{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Piedra FA"],"funding":["National Institute of Environmental Health Sciences","U.S. Department of Defense"],"pagination":["e0172953"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5340370"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(3)"],"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"],"journal":["PloS one"],"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."],"pmcid":["PMC5340370"],"funding_grant_id":["T32-07254","W81XWH1010146"],"pubmed_authors":["Avadhanula V","Piedra PA","Mei M","Aideyan L","Mehta R","Garofalo RP","Piedra FA"],"additional_accession":[]},"is_claimable":false,"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.","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","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017","modification":"2026-05-30T01:50:42.381Z","creation":"2019-03-26T22:52:58Z"},"accession":"S-EPMC5340370","cross_references":{"pubmed":["28267794"],"doi":["10.1371/journal.pone.0172953"]}}