In vitro studies confirm that the two viruses infect different cell types, and generate different cytopathic effects, cytokine and growth factor responses.
Murine roseolovirus (MRV) infection experiments are only partially supportive of role of HHV-6A/B in Alzheimer’s disease
While MRV administered peripherally led to brain infection and neuroinflammation, it did not increase Aß deposition
HHV-6A promotes inflammation in astrocytoma cells by dysregulating autophagy
Infection increases ROS, induces ER stress and activates STAT3, NF-κB and mTOR pathways.
EBV and HHV-6 plasma viremia is infrequent at Day 7 during acute COVID-19
Other studies have suggested that reactivation of these viruses could theoretically contribute to a hyperinflammatory state or autoimmune disorders in acute COVID-19, but this study does not provide evidence of that.
Does inherited chromosomal integration of HHV-6 at 9q increase the risk of malignancy?
A large study of iciHHV-6 integration sites found integration at 9q more common in hematologic malignancies—but the study lacked power to draw firm conclusions.
Development of highly sensitive technique for detecting viral DNA sequences in cell-free plasma
Isolating DNA fragments less than 120 base pairs enriches for viral vs. cellular DNA.
G-1082A polymorphism of IL-10 may protect against HHV-6/EBV adenoid hypertrophy
The presence of HHV-6 and EBV DNA in nasal secretions correlates with the degree of adenoid hypertrophy in children.
HHV-6A U14 protein and NFκB activate each other
The late protein U14 of HHV-6A can induce the pro-inflammatory transcription factor NFκB, and NFκB, in turn, can encourage the replication of HHV-6A.
Different isoforms of CD46 affect infectivity and replication of HHV-6A and HHV-6B
While CD134 remains the more important receptor for HHV-6B, HHV-6B can use the CD46 receptor when a T cell has the C1 isoform of CD46.
HHV-6B may enter cells that don’t express CD134 via the nectin-2 receptor
If confirmed, finding could explain ability of HHV-6B to infect salivary, liver and neural cells.
HHV-6A and HCMV induce pro-fibrotic miRNA expression pattern in infected host cells
Pattern consistent with clinical studies suggesting these viruses may be one trigger of systemic sclerosis.
HHV-6 miRNA inhibits host miRNA to trigger reactivation from latency
A viral miRNA disrupts mitochondrial architecture, suppresses type I interferon production, is necessary for productive infection and for virus reactivation, all by inhibiting multiple members of the host miR-30 family—creating a therapeutic target to suppress reactivation.
4C-seq genomic methodology used to examine HHV-6A integration sites
Chromatin interactions help silence transcription of HHV-6A genes following integration
The effects of HHV-6B infection on immune checkpoint inhibition
HHV-6B infection of primary monocytes induces cell-associated and soluble PD-L1 production, increased intracellular ROS and activation of STAT1 and STAT3 pathways
The importance of individual glycoprotein components of the HHV-6A/6B envelope tetramer on essential viral functions
The combination of gQ1 and gQ2 tetramer components of both HHV-6A/6B are important for viral propagation, probably by affecting attachment to their different receptors.