Article Text

PDF
Fatal circumstances of human herpesvirus 6 infection: transcriptosome data analysis suggests caution in implicating HHV-6 in the cause of death
  1. Consolato Sergi1,
  2. Edith Daum2,
  3. Ingo Pedal3,
  4. Bärbel Hauröder4,
  5. Paul Schnitzler5
  1. 1Institute of Pathology, Medical University of Innsbruck, Austria
  2. 2Department of Virology, University Hospital, Heidelberg, Germany
  3. 3Institute of Forensic Medicine, University Hospital, Heidelberg, Germany
  4. 4Central Medical Institute of Federal Armed Forces, Koblenz, Germany
  5. 5Department of Virology, University Hospital, Heidelberg, Germany
  1. Professor Consolato Sergi, Medical University Innsbruck, Muellerstrasse 44, AT-6020 Innsbruck, Austria; consolato.sergi{at}i-med.ac.at

Statistics from Altmetric.com

Human herpesvirus 6 (HHV-6), a T-lymphotropic enveloped double stranded DNA virus of the Herpesviridae family, can be divided into two major variants, designated A and B. The B variant is associated with exanthema subitum (roseola infantum, 6th disease), characterised by fever and lymphadenopathy, followed or not by a maculo-papular rash primarily on the neck and trunk. HHV-6, however, is also an important opportunistic agent in patients with impaired immune systems. In recent years, increased antibody titres and positive amplification of the viral genome by PCR have been shown in chronic fatigue syndrome, lymphoproliferative diseases, autoimmune thyroiditis, Sjögren syndrome, rheumatoid arthritis, Crohn’s disease, and sarcoidosis.1 Complications of primary infection in infancy and childhood and simultaneous occurrence of sudden death or short-term mortality include pneumonitis, hepatosplenomegaly, fulminant hepatitis, aseptic meningitis, intussusception, thrombocytopenic purpura, fatal haemophagocytic syndrome, and disseminated infection.24

However, the aetiological contribution of the virus in fatal cases is still debated and the presence of HHV-6 in a latent status supports the possibility that viral DNA may be amplified in tissue without clinical signs for any of the related diseases. In order to examine the relationship of causality between HHV-6 infection and mortality in infants and children, we investigated HHV-6 infection in four children, who died suddenly or shortly after hospital admission.

Index cases

Case 1 is a female baby (body weight 2580 g, body length 47 cm) born by vaginal delivery following 37 weeks’ gestation (Apgar 7/8/9). There was a history of twin pregnancy, with death of the co-twin in the 16th week of gestation and tocolysis from the 24th week of gestation. Following rupture of the membranes, the amniotic liquid was green. Leucocytosis (40 200/µl), thrombocytopenia (14 000/µl), and C-reactive protein of 1.1 mg/dl were found. Antibiotic therapy (penicillin and claforan) was started. She fed orally and became stabile. …

View Full Text

Request permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.