HHV-6 & Epilepsy
HHV-6 & Epilepsy
Neurologists from the West China Hospital examined Mesial Temporal Lobe Epilepsy surgical resections using nested PCR and immunohistochemistry and found HHV-6B in the brain tissue of 28% of 32 resected brain tissues compared to only 8% of controls. The Chinese group also found that an inflammatory marker, NF-kB, was upregulated in the glial cells of patients positive for HHV-6B. The virus was found in the subset of patients with a history of febrile seizures (Li 2011).
This confirmed an earlier report from 2007 by investigators at the NINDS who reported finding HHV-6B replication in the hippocampal astrocytes in two thirds of 24 patients with mesial temporal sclerosis, but not in patients with other causes of epilepsy. They speculated that HHV-6B might cause seizures by interfering with the astrocyte’s ability to transport glutamate (Fotheringham 2007).
A German group found HHV-6 DNA in 56% of MTLE patients with a history of encephalitis, but not in the patients with a history of complex febrile seizures. However, this group used formalin-fixed, paraffin embedded tissues for their nested PCR study, considered by many to be a less sensitive method for the detection of HHV-6. Recent studies have shown that fresh or flash frozen tissues are far more sensitive because beta herpesvirus DNA is degraded when FFPE tissues are used, and that the DNA also degrades significantly with the passage of time.
HHV-6 & Status Epilepticus
An NIH supported multi-site study of the role of primary HHV-6 & 7 infection in children with febrile status epilepticus (FSE) found 33% of 63 infants showed evidence of HHV-6 infection while 7.9% of 63 had HHV-7 infection. (Epstein, Abstract from 2011 International Conference on HHV-6 & 7)
Download a copy of The HHV-6 Foundation’s 2012 AAN Meeting Packet on “HHV-6 in Epilepsy & Seizures,” which has a collection of select abstracts and publications on HHV-6 in Epilepsy & Seizures.
Key Papers: HHV-6 & Epilepsy