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.
HHV-6A protein identified in as the target of HHV-6 specific oligoclonal bands in MS
HHV-6A major capsid protein identified in CSF of MS patients: a case of molecular mimicry?
NINDS finds 38% of MS patients harbor HHV-6 or EBV specific oligoclonal bands
A new study from NIH/NINDS further strengthens the relationship between HHV-6, EBV, and multiple sclerosis.
NIH Laboratory develops novel marmoset model of HHV-6A & HHV-6B infection
Dr. Steven Jacobson’s laboratory at the US National Institute of Health has developed a novel marmoset model for the study of HHV-6 infection.
Increased prevalence of HHV-6 antibodies discovered in multiple sclerosis patients
An increased prevalence of HHV-6 U94/REP antibodies found among Tunisian MS patients.
HHV-6 active replication genetically linked to poor treatment response among MS patients
Strong evidence of a genetic link between HHV-6 active replication and poor IFN-B treatment response among multiple sclerosis patients
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