In vitro studies confirm that the two viruses infect different cell types, and generate different cytopathic effects, cytokine and growth factor responses.
HHV-6A promotes inflammation in astrocytoma cells by dysregulating autophagy
Infection increases ROS, induces ER stress and activates STAT3, NF-κB and mTOR pathways.
New seroepidemiological evidence that HHV-6 contributes to MS disease progression
Longitudinal study of people with a single initial episode of demyelination provides stronger evidence for HHV-6 than EBV in the pathogenesis of MS, but the evidence is not robust.
A relationship between human endogenous retroviruses and HHV-6A/B in multiple sclerosis patients
Significant positive correlations were found between HERV family proteins and antibodies to HHV-6A/B but not antibodies to EBV
CMV infection may diminish the risk of developing MS
Studies conducted on serum obtained before development of MS indicate possible protective role
Detection of HHV-6 miRNA in Multiple Sclerosis patients
HHV-6 miRNAs and antibodies were identified and significantly correlated with each other in serum and CSF of MS patients
Metagenomic and reverse transcriptase methodologies employed to detect herpesvirus DNA in spinal fluid of multiple sclerosis (MS) patients
Study provides little evidence for or against a possible role for HHV-6 or EBV in the pathogenesis of MS
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.
Large serologic study incriminates both EBV and HHV-6A as triggers of multiple sclerosis
HHV-6A infection at any age, and EBV infection after age 20, were found to be significant risk factors
A review of the role of HHV-6A in multiple sclerosis and HHV-6B in epilepsy
Neuroscientists at Karolinska Institute in Sweden summarized the growing literature linking HHV-6A/B to both illnesses.
A review of evidence linking HHV-6A/B to neurological diseases: association or causation?
A thorough review examines the possible role of HHV-6A/B in febrile seizures, mesial temporal lobe epilepsy, multiple sclerosis and Alzheimer’s disease, proposing evidence to distinguish association from causation.
HHV6A/B as a clinical marker of multiple sclerosis relapse during the postpartum period
HHV-6 IgM antibodies were higher in pregnant MS patients than in healthy controls. Women with elevated HHV-6 IgM titers were more likely to relapse postpartum.
Lifestyle factors interact with HHV-6A in the development of multiple sclerosis
Smoking, low ultraviolet radiation exposure, and low vitamin D levels interact with HHV-6A to increase the risk of developing multiple sclerosis
Latent HHV-6, mitochondrial fragmentation and a hypometabolic state in ME/CFS patients
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.
HHV-6A (but not HHV-6B) linked to increased risk of multiple sclerosis
Karolinska Institute researchers developed a novel serological assay to determine that individuals with antibodies to HHV-6A early proteins are more likely to develop MS. HHV-6A antibodies were the highest in the presence of elevated EBV antibodies, suggesting that the two viruses could jointly contribute to the development of MS.