For example, CMV seropositivity was associated with the equivalent of almost 12 years of chronological age.A group at University of Rochester demonstrated that the HHV-6A latency gene, U94, inhibits migration of cells involved in myelin repair.The authors suggest reduced immunity may be one reason why past studies have found increased levels of HHV-6 DNA in the brains of Alzheimer’s patients compared to controls.Japanese investigators from Kobe University identified CXC11 as a chemokine uniquely expressed in primary HHV-6B infections.At 100 days after transplantation, the overall survival rate was just 58.3%, compared with 80.5% for patients who did not develop encephalitis.High-dose antiviral therapy was shown to mitigate high mortality rates in these patients.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.
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.
They also confirmed a previous finding that cytokine CCL2 (MCP-1) plays a role in HHV-6B primary infections.
Both CXCL11 and CCL2 are expressed in several neuroinflammatory conditions including epilepsy, Alzheimer’s disease and traumatic brain injury.
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.The authors believe that MRV will be a useful mouse model to study the impact of HHV-6 & 7 in humans.