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.
Karolinska study on HHV-6A serology highlighted at major MS conference, ECTRIMS
HHV-6 is rarely discussed at the major multiple sclerosis meetings but this year, Anna Fogdell-Hahn from Karolinska Institute was a featured speaker at the 35th meeting of the European Committee for Treatment and Research in Multiple Sclerosis.
Infection with HHV-6A/B speeds progression of disease in marmoset model of MS
Marmosets infected with HHV-6A/B intranasally were initially asymptomatic but later developed significantly accelerated disease and died in a shorter period of time. HHV-6 proteins were found at high levels in the brain lesions.
Latent HHV-6A may impair myelin repair in multiple sclerosis
A group at University of Rochester demonstrated that the HHV-6A latency gene, U94, inhibits migration of cells involved in myelin repair. Inefficient myelin repair is associated with progression MS, and the ability of HHV-6A to impede this process suggests that it could be involved in the progression of MS, and raises questions about the virus’s role in other chronic demyelinating diseases.
HHV-6 U24 tightly linked to specific E3 ubiquitin ligases
The group that recently discovered a ligand for U24 has expanded upon their previous experiments to further elucidate the viral protein’s interactions and functions as they pertain to MS.
New evidence linking HHV-6A U24 protein to MS
HHV-6 has been linked in numerous studies to multiple sclerosis. Now, investigators at the University of British Columbia have published new data suggesting that HHV-6A may be a key player in the development of multiple sclerosis. The investigators propose that the viral protein U24 may dysregulate myelination.
CXCL11 and CCL2 are specific to HHV-6B in febrile infants
Japanese investigators from Kobe University identified CXC11 as a chemokine uniquely expressed in primary HHV-6B infections. They also confirmed a previous finding that cytokine CCL2 (MCP-1) plays a role in HHV-6B primary infections. Both CXCL11 and CCL2 are expressed in several neuroinflammatory conditions including epilepsy, Alzheimer’s disease and traumatic brain injury.
New research shows HLA modulation caused by acute HHV-6A infection of mesothelial cells
HHV-6A infection of mesothelial cells causes HLA molecule modulation. This study demonstrates, for the first time, that human mesothelial cells are susceptible to HHV-6A infection. They also show that the virus causes modulated HLA expression on the cell surface, inducing the de novo expression of HLA class II and HLA-G
HHV-6 antibody level correlates with relapse and progression in MS patients
Anti-HHV-6 IgG titer may be a useful prognostic factor in predicting relapsing-remitting MS clinical course
Two types of HHV-6 positivity in CNS demyelinating disease
New study shows HHV-6 may induce demyelination through both B and T-cell reaction. HHV-6 oligoclonal bands were also found in cases of clinically isolated syndrome.