27.6% of Japanese mothers with iciHHV6 had a spontaneous abortion compared to 14.8% of controls. iciHHV6 mothers were also 6.4X more likely to have two or more spontaneous abortions.
Three top experts on HHV-6A/B teamed up to write a comprehensive review and propose criteria for establishing HHV-6A/B to MS, epilepsy and Alzheimer’s disease.
Six-month overall survival was 96% in the treated group compared to 72% in the untreated group.
Surprisingly, 72% of integrated genomes were found on chromosome 22q. Solo-DR sequences of HHV-6B were left behind after excision and reactivation.
Dysregulation of the microRNA miR155 is associated with pathophysiological progression of Alzheimer’s disease. HHV-6A has been shown to suppress miR155.
Japanese investigators show that a protein expressed by latent HHV-6B in astrocytes, results in an influx of extra-cellular calcium, triggering the onset of depression.
A large UK study utilizing RNA sequencing metagenomics of placental samples identified HHV-6 RNA in 6.1% of pre-eclampsia cases and 2.2% of healthy pregnancies. HHV-6 was the only virus found and it was iciHHV-6 in 70% of cases.
HHV-6/7 DNA was found in the plasma of 19.6% of epilepsy patients compared to none of the controls. Protein expression indicating active infection was found in 53% of the HHV-6/7 positive patients.
So far only one case report has documented HHV-6B reactivation in COVID-19, but the rise in Kawasaki-like symptoms and pityriasis rosea has at least one dermatology group suspicious of HHV-6/7 reactivation.
High dose steroids given in the first week appears to prevent HHV-6 reactivation in DRESS/DIHS patients by suppressing T-cell activation and serum interleukin-2 receptor (sIL-2R) levels. In contrast, a late start of steroid therapy resulted in a persistently high viral load for at least three weeks.
The mechanisms leading to HHV-6A/B integration are a subject of intense research by several laboratories. A new paper in PLoS Pathogens provides some understanding as to how HHV-6A/B may integrate host chromosomes.
A team of virologists and metabolomics specialists collaborated to demonstrate how chromosomally integrated HHV-6 can be stimulated to secrete factors that simultaneously cause mitochondrial fragmentation, a reduction in intracellular ATP reserve and an expanded antiviral defense by their neighboring cells.
Herpesvirus co-infections, particularly HHV-6 and CMV, cause severe lymphopenia, pneumonia, and an increased risk of acquiring bacterial and fungal infections in non-transplant acute leukemia patients undergoing chemotherapy.
Patients with DRESS/DIHS hypersensitivity reactions and active HHV-6 often develop autoimmune diseases such as type 1 diabetes and autoimmune thyroiditis. Investigators at National Taiwan University Hospital believe that IP-10 is key to this process.
Allogenic transplant patients who received prophylactic oral brincidofovir as part of a CMV trial had a reduced HHV-6B reactivation and lower viral loads.