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Article: T-cell immunity to subclinical cytomegalovirus infection reduces cardiac allograft disease

TitleT-cell immunity to subclinical cytomegalovirus infection reduces cardiac allograft disease
Authors
KeywordsAtherosclerosis
Immune system
Lymphocytes
Rejection
Transplantation
Viruses
Issue Date2006
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://circ.ahajournals.org
Citation
Circulation, 2006, v. 114 n. 15, p. 1608-1615 How to Cite?
AbstractBACKGROUND - Asymptomatic cytomegalovirus (CMV) replication is frequent after cardiac transplantation in recipients with pretransplantation CMV infection. How subclinical viral replication influences cardiac allograft disease remains poorly understood, as does the importance of T-cell immunity in controlling such replication. METHODS AND RESULTS - Thirty-nine cardiac recipients who were pretransplantation CMV antibody positive were longitudinally studied for circulating CMV-specific CD4 and CD8 T-cell responses, CMV viral load in blood neutrophils, and allograft rejection during the first posttransplantation year. Nineteen of these recipients were also analyzed for changes of coronary artery intimal, lumen, and whole-vessel area. All recipients received early prophylactic therapy with ganciclovir. No recipients developed overt CMV disease. Those with detectable levels of CMV-specific CD4 T cells in the first month after transplantation were significantly protected from high mean and peak posttransplantation viral load (P<0.05), acute rejection (P<0.005), and loss of allograft coronary artery lumen (P<0.05) and of whole-vessel area (P<0.05) compared with those who lacked this immune response. The losses of lumen and vessel area were both significantly correlated with the time after transplantation at which a CD4 T-cell response was first detected (P<0.05) and with the cumulative graft rejection score (P<0.05). CONCLUSIONS - The early control of subclinical CMV replication after transplantation by T-cell immunity may limit cardiac allograft rejection and vascular disease. Interventions to increase T-cell immunity might be clinically useful in limiting these adverse viral effects. © 2006 American Heart Association, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/125251
ISSN
2015 Impact Factor: 17.047
2015 SCImago Journal Rankings: 7.853
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTu, Wen_HK
dc.contributor.authorPotena, Len_HK
dc.contributor.authorStepickBiek, Pen_HK
dc.contributor.authorLiu, Len_HK
dc.contributor.authorDionis, KYen_HK
dc.contributor.authorLuikart, Hen_HK
dc.contributor.authorFearon, WFen_HK
dc.contributor.authorHolmes, THen_HK
dc.contributor.authorChin, Cen_HK
dc.contributor.authorCooke, JPen_HK
dc.contributor.authorValantine, HAen_HK
dc.contributor.authorMocarski, ESen_HK
dc.contributor.authorLewis, DBen_HK
dc.date.accessioned2010-10-31T11:20:01Z-
dc.date.available2010-10-31T11:20:01Z-
dc.date.issued2006en_HK
dc.identifier.citationCirculation, 2006, v. 114 n. 15, p. 1608-1615en_HK
dc.identifier.issn0009-7322en_HK
dc.identifier.urihttp://hdl.handle.net/10722/125251-
dc.description.abstractBACKGROUND - Asymptomatic cytomegalovirus (CMV) replication is frequent after cardiac transplantation in recipients with pretransplantation CMV infection. How subclinical viral replication influences cardiac allograft disease remains poorly understood, as does the importance of T-cell immunity in controlling such replication. METHODS AND RESULTS - Thirty-nine cardiac recipients who were pretransplantation CMV antibody positive were longitudinally studied for circulating CMV-specific CD4 and CD8 T-cell responses, CMV viral load in blood neutrophils, and allograft rejection during the first posttransplantation year. Nineteen of these recipients were also analyzed for changes of coronary artery intimal, lumen, and whole-vessel area. All recipients received early prophylactic therapy with ganciclovir. No recipients developed overt CMV disease. Those with detectable levels of CMV-specific CD4 T cells in the first month after transplantation were significantly protected from high mean and peak posttransplantation viral load (P<0.05), acute rejection (P<0.005), and loss of allograft coronary artery lumen (P<0.05) and of whole-vessel area (P<0.05) compared with those who lacked this immune response. The losses of lumen and vessel area were both significantly correlated with the time after transplantation at which a CD4 T-cell response was first detected (P<0.05) and with the cumulative graft rejection score (P<0.05). CONCLUSIONS - The early control of subclinical CMV replication after transplantation by T-cell immunity may limit cardiac allograft rejection and vascular disease. Interventions to increase T-cell immunity might be clinically useful in limiting these adverse viral effects. © 2006 American Heart Association, Inc.en_HK
dc.languageengen_HK
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://circ.ahajournals.orgen_HK
dc.relation.ispartofCirculationen_HK
dc.rightsThis is a non-final version of an article published in final form in (provide complete journal citation)-
dc.subjectAtherosclerosisen_HK
dc.subjectImmune systemen_HK
dc.subjectLymphocytesen_HK
dc.subjectRejectionen_HK
dc.subjectTransplantationen_HK
dc.subjectVirusesen_HK
dc.subject.meshCD4-Positive T-Lymphocytes - immunology - pathology-
dc.subject.meshCD8-Positive T-Lymphocytes - immunology - pathology-
dc.subject.meshCoronary Artery Disease - etiology - immunology - pathology - prevention and control-
dc.subject.meshCytomegalovirus Infections - drug therapy - immunology - pathology-
dc.subject.meshHeart Transplantation - adverse effects - immunology - pathology-
dc.titleT-cell immunity to subclinical cytomegalovirus infection reduces cardiac allograft diseaseen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0009-7322&volume=114&issue=15&spage=1608&epage=1615&date=2006&atitle=T-cell+immunity+to+subclinical+cytomegalovirus+infection+reduces+cardiac+allograft+diseaseen_HK
dc.identifier.emailTu, W:wwtu@hkucc.hku.hken_HK
dc.identifier.authorityTu, W=rp00416en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1161/CIRCULATIONAHA.105.607549en_HK
dc.identifier.pmid17015794-
dc.identifier.scopuseid_2-s2.0-33749601263en_HK
dc.identifier.hkuros179389en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33749601263&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume114en_HK
dc.identifier.issue15en_HK
dc.identifier.spage1608en_HK
dc.identifier.epage1615en_HK
dc.identifier.isiWOS:000241077600011-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTu, W=7006479236en_HK
dc.identifier.scopusauthoridPotena, L=6602877926en_HK
dc.identifier.scopusauthoridStepickBiek, P=6505903698en_HK
dc.identifier.scopusauthoridLiu, L=14832848200en_HK
dc.identifier.scopusauthoridDionis, KY=14123041200en_HK
dc.identifier.scopusauthoridLuikart, H=6602985010en_HK
dc.identifier.scopusauthoridFearon, WF=7003425177en_HK
dc.identifier.scopusauthoridHolmes, TH=35857851000en_HK
dc.identifier.scopusauthoridChin, C=7202170768en_HK
dc.identifier.scopusauthoridCooke, JP=7202378672en_HK
dc.identifier.scopusauthoridValantine, HA=35430802300en_HK
dc.identifier.scopusauthoridMocarski, ES=7006866600en_HK
dc.identifier.scopusauthoridLewis, DB=7404750928en_HK

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