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Chromosomal integration of the HHV-6 genome as a possible cause of HHV-6 detection in cardiac tissues
  1. Volker Strenger1,
  2. Stephan W Aberle2,
  3. Gerald Wendelin1,
  4. Klaus Pfurtscheller1,
  5. Elisabeth P Nacheva3,
  6. Gerfried Zobel1,
  7. Bert Nagel1
  1. 1Department of Pediatrics and Adolescent Medicine, Medical University of Graz, Graz, Austria
  2. 2Clinical Institute of Virology, Medical University of Vienna, Vienna, Austria
  3. 3Department of Haematology, Royal Free & University College Medical School, London, UK
  1. Correspondence to Dr Volker Strenger, Department of Paediatrics and Adolescent Medicine, Medical University of Graz, Auenbruggerplatz 30, A-8036 Graz, Austria; volker.strenger{at}

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With interest we read the article published by Comar et al. The authors analysed 35 explanted hearts from children with idiopathic dilated cardiomyopathy (DCM, n=16) or congenital heart disease (CHD, n=11) for the presence of human herpes virus 6 (HHV-6) DNA. They found the HHV-6 B genome in 43.7% and 21% of patients with DCM and CHD, respectively. DNA load ranged from 1.56×102 to 8.6×102 copies/μg DNA (mean 3.06×102 copies/μg).

The authors conclude that there might be associations between the myocardial disease and a latent HHV-6 infection.1 However, if HHV-6 DNA is detected in tissue specimens, chromosomal integration of the HHV-6 genome (chromosomally-integrated HHV-6 (CIHHV-6)) should be considered, and further analyses should be undertaken.2,3 We report a case where detection of HHV-6 DNA initially (mis-)led to the diagnosis of HHV-6 associated myocarditis.

A 4-year-old girl was admitted with fever and reduced general condition. Echocardiography revealed an enlarged left atrium and left ventricle, severely reduced contractility and moderate mitral valve regurgitation consistent with DCM. Haemodynamics deteriorated with recurrent arrhythmias, hypotension …

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  • Competing interests None.

  • Provenance and peer review Not commissioned; externally peer reviewed.