title: Does influenza A infection increase oxidative damage?
abstract: Considerable data implicate oxidative damage in influenza pathogenesis. We examined temporal changes in oxidative damage using accurate biomarkers in an adult cohort with acute influenza infection and their relationships with clinical parameters. Clinical information and blood samples were collected during their acute illness and 3 months later. A fatigue questionnaire was administered 3 months following influenza infection. Thirty-five patients (mean age, 34 years) with polymerase chain reaction-confirmed influenza A infection were included; all patients returned for follow-up assessments. Adjusted levels of plasma F2-isoprostanes, total hydroxyeicosatetraenoic products (HETEs), 7β-hydroxycholesterol and 7-ketocholesterol, serum gamma-glutamyltransferase, and high-sensitivity C-reactive protein (hsCRP) were increased during the acute illness compared with age-matched controls. Despite clinical recovery, levels of these biomarkers remained higher at month 3 compared with controls. A proportion of patients had persistent symptoms such as fatigue (23%), myalgia (14%), and arthralgia (11%) at month 3. Patients with significant fatigue had higher baseline levels of plasma F2-isoprostanes, F4-neuroprostanes, and total HETEs compared to those without fatigue. By contrast, patients with persistent arthralgia and myalgia had higher baseline levels of serum hsCRP compared to those without these symptoms. Our observations lead to the hypothesis that oxidative damage participates in the pathogenesis of influenza infection and postinfectious fatigue.
authors.affiliation: 1 Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore , Singapore, Singapore .
authors.forename: Mary P E
authors.initials: MP
authors.lastname: Ng
authors.forename: Jetty C Y
authors.initials: JC
authors.lastname: Lee
authors.forename: Wai Mun
authors.initials: WM
authors.lastname: Loke
authors.forename: Leonard L L
authors.initials: LL
authors.lastname: Yeo
authors.forename: Amy M L
authors.initials: AM
authors.lastname: Quek
authors.forename: Erle C H
authors.initials: EC
authors.lastname: Lim
authors.forename: Barry
authors.initials: B
authors.lastname: Halliwell
authors.forename: Raymond Chee-Seong
authors.initials: RC
authors.lastname: Seet
mesh_terms: D000328:Adult; D018771:Arthralgia / Q000097:blood / Q000209:etiology / Q000378:metabolism / Q000821:virology; D015415:Biomarkers / Q000097:blood / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D028441:F2-Isoprostanes / Q000097:blood; D005221:Fatigue / Q000097:blood / Q000209:etiology / Q000378:metabolism / Q000821:virology; D005260:Female; D006801:Humans; D006893:Hydroxyeicosatetraenoic Acids / Q000097:blood; D009980:Influenza A virus; D007251:Influenza, Human / Q000097:blood / Q000150:complications* / Q000378:metabolism / Q000473:pathology*; D008297:Male; D063806:Myalgia / Q000097:blood / Q000209:etiology / Q000378:metabolism / Q000821:virology; D058632:Neuroprostanes / Q000097:blood; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000502:physiology*
chemical_list: D015415:Biomarkers; D028441:F2-Isoprostanes; D006893:Hydroxyeicosatetraenoic Acids; D058632:Neuroprostanes; D002097:C-Reactive Protein