F Freymuth (Professeur de virologie, biologiste des Hôpitaux)
{"title":"Virus respiratoire syncytial et virus para-influenza humains : clinique","authors":"F Freymuth (Professeur de virologie, biologiste des Hôpitaux)","doi":"10.1016/j.emcped.2003.06.003","DOIUrl":null,"url":null,"abstract":"<div><p>The respiratory syncytial virus (RSV) causes 50% to 90% of all bronchiolitis cases in infants. The occurrence and severity of bronchiolitis are dependent on patient-related factors (preterm birth, comorbidities, individual susceptibility), virus-related factors (RSV A), and environmental factors (pollution, environmental tobacco smoke, and others). Mortality rates in infants with bronchiolitis range from 0.005% to 0.2% according to patient-related factors. The pathophysiology of RSV bronchiolitis is unknown but clearly involves direct effects of the virus on the airway epithelium, airway immaturity, and recently identified effects of the inflammatory response. Immunopathologic mechanisms (e.g., IgE antibodies and CD4<sup>+</sup> Th2 cells) play a role in some infants or in severe forms. Complete immunity to the virus is never achieved, and repeat infections are common in the young and the elderly, in whom the RSV causes about 5% of all lower respiratory tract infections. VPI3 infections usually cause bronchiolitis, whereas VPI1 and VPI2 infections manifest chiefly as laryngotracheitis. Little is known about the clinical expression of VPI4 infection. Bronchiolitis due to hMPV is indistinguishable from RSV bronchiolitis.</p></div>","PeriodicalId":100441,"journal":{"name":"EMC - Pédiatrie","volume":"1 1","pages":"Pages 18-27"},"PeriodicalIF":0.0000,"publicationDate":"2004-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.emcped.2003.06.003","citationCount":"2","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"EMC - Pédiatrie","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1762601303000119","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 2
Abstract
The respiratory syncytial virus (RSV) causes 50% to 90% of all bronchiolitis cases in infants. The occurrence and severity of bronchiolitis are dependent on patient-related factors (preterm birth, comorbidities, individual susceptibility), virus-related factors (RSV A), and environmental factors (pollution, environmental tobacco smoke, and others). Mortality rates in infants with bronchiolitis range from 0.005% to 0.2% according to patient-related factors. The pathophysiology of RSV bronchiolitis is unknown but clearly involves direct effects of the virus on the airway epithelium, airway immaturity, and recently identified effects of the inflammatory response. Immunopathologic mechanisms (e.g., IgE antibodies and CD4+ Th2 cells) play a role in some infants or in severe forms. Complete immunity to the virus is never achieved, and repeat infections are common in the young and the elderly, in whom the RSV causes about 5% of all lower respiratory tract infections. VPI3 infections usually cause bronchiolitis, whereas VPI1 and VPI2 infections manifest chiefly as laryngotracheitis. Little is known about the clinical expression of VPI4 infection. Bronchiolitis due to hMPV is indistinguishable from RSV bronchiolitis.