(Circulation. 2000;101:231.)
© 2000 American Heart Association, Inc.
Brief Rapid Communications |
Enteroviral Capsid Protein VP1 Is Present in Myocardial Tissues From Some Patients With Myocarditis or Dilated Cardiomyopathy
From the Molecular Pathology Section, Division of Biomedical Sciences (Y.L., L.C.A., H.Z.) and Infectious Disease and Medical Microbiology (H.Z.), Imperial College of Science, Technology, and Medicine, London, UK; Laboratoire de Bactériologie-Virologie (Y.L., T.B., B.P.) and Laboratoire d’Anatomo-Pathologie (J.-F.M.), Faculté de Médecine Jacques Lisfranc, Saint-Etienne, and Laboratoire de Virologie, Faculté de Médecine, Lille (L.A.), France; and Key Laboratory of Viral Heart Disease, Ministry of Public Health, Zhongshan Hospital, Shanghai Medical University, PRC (Y.L., T.P., Y.Y.).
Correspondence to Dr Hongyi Zhang, Molecular Pathology, DBS, SAF Building, ICSTM, Exhibition Road, London SW7 2AZ, UK. E-mail h.zhang{at}ic.ac.uk
Background—There are still discrepancies in the association of enterovirus and myocardial disease, partially due to lack of data on the detection of virus antigens in tissues. It is desirable to localize enteroviral antigens so as to establish a link between the two and to study mechanisms of virus persistence.
Methods and Results—Nineteen fixed explanted or postmortem
myocardial samples were obtained from patients with myocarditis or
dilated cardiomyopathy (DCM). Control samples were
collected from 11 subjects who had died accidentally or of
noncardiovascular disease. Viral antigen was detected
by an improved immunohistochemical technique using an enterovirus
group–specific antibody to viral capsid protein VP1. Nine of 11
myocarditis cases (81.8%) and 6 of 8 DCM cases (75%) were positive.
Signals were localized in the cytoplasm of myocytes. Intense
immunostaining was observed in acute myocarditis,
whereas VP1 was detected in scattered myocytes in chronic myocarditis
or DCM. Enteroviral RNA was detected in 6 of 11 myocarditis samples
(54.5%) and 3 of 8 DCM samples (37.5%) by the reverse
transcription–nested polymerase chain reaction, correlating with
antigen detection (
=0.6±0.21). Neither viral antigen nor RNA was
detected in any controls.
Conclusions—Our findings demonstrate a direct link between enterovirus infection and some myocarditis or DCM cases. The pattern of VP1 detection may correlate with disease stage and severity. The data suggest that viral protein synthesis may be involved in persistent enterovirus infection in the pathogenesis of DCM.
Key Words: cardiomyopathy • myocarditis • viruses • antigens • immunohistochemistry
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