title: Respiratory syncytial virus, airway inflammation, and FEV1 decline in patients with chronic obstructive pulmonary disease.
abstract: BACKGROUND
  Respiratory syncytial virus (RSV) is increasingly recognized as an important pathogen in adults with cardiopulmonary disease. It has been associated with acute exacerbations of chronic obstructive pulmonary disease (COPD); however, it has also been detected in the lower airway in the stable state, but the consequences of RSV in stable disease have not previously been determined. We therefore studied the consequences of RSV persistence in adults with COPD and its effect on airway inflammation and lung function decline.
  
  
  METHODS
  A total of 241 sputum samples from 74 patients with COPD (FEV(1)% predicted, 39.2%; interquartile range, 29.6-57.8%) were collected quarterly in the stable state over 2 yr. RSV was detected by polymerase chain reaction (PCR), quantitative microbiology was performed, and inflammatory cytokines were quantified by ELISA.
  
  
  RESULTS
  RSV RNA was detected in 32.8% of sputum samples. Patients in whom RSV was more frequently detected (> 50% of samples RSV PCR-positive, n=18) had higher airway inflammation and faster FEV(1) decline over the study (101.4 ml/yr [95% confidence interval, 57.1-145.8]) compared with those with less frequent detection of RSV (n=56; 51.2 ml/yr [31.7-70.8]; p=0.01). The observed relationship between RSV detection and accelerated lung function decline was independent of smoking status, exacerbation frequency, and lower airway bacterial load.
  
  
  CONCLUSIONS
  Persistent RSV detection in patients with COPD is associated with airway inflammation and accelerated decline in FEV(1). Chronic RSV infection may be a novel therapeutic target to alter the natural history of COPD.
authors.affiliation: Academic Unit of Respiratory Medicine, University College London, Royal Free and University College Medical School, Hampstead Campus, Rowland Hill Street, London, NW3 2PF, UK.
authors.forename: Tom M A
authors.initials: TM
authors.lastname: Wilkinson
authors.forename: Gavin C
authors.initials: GC
authors.lastname: Donaldson
authors.forename: Sebastian L
authors.initials: SL
authors.lastname: Johnston
authors.forename: Peter J M
authors.initials: PJ
authors.lastname: Openshaw
authors.forename: Jadwiga A
authors.initials: JA
authors.lastname: Wedzicha
mesh_terms: D000368:Aged; D016207:Cytokines / Q000378:metabolism*; D018450:Disease Progression; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005500:Follow-Up Studies; D005541:Forced Expiratory Volume / Q000502:physiology*; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D011446:Prospective Studies; D029424:Pulmonary Disease, Chronic Obstructive / Q000378:metabolism / Q000503:physiopathology / Q000821:virology; D012367:RNA, Viral / Q000032:analysis; D012136:Respiratory Syncytial Viruses / Q000235:genetics / Q000302:isolation & purification*; D012720:Severity of Illness Index; D013183:Sputum / Q000378:metabolism / Q000821:virology
chemical_list: D016207:Cytokines; D012367:RNA, Viral