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.
Neonatal murine roseolovirus infection induces autoimmunity
Early infection interferes with normal thymocyte development and disrupts central tolerance resulting in autoimmune disease later in life. Only infection during this critical time period resulted in autoimmunity.
Updated mapping and proposed new annotation of the HHV-6B transcriptome
An analysis of the kinetics of gene expression during infection of human Molt-3 T-cells agrees with previous studies, but also demonstrates unique findings.
A large scale whole genome sequencing study sheds light on HHV-6 integration events
Investigators at the Riken Institute in Japan developed new computational methods to detect virus induced structural variants in the human genome
New technique for precisely identifying integration site of HHV-6 in telomeres
Using whole genome optical mapping, investigators found that contrary to previous findings, the length of telomeres with viral integration was not unusually short.
A comprehensive review of the role and potential functions HHV-6A/B U94
The review covers the role the U94 gene product plays in the virus’s life cycle, replication, and latency, as well as in the immune response.
The role of HHV-6 in dysregulating autophagy
HHV-6, like some other herpesviruses, dysregulates autophagy in multiple cell types, with important biological consequences.
HHV-6 linked to intrauterine growth restriction via the human leukocyte antigen-G dysregulation
A small study found a strong association between HHV-6 infection of the placenta and intrauterine growth restriction—a finding consistent with other evidence linking HHV-6 to several reproductive diseases.
HHV-6A and 7 infection of T cells downregulates the protein tyrosine phosphatase, CD45
CD45, important in T cell receptor signaling, may be one mechanism by which roseolaviruses evade immune detection and help achieve latency
HHV-6A, HHV-6B, and HHV-7 have differential impact on intracellular DNA sensors of NK cells
Cytokine and chemokine responses were very similar in HHV-6B and HHV-7 infections. The results were starkly different for HHV-6A.
University of Washington’s Clinical Laboratory in the News
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 …