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.
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.
Authors: Oscar H Del Brutto; Naoum P Issa; Perla Salgado; Victor J Del Brutto; Mauricio Zambrano; Julio Lama; Héctor H García Journal: Am J Trop Med Hyg Date: 2016-11-14 Impact factor: 2.345
Authors: Luca Bartolini; Eleonora Piras; Kathryn Sullivan; Sean Gillen; Adrian Bumbut; Cheng-Te Major Lin; Emily C Leibovitch; Jennifer S Graves; Emmanuelle L Waubant; James M Chamberlain; William D Gaillard; Steven Jacobson Journal: Front Neurol Date: 2018-10-05 Impact factor: 4.003
Authors: William H Theodore; Emily Leibovitch; Bridgette J Billioux; Sara K Inati; Kareem Zaghloul; John Heiss; William D Gaillard; Steven Jacobson Journal: Epilepsia Open Date: 2021-08-08