File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Delayed clearance of viral load and marked cytokine activation in severe cases of pandemic H1N1 2009 influenza virus infection

TitleDelayed clearance of viral load and marked cytokine activation in severe cases of pandemic H1N1 2009 influenza virus infection
Authors
Issue Date2010
PublisherOxford University Press. The Journal's web site is located at http://www.oxfordjournals.org/our_journals/cid/
Citation
Clinical Infectious Diseases, 2010, v. 50 n. 6, p. 850-859 How to Cite?
AbstractBackground: Infections caused by the pandemic H1N1 2009 influenza virus range from mild upper respiratory tract syndromes to fatal diseases. However, studies comparing virological and immunological profile of different clinical severity are lacking. Methods: We conducted a retrospective cohort study of 74 patients with pandemic H1N1 infection, including 23 patients who either developed acute respiratory distress syndrome (ARDS) or died (ARDS-death group), 14 patients with desaturation requiring oxygen supplementation and who survived without ARDS (survived-withoutARDS group), and 37 patients with mild disease without desaturation (mild-disease group). We compared their pattern of clinical disease, viral load, and immunological profile. Results: Patients with severe disease were older, more likely to be obese or having underlying diseases, and had lower respiratory tract symptoms, especially dyspnea at presentation. The ARDS-death group had a slower decline in nasopharyngeal viral loads, had higher plasma levels of proinflammatory cytokines and chemokines, and were more likely to have bacterial coinfections (30.4%), myocarditis (21.7%), or viremia (13.0%) than patients in the survived-without-ARDS or the mild-disease groups. Reactive hemophagocytosis, thrombotic phenomena, lymphoid atrophy, diffuse alveolar damage, and multiorgan dysfunction similar to fatal avian influenza A H5N1 infection were found at postmortem examinations. Conclusions: The slower control of viral load and immunodysregulation in severe cases mandate the search for more effective antiviral and immunomodulatory regimens to stop the excessive cytokine activation resulting in ARDS and death. © 2010 by the Infectious Diseases Society of America. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/125075
ISSN
2021 Impact Factor: 20.999
2020 SCImago Journal Rankings: 3.440
ISI Accession Number ID
Funding AgencyGrant Number
Providence Foundation Limited
University Grant Council
Research Fund for the Control of Infectious Diseases (RFCID)
Food and Health Bureau of the Hong Kong SAR Government
Funding Information:

The Providence Foundation Limited in memory of the late Dr Lui Hac Minh, the University Grant Council, and the Research Fund for the Control of Infectious Diseases (RFCID) of the Food and Health Bureau of the Hong Kong SAR Government.

References

 

DC FieldValueLanguage
dc.contributor.authorTo, KKWen_HK
dc.contributor.authorHung, IFNen_HK
dc.contributor.authorLi, IWSen_HK
dc.contributor.authorLee, KLen_HK
dc.contributor.authorKoo, CKen_HK
dc.contributor.authorYan, WWen_HK
dc.contributor.authorLiu, Ren_HK
dc.contributor.authorHo, KYen_HK
dc.contributor.authorChu, KHen_HK
dc.contributor.authorWatt, CLen_HK
dc.contributor.authorLuk, WKen_HK
dc.contributor.authorLai, KYen_HK
dc.contributor.authorChow, FLen_HK
dc.contributor.authorMok, Ten_HK
dc.contributor.authorBuckley, Ten_HK
dc.contributor.authorChan, JFWen_HK
dc.contributor.authorWong, SSYen_HK
dc.contributor.authorZheng, Ben_HK
dc.contributor.authorChen, Hen_HK
dc.contributor.authorLau, CCYen_HK
dc.contributor.authorTse, Hen_HK
dc.contributor.authorCheng, VCCen_HK
dc.contributor.authorChan, KHen_HK
dc.contributor.authorYuen, KYen_HK
dc.date.accessioned2010-10-31T11:09:59Z-
dc.date.available2010-10-31T11:09:59Z-
dc.date.issued2010en_HK
dc.identifier.citationClinical Infectious Diseases, 2010, v. 50 n. 6, p. 850-859en_HK
dc.identifier.issn1058-4838en_HK
dc.identifier.urihttp://hdl.handle.net/10722/125075-
dc.description.abstractBackground: Infections caused by the pandemic H1N1 2009 influenza virus range from mild upper respiratory tract syndromes to fatal diseases. However, studies comparing virological and immunological profile of different clinical severity are lacking. Methods: We conducted a retrospective cohort study of 74 patients with pandemic H1N1 infection, including 23 patients who either developed acute respiratory distress syndrome (ARDS) or died (ARDS-death group), 14 patients with desaturation requiring oxygen supplementation and who survived without ARDS (survived-withoutARDS group), and 37 patients with mild disease without desaturation (mild-disease group). We compared their pattern of clinical disease, viral load, and immunological profile. Results: Patients with severe disease were older, more likely to be obese or having underlying diseases, and had lower respiratory tract symptoms, especially dyspnea at presentation. The ARDS-death group had a slower decline in nasopharyngeal viral loads, had higher plasma levels of proinflammatory cytokines and chemokines, and were more likely to have bacterial coinfections (30.4%), myocarditis (21.7%), or viremia (13.0%) than patients in the survived-without-ARDS or the mild-disease groups. Reactive hemophagocytosis, thrombotic phenomena, lymphoid atrophy, diffuse alveolar damage, and multiorgan dysfunction similar to fatal avian influenza A H5N1 infection were found at postmortem examinations. Conclusions: The slower control of viral load and immunodysregulation in severe cases mandate the search for more effective antiviral and immunomodulatory regimens to stop the excessive cytokine activation resulting in ARDS and death. © 2010 by the Infectious Diseases Society of America. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://www.oxfordjournals.org/our_journals/cid/en_HK
dc.relation.ispartofClinical Infectious Diseasesen_HK
dc.subject.meshCohort Studies-
dc.subject.meshCytokines - blood-
dc.subject.meshInfluenza A Virus, H1N1 Subtype - isolation and purification-
dc.subject.meshInfluenza, Human - immunology - pathology - virology-
dc.subject.meshViral Load-
dc.titleDelayed clearance of viral load and marked cytokine activation in severe cases of pandemic H1N1 2009 influenza virus infectionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1058-4838&volume=50&issue=6&spage=850&epage=859&date=2010&atitle=Delayed+clearance+of+viral+load+and+marked+cytokine+activation+in+severe+cases+of+pandemic+H1N1+2009+influenza+virus+infection-
dc.identifier.emailTo, KKW: kelvinto@hkucc.hku.hken_HK
dc.identifier.emailHung, IFN: ivanhung@hkucc.hku.hken_HK
dc.identifier.emailChan, JFW: jfwchan@hku.hken_HK
dc.identifier.emailWong, SSY: samsonsy@hkucc.hku.hken_HK
dc.identifier.emailZheng, B: bzheng@hkucc.hku.hken_HK
dc.identifier.emailChen, H: hlchen@hku.hken_HK
dc.identifier.emailTse, H: htse@hkucc.hku.hken_HK
dc.identifier.emailYuen, KY: kyyuen@hkucc.hku.hken_HK
dc.identifier.authorityTo, KKW=rp01384en_HK
dc.identifier.authorityHung, IFN=rp00508en_HK
dc.identifier.authorityChan, JFW=rp01736en_HK
dc.identifier.authorityWong, SSY=rp00395en_HK
dc.identifier.authorityZheng, B=rp00353en_HK
dc.identifier.authorityChen, H=rp00383en_HK
dc.identifier.authorityTse, H=rp00519en_HK
dc.identifier.authorityYuen, KY=rp00366en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1086/650581en_HK
dc.identifier.pmid20136415-
dc.identifier.scopuseid_2-s2.0-77749282915en_HK
dc.identifier.hkuros173891en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77749282915&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume50en_HK
dc.identifier.issue6en_HK
dc.identifier.spage850en_HK
dc.identifier.epage859en_HK
dc.identifier.eissn1537-6591-
dc.identifier.isiWOS:000274656000009-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTo, KKW=14323807300en_HK
dc.identifier.scopusauthoridHung, IFN=7006103457en_HK
dc.identifier.scopusauthoridLi, IWS=24464179500en_HK
dc.identifier.scopusauthoridLee, KL=35315784200en_HK
dc.identifier.scopusauthoridKoo, CK=35946195400en_HK
dc.identifier.scopusauthoridYan, WW=7402221587en_HK
dc.identifier.scopusauthoridLiu, R=36087869100en_HK
dc.identifier.scopusauthoridHo, KY=36025095900en_HK
dc.identifier.scopusauthoridChu, KH=7402452789en_HK
dc.identifier.scopusauthoridWatt, CL=7005965559en_HK
dc.identifier.scopusauthoridLuk, WK=7005237832en_HK
dc.identifier.scopusauthoridLai, KY=36091351800en_HK
dc.identifier.scopusauthoridChow, FL=36024951200en_HK
dc.identifier.scopusauthoridMok, T=8706357200en_HK
dc.identifier.scopusauthoridBuckley, T=7101745369en_HK
dc.identifier.scopusauthoridChan, JFW=24278817900en_HK
dc.identifier.scopusauthoridWong, SSY=13310021400en_HK
dc.identifier.scopusauthoridZheng, B=7201780588en_HK
dc.identifier.scopusauthoridChen, H=26643315400en_HK
dc.identifier.scopusauthoridLau, CCY=8398162900en_HK
dc.identifier.scopusauthoridTse, H=7006070596en_HK
dc.identifier.scopusauthoridCheng, VCC=23670479400en_HK
dc.identifier.scopusauthoridChan, KH=7406034307en_HK
dc.identifier.scopusauthoridYuen, KY=36078079100en_HK
dc.identifier.citeulike6649981-
dc.identifier.issnl1058-4838-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats