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Pediatrics. 2014 Jun;133(6):e1541-7. doi: 10.1542/peds.2013-3344. Epub 2014 May 12.

Delayed primary HHV-7 infection and neurologic disease.

Author information

1
Division of Infectious Diseases, Department of Paediatrics, kevin.schwartz@sickkids.ca.
2
Division of Microbiology, Department of Paediatric Laboratory Medicine, and.
3
Virus Reference Department, Health Protection Agency Microbiology Service Division, London, United Kingdom;Department of Infection, Division of Infection and Immunity, University College London, London, United Kingdom; and.
4
Department of Infection, Division of Infection and Immunity, University College London, London, United Kingdom; and.
5
Divisions of Neurology, Department of Paediatrics.
6
Department of Pediatrics Children's Hospital of Philadelphia, University of Pennsylvania, Philadelphia, PennsylvaniaResearch Institute, The Hospital for Sick Children, University of Toronto, Toronto, Canada;
7
Division of Paediatric Medicine, Department of Paediatrics.
8
Division of Infectious Diseases, Department of Paediatrics.

Abstract

BACKGROUND:

Primary human herpesvirus 7 (HHV-7) infection occurs almost universally during the first 5 years of life and is rarely accompanied by central nervous system (CNS) symptoms such as febrile seizures. The present retrospective study investigated the role of primary HHV-7 infection in CNS disease in children, including adolescents.

METHODS:

The study included all children who had neurologic disease aged younger than 18 years seen at the Hospital for Sick Children, Toronto, Canada, between April 1, 1998 and December 31, 2011, whose cerebrospinal fluid (CSF) was found by polymerase chain reaction to contain HHV-7 DNA. Where sera were available, HHV-7 IgG antibody titers and avidity were measured to differentiate primary from past infection.

RESULTS:

HHV-7 DNA was detected in the CSF of 57 (1.9%) of the 2972 children tested. In 3 adolescents primary HHV-7 infection (low avidity IgG) was confirmed as the cause of neurologic disease, 2 who had encephalitis and 1 who had Guillain-Barré syndrome. Eighteen children had possible HHV-7 disease (no alternative cause identified and indeterminate antibody result or serum not available), 7 encephalitis, 8 meningitis, and 3 demyelinating disorders. HHV-7 disease was excluded in 36 children on the basis of past infection (high IgG avidity) and/or an alternative cause.

CONCLUSIONS:

Primary HHV-7 infection delayed into adolescence can cause serious neurologic disease. HHV-7 DNA in CSF alone is insufficient to prove an etiologic association. Combining CSF polymerase chain reaction with serology is essential to prove primary infection when investigating HHV-7 CNS disease.

KEYWORDS:

CNS; Guillain-Barré syndrome; HHV-7; child; encephalitis; meningitis

PMID:
24819578
DOI:
10.1542/peds.2013-3344
[Indexed for MEDLINE]

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