Patients with viral loads suggestive of iciHHV-6 had the greatest risk of developing demyelinating disease.
In vitro studies confirm that the two viruses infect different cell types, and generate different cytopathic effects, cytokine and growth factor responses.
Infection increases ROS, induces ER stress and activates STAT3, NF-κB and mTOR pathways.
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.
Significant positive correlations were found between HERV family proteins and antibodies to HHV-6A/B but not antibodies to EBV
Studies conducted on serum obtained before development of MS indicate possible protective role
HHV-6 miRNAs and antibodies were identified and significantly correlated with each other in serum and CSF of MS patients
Study provides little evidence for or against a possible role for HHV-6 or EBV in the pathogenesis of MS
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.
HHV-6A infection at any age, and EBV infection after age 20, were found to be significant risk factors
Neuroscientists at Karolinska Institute in Sweden summarized the growing literature linking HHV-6A/B to both illnesses.
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.
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.
Smoking, low ultraviolet radiation exposure, and low vitamin D levels interact with HHV-6A to increase the risk of developing multiple sclerosis
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.