<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Piedra FA</submitter><funding>National Institute of Environmental Health Sciences</funding><funding>U.S. Department of Defense</funding><pagination>e0172953</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5340370</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(3)</volume><pubmed_abstract>Respiratory syncytial virus (RSV) causes significant infant morbidity and mortality. For decades severe RSV-induced disease was thought to result from an uncontrolled host response to viral replication, but recent work suggests that a strong innate immune response early in infection is protective. To shed light on host-virus interactions and the viral determinants of disease, copy numbers of five RSV genes (NS1, NS2, N, G, F) were measured by quantitative real-time polymerase chain reaction (qPCR) in nasal wash samples from children with RSV-associated bronchiolitis. Correlations were sought with host cytokines/chemokines and biomarkers. Associations with disposition from the emergency department (hospitalized or sent home) and pulse oximetry O2 saturation levels were also sought. Addition</pubmed_abstract><journal>PloS one</journal><pubmed_title>The interdependencies of viral load, the innate immune response, and clinical outcome in children presenting to the emergency department with respiratory syncytial virus-associated bronchiolitis.</pubmed_title><pmcid>PMC5340370</pmcid><funding_grant_id>T32-07254</funding_grant_id><funding_grant_id>W81XWH1010146</funding_grant_id><pubmed_authors>Avadhanula V</pubmed_authors><pubmed_authors>Piedra PA</pubmed_authors><pubmed_authors>Mei M</pubmed_authors><pubmed_authors>Aideyan L</pubmed_authors><pubmed_authors>Mehta R</pubmed_authors><pubmed_authors>Garofalo RP</pubmed_authors><pubmed_authors>Piedra FA</pubmed_authors></additional><is_claimable>false</is_claimable><name>The interdependencies of viral load, the innate immune response, and clinical outcome in children presenting to the emergency department with respiratory syncytial virus-associated bronchiolitis.</name><description>Respiratory syncytial virus (RSV) causes significant infant morbidity and mortality. For decades severe RSV-induced disease was thought to result from an uncontrolled host response to viral replication, but recent work suggests that a strong innate immune response early in infection is protective. To shed light on host-virus interactions and the viral determinants of disease, copy numbers of five RSV genes (NS1, NS2, N, G, F) were measured by quantitative real-time polymerase chain reaction (qPCR) in nasal wash samples from children with RSV-associated bronchiolitis. Correlations were sought with host cytokines/chemokines and biomarkers. Associations with disposition from the emergency department (hospitalized or sent home) and pulse oximetry O2 saturation levels were also sought. Addition</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017</publication><modification>2026-05-30T01:50:42.381Z</modification><creation>2019-03-26T22:52:58Z</creation></dates><accession>S-EPMC5340370</accession><cross_references><pubmed>28267794</pubmed><doi>10.1371/journal.pone.0172953</doi></cross_references></HashMap>