A broadscale investigation of the ovarian cancer oncobiome using a microarray system PathoChip found HHV-6A sequences at or near genes associated with tumorigenesis in ovarian cancer tissue samples.
Dense infection of the hippocampus in primary HHV-6B encephalitis
The autopsy of an infant with HHV-6B encephalitis showed a 4-5 fold increase in the viral load of the hippocampus compared to other parts of the brain. Neurons, oligodendrocytes and vascular endothelial cells were infected, but not astrocytes or microglia.
HHV-6 infection of NK cells causes dramatic changes in miRNA and transcription factors that govern immune function
Italian investigators showed that HHV-6A and -6B infection of natural killer cells have a remarkable effect on the expression of miRNAs and transcription factors, which in turn control natural killer cell development, maturation and function.
Deep sequencing analysis finds HHV-6, CMV and EBV in a subset of stomach and colon cancers
A team at University of Pittsburgh analyzed a large database of deep sequencing data from tumor and control tissues to look for viral sequences in 22 different cancers. They were surprised to find several herpesviruses in gastrointestinal cancers but not in control tissues.
HHV-6 acute liver failure in an immunocompetent child: case report
HHV-6 is rarely identified as the cause of liver dysfunction in immunocompetent children, in part because HHV-6 is not included in routine testing, and HHV-6 infections can be highly localized to the liver. In this case, an alert team in Arizona identified HHV-6 by needle biopsy.
HHV-6 myelitis after cord blood transplantation
Japanese investigators described HHV-6 myelitis in patients who had received cord blood transplantations and report that where HHV-6 reactivation is suspected, early antiviral intervention can dramatically improve patient outcomes.
HHV-6B reactivates first, proceeds to end organ disease faster in transplant patients
Investigators at Fred Hutch Cancer Research Center found that HHV-6B is the first DNA virus to reactivate at a median of 3 weeks, compared to CMV, EBV and Adenovirus at 5-6 weeks. HHV-6B also peaked rapidly, unlike other DNA viruses that took 3-6 weeks to reach peak viral load. HHV-6B reactivation resulted in increased mortality after 100 days.
Ancient iciHHV-6 genomes vary considerably from community strains, but still capable of reactivation
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 24,000 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.
HHV-6 shedding correlates negatively with IL-6 and other inflammatory cytokines in HIV+ patients on antiretroviral therapy
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.
New HHV-6 NIH grants awarded in 2017
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.
HHV-6 reactivation associated with fever after autologous transplantation
Half of autologous hematopoietic cell transplant patients with HHV-6 reactivation exhibit fever plus a collection of symptoms that include diarrhea, rash and pneumonia.
HHV-6B found in the islet cells of both type 1 diabetes patients and controls
Swedish investigators have found HHV-6 protein in the pancreatic islet cells of both type 1 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.
Review of HHV-6 in Liver Transplantation
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 39% to 11%.