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HHV-6B reactivation resulted in increased mortality after 100 days.

British researchers used molecular dating methods to determine that most strains of ici HHV-6 come from a small number of ancient human ancestors; the youngest found lived over 24,000 years ago.

A group from Italy’s University of Bologna report that genetic defects in antimicrobial defense mechanisms can leave some individuals vulnerable to sub-clinical infections that lead to cognitive decline as they age.

They found variations in specific antiviral genes that correlate with HHV-6 DNA levels in brain tissue and blood from patients with Alzheimer’s disease.

The viral load was higher in the islet cells than in surrounding tissues.

Unfortunately, they did not provide data on the difference between patients and controls in the viral load.

While HIV patients had increased shedding of EBV and CMV, there was no difference in shedding between patients and controls for HHV-6.

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HHV-6B also peaked rapidly, unlike other DNA viruses that took 3-6 weeks to reach peak viral load.

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.

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.

T-cell depleted stem cell transplant patients at Memorial Sloan Kettering Cancer Center with HHV-6 viremia, CMV viremia, or 2 or more viremias experienced longer hospital stays and were readmitted more often.