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High HHV-6B viral loads found in a subset of epilepsy brain resections

Investigators at the University of Bonn Medical Center in Germany have screened 346 fresh-frozen brain tissue resections from temporal lobe epilepsy 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. HHV-6B was also the only virus found in autopsy controls, but the viral load was significantly lower in controls relative to epilepsy patients (p>0.001). Furthermore, the group found that epilepsy patients with a history of seizures or encephalitis had a higher prevalence of HHV-6B DNA found in the brain tissue compared to controls. READ MORE

ApoE4+ epilepsy patients have higher HHV-6B viral loads and more seizures

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 and HHV-6B infection, resulting in a higher viral load and seizure frequency in these patients. HHV-6B DNA was found in 39% of 46 MTLE resections. However the prevalence increased to 57% in those also positive for ApoE4, compared to just 10% of controls. Significantly, viral loads of the HHV-6B+ patients were much higher in those with ApoE4. MTLE patients positive for  ApoE4 with HHV-6B DNA in their resected hippocampus tissue and 126 copies/million cells, compared to 11 copies/million cells in control HHV-6B+ trauma patients. READ MORE

Heart failure worsens in patients with persistent HHV-6B+ biopsies

Numerous case reports and studies have now tied HHV-6 to myocarditis and cardiomyopathies. To further investigate this relationship, investigators from one of the top cardiology clinics in Europe performed a study to determine the outcome of patients discovered to have HHV-6 in their cardiac tissue during the initial biopsy screen. In the patients who had a resolution of HHV-6B infection, there was a significant improvement in ejection fraction. However, in those with persistent or new onset HHV-6 infection, left ventricular function progressively worsened, suggesting that HHV-6 infection can contribute to heart failure. Unfortunately, most of the pathogens involved in cardiac disease cannot be found in the plasma and can only be detected reliably when identified within the heart tissue specimens. READ MORE

Diagnosing infections in myocardial biopsies: An interview with Uwe Kühl and Dirk Lassner

Cardiologist Uwe Kühl has published a number of important papers on the subject of viral persistence in progressive cardiac dysfunction, including a recent paper that demonstrated heart failure patients with active ciHHV6 improved on antiviral therapy. Dr. Dirk Lassner is laboratory director of IKDT, the lab that performs their virology testing. READ MORE

GP96: a breakthrough in understanding HHV-6 cell tropism

Bhupesh Prusty and Thomas Rudel of the University of Wuerzburg, Germany, in collaboration with Dr. Yasuko Mori of Japan, have shed new light on the long-standing mystery of HHV-6 cell tropsim. CD46 and CD134 serve as essential cell surface receptors for HHV-6A and HHV-6B, respectively. However, it has been postulated that additional unknown factors might be required for HHV-6 entry and survival inside the host cell. To better understand this phenomenon, Prusty and Rudel followed an unbiased proteomics screen and identified human chaperone protein GP96 as a key protein that directly interacts with HHV-6 on the host cell surface and guides it for cellular degradation. READ MORE

Cleveland clinic group finds important miRNA for HHV-6A

Investigators led by Eain Murphy of Cleveland Clinic have identified a viral microRNA (miRNA) for HHV-6A, named miR-U86, that targets the HHV-6A intermediate early gene U86. They also found that the target of this viral encoded miRNA is a critical transcriptional activator of HHV-6A, suggesting that it is involved in auto-regulation. READ MORE

RANBP2 mutation tied to HHV-6 acute necrotizing encephalopathy

Two new reviews conclude that HHV-6 acute necrotizing encephalopathy (ANE) is tied to a mutation of the RANBP2 gene. RANBP2 is a gene that codes for protein with an essential role in energy metabolism in neuronal cells, and a defect in this gene results in an energy breakdown when the cell is challenged by viral infections (such as with HHV-6, influenza, parainfluenza, varicella) as well as intracellular bacterial infections such as mycoplasma pneumonia. READ MORE