All cases found to be iciHHV-6 were assumed to be false positives.
Viral DNA and antigen found at higher levels in MTLE than in control brains.
Unique pathways and significantly elevated cytokines were associated with a small cohort of pediatric seizure patients.
NINDS investigators studied fresh resected brain tissue and found 29 of 54 positive for HHV-6 DNA. Previous studies using formalin fixed and paraffin embedded samples have yielded much lower rates of positivity.
HHV-6 most common virus found in nasopharyngeal aspirates from young children with febrile seizures, followed by influenza and adenovirus.
HHV-6/7 DNA was found in the plasma of 19.6% of epilepsy patients compared to none of the controls. Protein expression indicating active infection was found in 53% of the HHV-6/7 positive patients.
Swedish investigators set out to uncover the pathways that HHV-6B might utilize in triggering MTLE. They found that HHV-6B infection altered expression of MAPK genes, suggesting a possible pathogenic mechanisms of HHV-6B in mesial temporal lobe epilepsy.
A large prospective study in Africa adds weight to argument that HHV-6B infection is an important cause of febrile status epilepticus.
HHV-6B induces unique, region-specific DNA hypomethylation, and findings suggest that the epigenetic modification may facilitate HHV-6B integration.
Australian investigators studied 143 young children with febrile seizures for signs of viral infection and found that HHV-6 was the fifth most common virus after rhinovirus (22%), enterovirus (20%), adenovirus (21%) and influenza (13%). Overall, a virus was found in 71% of cases. Virus found in complex seizures was associated with HHV-6 (42%) or influenza (41%).
A fifth case of limbic encephalitis associated with GAD antibodies and HHV-6 infection has been reported, this time in an immunocompetent woman with chromosomally integrated HHV-6, epilepsy, and psychosis. The patient’s condition improved (with a drop in GAD antibody titers and stabilization of psychotic symptoms) in response to three weeks of antiviral therapy but relapsed when antiviral therapy was withdrawn.
Japanese investigators published findings suggesting that HHV-6B plays a pathogenic role in epilepsy by enhancing gene expression that induces neuroinflammation and sclerosis in the temporal lobe. HHV-6 DNA levels were significantly higher in the resected tissue of epilepsy patients with sclerosis compared to those without it.
Tetsushi Yoshikawa and Yoshiki Kawamura just published an important study linking HHV-6B in brain tissues to sclerosis in mesial temporal lobe epilepsy. We asked him about this future plans and whether he plans to treat these patients.
A team of Chinese investigators led by Dr. Jin-Mei Li at West China Hospital has identified a possible synergy between a polymorphism of Apolipoprotein E (ApoE) and HHV-6B infection, resulting in a higher viral load and seizure frequency in these patients.
Investigators at the University of Bonn Medical Center in Germany have screened 346 fresh-frozen brain tissue resections from temporal lobe epilepsy (TLE) patients for all nine herpesviruses as well as for RNA viruses including Paramyxovirinae, Phleboviruses, Enteroviruses, and Flavivirus, using qPCR. HHV-6B was the only virus identified.
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