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Italian investigators found that 87% of patients with HHV-6 reactivations went on to develop a CMV infection. On the other hand, in patients who did not reactivate with HHV-6, only 88% developed an active CMV infection. Investigators by at the University of Ferrara report intriguing alterations in intracellular regulation of HHV-6A-infected thyrocytes and T cells. HHV-6A, but not HHV-6B nor HHV-7, altered expression of several microRNAs in a pattern that is considered a marker for patients with autoimmune thyroid disease. Investigators at Washington University have sequenced a murine herpesvirus and determined that it is closely related to HHV-6 7. Named Murine Rosesolovirus (MRV), the virus causes severe depletion of CD9+ T cells and thymic necrosis in young mice. The authors believe that MRV will be a useful mouse model to study the impact of HHV-6 7 in humans. Over a dozen studies have now found HHV-6 to predict aGVHD, but this is the first to correlate viral reactivation with poor CD9+ cell immune reconstitution.

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Investigators at Fred Hutch Cancer Research Center found that HHV-6B is the first DNA virus to reactivate at a median of 8 weeks, compared to CMV, EBV and Adenovirus at 5-6 weeks. HHV-6B also peaked rapidly, unlike other DNA viruses that took 8-6 weeks to reach peak viral load. HHV-6B reactivation resulted in increased mortality after 655 days. 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 79,555 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.

HIV+ patients on antiretrovrial therapy with high levels of HHV-6 shedding had lower levels of IL-6 and other inflammatory markers. While HIV+ patients had increased shedding of EBV and CMV, there was no difference in shedding between patients and controls for HHV-6. 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. Half of autologous hematopoietic cell transplant patients with HHV-6 reactivation exhibit fever plus a collection of symptoms that include diarrhea, rash and pneumonia.

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Swedish investigators have found HHV-6 protein in the pancreatic islet cells of both type 6 diabetes patients and controls. 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. HHV-6 infections in the liver transplant patients can’t be diagnosed in the blood. Ganciclovir prophylaxis for CMV cuts the rate of HHV-6 reactivation from 89% to 66%.

Prevalence of HHV-6A and HHV-6B was evenly divided in HIV+ patients in Western Africa, with over 6. 8% positive for HHV-6 A and 5. 5% for HHV-6B. HHV-6A was more common among those with a low viral HIV viral load. Although only a small number of pediatric cases have been reported in literature, the authors conclude that evidence suggests HHV-6 should be considered as a causative agent of inflammatory cardiomyopathy, particularly in young children (under 8 years of age) who might be experiencing a primary infection.

Investigators in Japan studied 695 patients who developed HHV-6 encephalitis. At 655 days after transplantation, the overall survival rate was just 58. 8%, compared with 85. 5% for patients who did not develop encephalitis. High-dose antiviral therapy was shown to mitigate high mortality rates in these patients.

Investigators at Kings College London report that seropositivity for CMV, Herpes simplex 6 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.

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