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HHV-6B reactivates first, proceeds to end organ disease faster in transplant patients

In All, Transplant Complications by Kristin Loomis

Investigators at Fred Hutch Cancer Research Center found that HHV-6B is the first DNA virus to reactivate at a median of 3 weeks, compared to CMV, EBV and Adenovirus at 5-6 weeks. HHV-6B also peaked rapidly, unlike other DNA viruses that took 3-6 weeks to reach peak viral load. HHV-6B reactivation resulted in increased mortality after 100 days.

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Ancient iciHHV-6 genomes vary considerably from community strains, but still capable of reactivation

In All, ciHHV-6 by Kristin Loomis

British researchers used molecular dating methods to determine that most strains of iciHHV-6 come from a small number of ancient human ancestors; the youngest found lived over 24,000 years ago. These ancient strains vary considerably from modern non-inherited strains of HHV-6A and appear just as likely to activate as their more modern cousins.

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New HHV-6 NIH grants awarded in 2017

In All by Kristin Loomis

Two new NIH grants awarded for studies related to HHV-6A and CNS disease. A Stanford group was also funded to develop whole genome sequencing platform to study HHV-6 and four other viruses post-transplant.

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Multiple herpesvirus infections lead to telomere shortening

In All, ciHHV-6 by Kristin Loomis

Investigators at Kings College London report that seropositivity for CMV, Herpes simplex 1 and HHV-6 are all associated with a significant shortening of telomeres over a three-year period. Furthermore, the magnitude of the changes was large. For example, CMV seropositivity was associated with the equivalent of almost 12 years of chronological age.

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Latent HHV-6A may impair myelin repair in multiple sclerosis

In All, CNS Disease, Multiple Sclerosis by Kristin Loomis

A group at University of Rochester demonstrated that the HHV-6A latency gene, U94, inhibits migration of cells involved in myelin repair. Inefficient myelin repair is associated with progression MS, and the ability of HHV-6A to impede this process suggests that it could be involved in the progression of MS, and raises questions about the virus’s role in other chronic demyelinating diseases.