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.
A Japanese group found that ciHHV6 genes encoding for immunoglobulins were decreased in ciHHV6 individuals, possibly modulating immune responses.
Cytokine and chemokine responses were very similar in HHV-6B and HHV-7 infections. The results were starkly different for HHV-6A.
This multiplex qualitative test for cerebrospinal fluid helps physicians diagnose HHV-6 encephalitis quickly, but interpretation must take into account imaging, ciHHV-6 status and other markers.
Keith Jerome and Alex Greninger’s virology lab at University of Washington was one of the first in the nation with a test for SARS CoV-2 and they are credited with helping to identify the first confirmed US case of the virus in January. Keith Jerome, MD, PhD, Director, and Alex Greninger, MD, PhD, Assistant Director of the University of Washington Virology Laboratory in Seattle. Greninger was featured in an interview in GQ, titled “The Infuriating Story of How the Government Stalled Coronavirus Testing” that he began developing the test early in January, when the sequence was first announced. Since then, he and his team have worked tirelessly to expand capacity in-house to diagnose more patients. A clip of a PBS …
Researchers led by Yasuko Mori of Kobe University in Japan have developed an animal model will be useful for studying the pathogenicity of HHV-6B in conditions such as acute GVHD and idiopathic pneumonia
RNA-Seq analysis of cells from skin and blood identified both HHV-6 and JAK-STAT pathways inhibitors as potential targets. Central memory CD4+T cells were enriched with HHV-6B.