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Latent HHV-6A may impair myelin repair in multiple sclerosis

In All, CNS Disease, Multiple Sclerosis by Kristin Loomis

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.

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CXCL11 and CCL2 are specific to HHV-6B in febrile infants

In All, Alzheimer's Disease, Multiple Sclerosis by Kristin Loomis

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.

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New research shows HLA modulation caused by acute HHV-6A infection of mesothelial cells

In All, Endocrine Conditions, Latest Scientific News, Multiple Sclerosis by Kristin Loomis

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