Pathogenic Role of Human Herpesvirus 6B Infection in Mesial Temporal Lobe Epilepsy

• Published in: The Journal of infectious diseases Vol. 212; no. 7; pp. 1014 - 1021
• Main Authors: Kawamura, Yoshiki, Nakayama, Ai, Kato, Taichi, Miura, Hiroki, Ishihara, Naoko, Ihira, Masaru, Takahashi, Yukitoshi, Matsuda, Kazumi, Yoshikawa, Tetsushi
• Format: Journal Article
• Language: English
• Published: United States Oxford University Press 01-10-2015
• Subjects: Adolescent; Adult; Amygdala - virology; Chemokine CCL2; Child; Child, Preschool; DNA, Viral - genetics; Epilepsy, Temporal Lobe - pathology; Epilepsy, Temporal Lobe - virology; Female; Gene Expression Regulation, Viral; Herpesvirus 6, Human - genetics; Herpesvirus 6, Human - pathogenicity; Hippocampus - virology; Human herpesvirus 6; Human herpesvirus 6B; Humans; Infant; Male; Middle Aged; Real-Time Polymerase Chain Reaction; RNA, Messenger - genetics; RNA, Viral - genetics; Roseolovirus Infections - pathology; Roseolovirus Infections - virology; Virus Activation; VIRUSES; Young Adult; human herpesvirus 6; lobe; mesial temporal sclerosis
• ISSN: 0022-1899; 1537-6613
• DOI: 10.1093/infdis/jiv160

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.