
schema:url	https://doi.org/10.3389/fcimb.2019.00075
resource representing a document's title	Contribution of Fcγ Receptor-Mediated Immunity to the Pathogenesis Caused by the Human Respiratory Syncytial Virus
has PubMed Central identifier	PMC6450440
has PubMed identifier	30984626
schema:publication	Front Cell Infect Microbiol
resource representing a document's body	covid:889915a03b21c44b0c3d21f13fb8d04a7cdd0f50#body_text
is schema:about of	named entity 'PATHOGENESIS' named entity 'immunization' named entity 'viral entry' named entity 'disease' named entity 'infants' named entity 'effects' named entity 'promote' named entity 'disease' named entity 'INFECTIVITY' named entity 'IMMUNE COMPLEXES' named entity 'EXTENDING' named entity 'INACTIVATED' named entity 'RECEPTORS' named entity 'CONTAINING' named entity 'CONTRIBUTE ' named entity 'ENTRY INTO HOST' named entity 'PATHOGENESIS' named entity 'THERAPEUTIC' named entity 'EFFECTS' named entity 'ADDITION' named entity 'VACCINE DEVELOPMENT' named entity 'SYMPTOMS' named entity 'LOW' named entity 'BRONCHIOLITIS' named entity 'HAVE' named entity 'CHILDREN' named entity 'TISSUE' named entity 'IMMUNE CELLS' named entity 'ASTHMA' named entity 'NEW' named entity 'ALL AGES' named entity 'IMMUNE RESPONSE' named entity 'FREQUENT' named entity 'EXCESSIVE' named entity 'THEIR' named entity 'ENHANCED' named entity 'UNDERLYING' named entity 'ACUTE' named entity 'DISCUSS' named entity 'LOWER RESPIRATORY TRACT INFECTIONS' named entity 'PROPHYLACTIC' named entity 'RESPIRATORY' named entity 'HRSV' named entity 'LIKELY' named entity 'LINES' named entity 'DISEASE' named entity 'CAUSE' named entity 'DAMAGE' named entity 'EVALUATING' named entity 'NATURAL' named entity 'AIRWAYS' named entity 'INFLAMMATORY RESPONSE' named entity 'PNEUMONIA' named entity 'INFANTS' named entity 'MECHANISMS' named entity 'VIRAL INFECTION' named entity 'ICS' named entity 'LIMITED' named entity 'ANTIBODIES' named entity 'UNDERSTANDING' named entity 'VIRUS CLEARANCE' named entity 'SUPPORTED' named entity 'INFLAMMATORY' named entity 'HOSPITALIZATION'

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