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Article: Does influenza A infection increase oxidative damage?

TitleDoes influenza A infection increase oxidative damage?
Authors
Issue Date2014
PublisherMary Ann Liebert, Inc Publishers. The Journal's web site is located at http://www.liebertpub.com/ars
Citation
Antioxidants & Redox Signaling, 2014, v. 21 n. 7, p. 1025-1031 How to Cite?
AbstractConsiderable 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), 7beta-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.
Persistent Identifierhttp://hdl.handle.net/10722/196828
ISSN
2015 Impact Factor: 7.093
2015 SCImago Journal Rankings: 3.134
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorNg, MPE-
dc.contributor.authorLee, JCY-
dc.contributor.authorLoke, WM-
dc.contributor.authorYeo, LLL-
dc.contributor.authorQuek, AML-
dc.contributor.authorLim, ECH-
dc.contributor.authorHalliwell, B-
dc.contributor.authorSeet, RCS-
dc.date.accessioned2014-04-29T03:44:52Z-
dc.date.available2014-04-29T03:44:52Z-
dc.date.issued2014-
dc.identifier.citationAntioxidants & Redox Signaling, 2014, v. 21 n. 7, p. 1025-1031-
dc.identifier.issn1523-0864-
dc.identifier.urihttp://hdl.handle.net/10722/196828-
dc.description.abstractConsiderable 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), 7beta-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.-
dc.languageeng-
dc.publisherMary Ann Liebert, Inc Publishers. The Journal's web site is located at http://www.liebertpub.com/ars-
dc.relation.ispartofAntioxidants & Redox Signaling-
dc.rightsThis is a copy of an article published in the Antioxidants & Redox Signaling © 2014 copyright Mary Ann Liebert, Inc.; Antioxidants & Redox Signaling is available online at: http://www.liebertonline.com-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleDoes influenza A infection increase oxidative damage?-
dc.typeArticle-
dc.identifier.emailLee, JCY: jettylee@hku.hk-
dc.identifier.authorityLee, JCY=rp01511-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1089/ars.2014.5907-
dc.identifier.pmid24673169-
dc.identifier.hkuros228734-
dc.identifier.volume21-
dc.identifier.issue7-
dc.identifier.spage1025-
dc.identifier.epage1031-
dc.identifier.isiWOS:000340542200002-
dc.publisher.placeUnited States-

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