Review summarizes experience from Japan and U.S.
Febrile status epilepticus in infants with MRI-confirmed brain abnormalities linked to temporal lobe epilepsy later in life
Surprisingly, although HHV-6B has been linked to febrile seizures, febrile status epilepticus and temporal lobe epilepsy, the report contains no mention of the virus.
BioFire assay identifies HHV-6 as the most frequent cause of meningoencephalitis in infants 4-11 months
All cases found to be iciHHV-6 were assumed to be false positives.
Another report links HHV-6B nucleic acid and antigen to mesial temporal lobe epilepsy
Viral DNA and antigen found at higher levels in MTLE than in control brains.
Abnormal cytokine levels in children with epilepsy suggest link to inflammation
Unique pathways and significantly elevated cytokines were associated with a small cohort of pediatric seizure patients.
Study of fresh brain tissue confirms a role for HHV-6 in mesial temporal sclerosis
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.
A clinically significant viral load of HHV6 DNA was found in children with febrile seizures
HHV-6 most common virus found in nasopharyngeal aspirates from young children with febrile seizures, followed by influenza and adenovirus.
Active HHV-6/7 infection found in subset of adult epilepsy patients
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.
MAPK upregulation by HHV-6B proposed as the mechanism behind link to epilepsy.
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.
Infants with HHV-6B seizures are 15X more likely to develop febrile status epilepticus
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 telomeric hypomethylation, possibly facilitating integration
HHV-6B induces unique, region-specific DNA hypomethylation, and findings suggest that the epigenetic modification may facilitate HHV-6B integration.
HHV-6 identified in 12% of simple and 42% of complex pediatric febrile seizures
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%).
GAD antibodies & HHV-6 limbic encephalitis – a case of molecular mimicry?
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.
Pathogenic role for HHV-6B in in mesial temporal lobe epilepsy
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.
Interview with Tetsushi Yoshikawa: Treating HHV-6B seizures
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.
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