Pathogenic Role of Human Herpesvirus 6B Infection in Mesial Temporal Lobe Epilepsy
- PMID: 25840441
- DOI: 10.1093/infdis/jiv160
Pathogenic Role of Human Herpesvirus 6B Infection in Mesial Temporal Lobe Epilepsy
Abstract
Background: Human herpesvirus 6B (HHV-6B) is the causative agent for exanthem subitum. HHV-6B was associated with mesial temporal sclerosis (MTS), leading to mesial temporal lobe epilepsy (MTLE). In this study, we sought to elucidate the pathogenic role of HHV-6B in patients with MTLE.
Methods: Seventy-five intractable MTLE patients, including 52 MTS patients and 23 non-MTS patients, were enrolled in this study. Resected hippocampus, amygdala, and mixed samples of amygdala and uncus samples were examined by real-time polymerase chain reaction (PCR) and reverse-transcriptase PCR to detect viral DNA and messenger RNA (mRNA), respectively. Host gene expressions, including neural markers, were measured using the TaqMan Gene Expression Assay.
Results: Detection of HHV-6 DNA was higher in MTS patients than non-MTS patients (median/interquartile range: 19.1/0-89.2 vs 0.0/0.0-0.0 copies/µg DNA; P = .004). HHV-6B viral DNA was determined in 12/27 HHV-6 DNA-positive samples, and no HHV-6B mRNA were detected in all samples. In MTS patients, expression of monocyte chemotactic protein-1 (P = .029) and glial fibrillary acidic protein (P = .043) were significantly higher in the amygdala samples with HHV-6 DNA than those without viral DNA.
Conclusions: This study suggests that HHV-6B may play an important role in the pathogenesis of MTS via modification of host gene expression.
Keywords: human herpesvirus 6; lobe; mesial temporal sclerosis.
© The Author 2015. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.
Comment in
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Human Herpesvirus 6 as a Viral Trigger in Mesial Temporal Lobe Epilepsy.J Infect Dis. 2015 Oct 1;212(7):1011-3. doi: 10.1093/infdis/jiv162. Epub 2015 Apr 3. J Infect Dis. 2015. PMID: 25840442 No abstract available.
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