1226Pathogenic role of human herpesvirus 6B in mesial temporal sclerosis

Background. Human herpesvirus 6B (HHV-6B) is the causative agent for exanthema subitum. This virus has been suggested to have neurovirulence based on the in-vivo and in-vitro studies. HHV-6B has been suggested to be associated with mesial temporal sclerosis (MTS) that results in mesial temporal lobe epilepsy. Aims of this study was to elucidate pathogenic role of HHV-6B in patients with MTS. Methods. Hippocampus, amygdala, and mixed samples of amygdala and uncus which were resected by surgery, were tested by real-time polymerase chain reaction (PCR) and reverse-transcriptase PCR (RT-PCR) for detection of nine human herpesviruses’ DNAs and measurement HHV-6B gene expression. Host gene expressions such as cytokines, chemokines, and neural markers were also measured by TaqMan Gene Expression Assay. Results. Seventy-five intractable temporal lobe epilepsy patients including 52 MTS patients and 23 non-MTS patients were enrolled in this study. HHV-6 DNA loads were significantly higher in MTS patients than non-MTS patients (median / interquartile range; 19.1 / 0 89.2 vs 0.0 / 0.0 – 0.0, P = 0.004). Seventeen of the 32 HHV-6 DNA positive samples were confirmed as HHV-6B based on the restriction fragment length polymorphisms analysis. Seven other human herpesviruses were rarely detected in these patients. No HHV-6B mRNA was detected in the 32 HHV-6 DNA positive brain tissues. In MTS patients, expressions of monocyte chemotactic protein-1 (P = 0.029) and glial fibrillary acidic protein (P = 0.043) in amygdala were significantly higher in the samples containing HHV-6 DNA (n = 7) than those lacking HHV-6 DNA (n = 18). No such difference was observed in the hippocampus. Conclusion. In contrast to other human herpesviruses, HHV-6 in particular HHV-6B can latently infect in limbic area. This study suggests that latently infected HHV-6B may play an important role in pathogenesis of MTS through modifying the host gene expressions. Disclosures. All authors: No reported disclosures.