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Infectious/Autoimmune Disorders

Role of HHV-6B Infection in Mesial Temporal Lobe Epilepsy

Authors:

John J Millichap ,

Northwestern University Feinberg School of Medicine, US
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J Gordon Millichap

Northwestern University Feinberg School of Medicine, US
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Abstract

Investigators from Fujita Health University, Toyoake, and National Epilepsy Center, Shizuoka, Japan, studied the pathogenic role of HHV-6B in patients with mesial temporal lobe epilepsy (MTLE). Of 75 intractable MTLE patients, 52 had mesial temporal sclerosis (MTS) and 23 were non-MTS patients.
How to Cite: Millichap, J.J. and Millichap, J.G., 2015. Role of HHV-6B Infection in Mesial Temporal Lobe Epilepsy. Pediatric Neurology Briefs, 29(5), p.40. DOI: http://doi.org/10.15844/pedneurbriefs-29-5-7
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  Published on 30 May 2015
 Accepted on 27 May 2015            Submitted on 20 May 2015

Investigators from Fujita Health University, Toyoake, and National Epilepsy Center, Shizuoka, Japan, studied the pathogenic role of HHV-6B in patients with mesial temporal lobe epilepsy (MTLE). Of 75 intractable MTLE patients, 52 had mesial temporal sclerosis (MTS) and 23 were non-MTS patients. Resected samples of hippocampus, amygdala, and mixed samples of amygdala and uncus were examined by real-time polymerase chain reaction (PCR) and reverse-transcriptase PCR to detect viral DNA and messenger RNA (mRNA), respectively. Detection of HHV-6 DNA was higher in MTS patients than non-MTS patients. Of 9 herpes viruses analyzed, HHV-6 was the most frequently detected. 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 and glial fibrillary acidic protein were significantly higher in the amygdala samples with HHV-6 DNA than those without viral DNA. The number of prolonged febrile seizures early in life was higher in the MTS patients than the non-MTS patients. HHV-6B may play an important role in the pathogenesis of MTS via modification of host gene expression. Latent infection rather than reactivation of HHV-6 probably contributes to the development of MTS. [1]

COMMENTARY. Prolonged febrile seizures or febrile status epilepticus (FSE) are associated with an increased risk of MTS and TLE, the subject of an ongoing, prospective multicenter study, the FEBSTAT study [2]. In 1964 and 1968, Falconer MA, Neurosurgeon at the Maudsley Hospital, London, UK, investigating the etiology of TLE, reported 13 (28%) of 47 cases with a history of infantile convulsions ascribed to fever [3, 4]. In comparison, 7 (15%) had a history of difficult birth. As early as 1956, Cavanagh and Meyer noted the high incidence of febrile convulsions preceding onset of TLE [5]. In the recent FEBSTAT study, HHV-6B viremia is reported in 54 of 169 subjects (32%) at the time of FSE [2].

A relationship between MTS and a history of febrile seizures and HHV-6B positivity is demonstrated in the current study [1]. Further, the viral load of HHV-6B correlates with markers that reflect inflammatory injury. Neuroinflammation is recognized as a key component of epilepsy pathogenesis [6]. If HHV-6-related febrile seizures are involved in the etiology of temporal sclerosis and TLE, antivirals that penetrate the blood-brain barrier administered at a young age for treatment of prolonged febrile seizures could prevent the development of MTLE [6].

Disclosures

The author(s) have declared that no competing interests exist.

References

  1. Kawamura, Y Nakayama, A Kato, T Miura, H Ishihara, N Ihira, M et al. (2015). Pathogenic Role of Human Herpesvirus 6B Infection in Mesial Temporal Lobe Epilepsy. J Infect Dis, Epub 2015 Apr 3.DOI: https://doi.org/10.1093/infdis/jiv160 [PubMed]  

  2. Epstein, LG Shinnar, S Hesdorffer, DC Nordli, DR Hamidullah, A Benn, EK et al. (2012). Human herpesvirus 6 and 7 in febrile status epilepticus: the FEBSTAT study. Epilepsia 53(9): 1481–8, DOI: https://doi.org/10.1111/j.1528-1167.2012.03542.x [PubMed]  

  3. Falconer, MA, Serafetinides, EA and Corsellis, JA (1964). Etiology and Pathogenesis of Temporal Lobe Epilepsy. Arch Neurol 10: 233–48, DOI: https://doi.org/10.1001/archneur.1964.00460150003001 [PubMed]  

  4. Falconer, MA and Taylor, DC (1968). Surgical treatment of drug-resistant epilepsy due to mesial temporal sclerosis. Etiology and significance. Arch Neurol 19(4): 353–61, DOI: https://doi.org/10.1001/archneur.1968.00480040019001 [PubMed]  

  5. Cavanagh, JB and Meyer, A (1956). Aetiological aspects of Ammon's horn sclerosis associated with temporal lobe epilepsy. Br Med J 2(5006): 1403–7, DOI: https://doi.org/10.1136/bmj.2.5006.1403 [PubMed]  

  6. Leibovitch, EC and Jacobson, S (2015). Human Herpesvirus 6 as a Viral Trigger in Mesial Temporal Lobe Epilepsy. J Infect Dis, Epub 2015 Apr 3.DOI: https://doi.org/10.1093/infdis/jiv162 [PubMed]  


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