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HHV-6 DR7 found to promote glioma development and progression

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.

$4 million in prizes for literature reviews that explain Alzheiemer’s

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 …

Research Priorities

Note: we welcome your input. Please send comments to: 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 …

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New findings on how HHV-6A/B U94 blocks angiogenesis

The HHV-6 latency gene U94 has been found to block angiogenesis, but the mechanisms behind this phenomenon have been unclear. A team lead by Roberta Rizzo and Elisabetta Caselli in Italy shed light on this process, opening the door to new potential molecular targets to pursue in treating diseases marked by improper vascularization.

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HHV-6A & B dysregulate autophagy differently in HSB-2 cells

A group led by Mara Cirone in Italy found that HHV-6B blocks autophagy in HSB-2 cells. Both HSV-1 and CMV have proteins that block autophagy, and HHV-6B carries genes that are homologues of those encoding for CMV’s anti-autophagy protein. Her next step is to study the impact of both HHV-6A and HHV-6B on autophagy in neuronal cells.


The NEJM rarely covers HHV-6, but did an excellent case history of this patient with HHV-6 reactivation in conjunction with DRESS. The patient was not treated with an antiviral in spite of a plasma HHV-6 DNA load of 112,836, extensive lymphadenopathy, rash and abnormal liver function tests. What did NEJM get wrong? They stated ciHHV6 could be ruled out because a) the viral load was only log 5 on a plasma DNA test and b) the viral load dropped to less than 500 copies/ml. The plasma viral load in a ciHHV-6 patient can fall below 500 copies/ml if the blood is centrifuged within a few hours. On the other hand, ciHHV-6 samples shipped overnight and centrifuged the next day, are …