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.
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.
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.
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.
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
Anti-HHV-6 IgG titer may be a useful prognostic factor in predicting relapsing-remitting MS clinical course
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 major capsid protein identified in CSF of MS patients: a case of molecular mimicry?
A new study from NIH/NINDS further strengthens the relationship between HHV-6, EBV, and multiple sclerosis.
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.
An increased prevalence of HHV-6 U94/REP antibodies found among Tunisian MS patients.
Strong evidence of a genetic link between HHV-6 active replication and poor IFN-B treatment response among multiple sclerosis patients
A new study shows that multiple sclerosis patients with HHV-6 have higher risk of relapse and poor response to IFN-beta treatment.
The trigger for neurological disease in a subset of patients with MS?
The administration of immune agents to patients (known as Interferon-Beta-1b, or IFN-beta, therapy) has been widely used in the treatment and maintenance of multiple sclerosis (MS). Additionally, it is known that the risk of MS exacerbation is much higher in patients with active HHV-6 infection than in patients with a latent infection of the virus (Lafuente 2006, 2007; Chapenko 2003). In this new study from Madrid, researchers examined the effectiveness of IFN-1b therapy in multiple sclerosis patients with active HHV-6 infection. By monitoring the HHV-6 DNA levels of MS patients undergoing IFN-beta therapy, investigators were able to find that patients with active HHV-6 infection had a higher risk of severe MS relapse and poor response to IFN-beta therapy than patients …