Israeli scientists have identified hundreds of new open reading frames, generating an unbiased atlas of the HHV-6 proteome. They also identified three highly abundant long non-coding RNAs.
Researchers from GlaxoSmithKline found a significant overlap in differentially expressed genes shared by those with herpesvirus infections, Alzheimer’s and Parkinson’s. On the other hand, there was no significant overlap between herpesviruses and Type 2 diabetes or Huntington’s disease.
Yasuko Mori, PhD, Professor of Clinical Virology at the Kobe University Graduate School of Medicine was awarded the HHV-6 Foundation’s Dharam Ablashi Lifetime Achievement Award at the 11th International Conference on HHV-6 & 7.
The U94 “latency” gene of HHV-6, interferes with breast cancer proliferation and potentiates chemotherapy.
A Chinese medicine that has been used for thousands of years, berberine inhibits replication of CMV at micromolar levels in vitro. It was also effective against drug resistant strains of CMV, as well against murine cytomegalovirus.
Alex Greninger, PhD, was awarded the Junior Investigator award for Basic Science at the 11th international HHV-6 & 7 Conference in Quebec City, Canada.
Xiafeng Zhou was awarded the Young Investigator Award for Clinical Research at the 11th International HHV-6 & 7 Conference in Quebec City, Canada.
A prospective study of allogenic stem cell transplant patients in Japan suggests that the percentage of CD134+ T cells could be used to predict which patients are vulnerable to HHV-6 reactivation. The authors propose that further investigation into the effect of elevated CD134+ T cells pre-transplant is warranted.
Rational vaccine design requires understanding details of protective immunity against each virus. Yasuko Mori and associates from Japan have now identified CD4+ and H-2Kd restricted CD8+ T-cell epitopes essential for HHV-6B viral entry, opening new possibilities for vaccines and immunotherapy.
Yasuko Mori and colleagues were successful in humanizing two neutralizing monoclonal antibodies to HHV-6B. The chimeric antibodies performed well enough to show promise for therapeutic use.
A Chinese group found HHV-6 direct repeat 7 in 48% of glioma tumors. Furthermore, they determined that DR7 overexpression could promote glioma cell migration, invasion and angiogenesis. Expression profiles showed that DR7 created an inflammatory microenvironment that enhanced degradation of the extracellular matrix.
A number of astronauts have complained about herpesvirus reactivations during flight, and several developed shingles. Investigators at NASA determined that space flight increases herpesvirus shedding in saliva, compared to levels before and after their missions.
The Oskar Fischer prize is named after a neuropathologist who was the first to describe neuritic plaques in 1907 in Prague. James Truchard, the former CEO and Chairman of National Instruments has donated funds for a prize to scientists who can review the existing medical literature to come up with a theory on what causes Alzheimer’s. Truchard points out that there have been 130,000 scientific papers on Alzheimer’s but that each paper focuses only on a narrow aspect of the disease and brain science. He wants someone to comb through all of the literature and find a unifying “big picture” explanation. “Just like someone like Einstein did in creating the theory of general relativity or Darwin did in looking at …
Note: we welcome your input. Please send comments to: Kristin_Loomis@HHV-6Foundation.org PROPOSED NEW PRIORITIES FOR ALZHEIMER’S RESEARCH Exploration of HHV-6A and HHV-7 in the development and progression of Alzheimer’s Disease Background: Two recent papers published in Neuron have strongly implicated herpesviruses in the pathogenesis of Alzheimer’s disease. Moir and Tanzi showed that amyloid plaques develop rapidly in response to infection by HHV-6A, HHV-6B and HSV1 (Eimer 2018). In addition, a comprehensive NIH funded “multiomic” evaluation of the Alzheimer’s brain tissue using next generation sequencing data strongly implicated two roseoloviruses: HHV-6A and HHV-7 (Readhead 2018). Among the findings: Contrary to popular belief, HHV-6A is not ubiquitous. Only HHV-6B, which is spread via the saliva, is ubiquitous. HHV-6A is not found in the …
Both infectious and UV-inactivated HHV-6A activate endogenous retrovirus envelope protein – but so does selective stimulation of HHV-6A’s CD46 receptor. This “cross-talk” between HHV-6A and endogenous retrovirus appears to play an important role in the pathogenesis of inflammatory diseases.