Japanese scientists were the first to suggest that HHV-6B may be a frequent cause of temporal lobe epilepsy (Uesugi et al , 2000). They found three out of six mesial temporal lobe resections were positive for HHV-6.

Interest in the association of HHV-6B in mesial temporal lobe epilepsy grew with the publication of findings by investigators at the NINDS (Donati 2003) that HHV-6B was found at pathogenic levels a subset of patients with mesial temporal lobe epilepsy (MTLE), suggesting a possible role of HHV-6 in the development of MTLE. HHV-6 DNA was

found in half of the MTLE biopsies but none of the neocortical epilepsy patients. Virus was found specifically in the astrocytes of the hippocampus and temporal lobe.

Jacobson and colleagues expanded on this study in 2007 by examining the brain tissue from patients who had surgeries to remove sections of the brain as therapy when no drugs were effective. They found that 11 out of 16 patients were clearly infected with HHV-6B at what appeared to be pathogenic levels. None of the controls (brain tissue resections from other conditions) were positive for

HHV-6. Furthermore, they found that the virus is concentrated in the temporal lobe and the region next to the temporal lobe but not the frontal and occipital lobes.

Finally, Jacobson’s group provided a theoretical explanation for how the virus could trigger epilepsy by showing that the virus reduces glutamate transport, a phenomenon associated with MTLE.