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.
An explanation for why HHV-6 reactivation and DRESS lead to autoimmunity
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.
Oral brincidofovir prophylaxis for CMV decreased incidence of HHV-6B viremia
Allogenic transplant patients who received prophylactic oral brincidofovir as part of a CMV trial had a reduced HHV-6B reactivation and lower viral loads.
iciHHV-6 may modulate human gene expression
A Japanese group found that ciHHV6 genes encoding for immunoglobulins were decreased in ciHHV6 individuals, possibly modulating immune responses.
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.
Multiplex FilmArray Meningitis/Encephalitis assay is useful for diagnosing HHV-6 encephalitis
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.
New humanized mouse model mimics HHV-6B pathogenesis
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
Single-cell RNA sequencing analysis implicates HHV-6B in DIHS/DRESS.
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.
Clonally expanded CD8 T cells in spinal fluid of Alzheimer’s patients suggest an adaptive immune response to pathogens
Researchers at the NIH used RNA-Seq cells from skin and blood to study the underlying mechanisms in DIHS/DRESS and identified both HHV-6 and JAK-STAT pathways as potential targets. Central memory CD4+T cells were enriched with HHV-6B.
Comprehensive annotations of HHV-6A/B reveal novel genomic features
Hundreds of new open reading frames were identified in a comprehensive Weizman Institute study that has generated a complete, unbiased atlas of the HHV-6A/B proteome.
HHV-6A detected in the skin biopsies of systemic sclerosis patients
A group led by Elisabetta Caselli at University of Ferrara discovered HHV-6A in the skin and elevated levels of HHV6-B in the peripheral blood of systemic sclerosis patients
NINDS/NIH investigators find very little HHV-6 RNA or DNA in either Alzheimer’s or control brains
A team led by Steven Jacobson, PhD at NINDS analyzed RNA-seq datasets from 901 brains, and found only 1.2% of Alzheimer’s patients and 0.4% of controls positive for HHV-6 RNA. They also found HHV-6 DNA in less than 4% of samples tested by ddPCR.
The debate continues over RNA-seq analysis of HHV-6A in Alzheimer’s
Two groups have challenged the widely-publicized 2018 study in 2018, that found increased HHV-6A & 7 abundance and an association with clinical and pathology scores in Alzheimer’s. The topic has become the focus vigorous debate.
Low sodium or SIADH may be an early indicator of HHV-6 encephalitis
A systematic review suggests that sodium imbalance is associated with HHV-6 encephalitis and syndrome of inappropriate diuretic hormone (SIADH) could serve as an early warning
HHV-6A induces dysregulation of autophagy in neurons and astrocytoma cells, increasing beta-amyloid and tau
Building on their prior work, an Italian team has shown that HHV-6A is able to induce dysregulation of autophagy in neurons and astrocytoma cells, increasing amyloid beta and tau production.