In an article published in the Pediatric Infectious Disease Journal, Tetsushi Yoshikawa’s team from Fujita Health University School of Medicine determined that the severe neutropenia in primary HHV-6B infection is tied to reduced platelet counts, lower RANTES and higher levels of MCP-1, MIG and IP-10.
A large-scale multiplex PCR assay developed by a team in Japan was used to study 13 DNA viruses in 105 allogenic hematopoietic stem cell transplant patients. They found that patients treated with steroids had a significantly higher risk of HHV-6 reactivation (p=0.027), and that HHV-6 was the only virus tied to the onset of acute GVHD (p=0.016).
A pivotal study, led by Michael Boeckh at the Fred Hutchinson Cancer Research Center, has determined that occult infections contribute to 57% of all cases of “idiopathic” pneumonia syndrome (IPS), a condition previously assumed to be non-infectious. HHV-6 was the dominant pathogen representing 29% of cases.
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.
A genetic polymorphism of the chemokine CXCL12 was found to be associated with a lower incidence of acute GVHD. Furthermore patients with this polymorphism or receiving cells with the polymorphism were less prone to early HHV-6 reactivation.
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.
Since both HHV-6 and EBV have been associated with an increased risk of autoimmune disease development, a group at the American University of Beirut studied whether viral DNA might be capable of triggering IL-17, a cytokine associated with autoimmune disease. They injected BALB/c mice intraperitoneally with either EBV or HHV-6A DNA. They found that both IL-17 and IL-23 were markedly elevated.
A group at the University of Pennsylvania performed a retroactive study of 29 pediatric patients hospitalized with drug hypersensitivity reactions and found that those who reactivated with HHV-6 had longer lengths of stay (11.5 days vs. 5. days) and more severe illness. They were not able to determine the impact of steroid administration in HHV-6 positive patients.
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.
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.
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.
Pitt Niehusmann has completed the largest study to date on the question of whether viruses play a role in refractory mesial temporal lobe epilepsy (MTLE), with 346 samples analyzed. We asked Pitt a few questions about his work.
Bhupesh Prusty and Thomas Rudel of 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.
Two new reviews conclude that HHV-6 acute necrotizing encephalopathy is tied to a mutation of the RANBP2 gene.