Research: Herpes virus and trigger of MS

Background: The role of herpes viruses as potential triggers of MS is still debated. 

Methods: Peripheral blood mononuclear cells from MSers and controls were treated with CpG sequences and infected in
vitro with HSV-1 (herpes simplex virus 1). Samples were analyzed for viral yield, TLR9 pathways,
cytokine secretion, NK cell activation and killer immunoglobulin-like
receptor (KIR) expression. 

CpG sequences – refer to a specific DNA sequence. In man these sequences are usually methylated, whilst in viruses and bacteria they are not. Unmethylated CpG sites can be detected by Toll-Like Receptor 9 or TLR9. TLR9 is one of the receptors the immune system uses to detect invading organisms – i.e. it is a danger signal.
Results: CpG treatment promoted an unexpected
sensitivity to herpes virus infection in a subset of MSers: TLR9
pathways did not show defects while NK cells presented decreased
degranulation and cytotoxicity and up-regulated the inhibitory KIR2DL2
receptor. CpG treatment of purified NK cells affected directly KIR2DL2
modulation and cell activation. 

NK or natural killer cells are an immune cell the body uses to fight infections and cancer. There is data that suggests MSers have a defect in the function of their NK cells. 

Conclusion: These data suggest potential
implications for viral pathogenesis of MS.

“I am not sure what potential implications they are referring to. The hypotheses have not been well-defined in this study, which makes their conclusion difficult to interpret. Pity they did not choose a more relevant virus to study; HSV-1 is the virus that causes herpes labialis or fever blisters. There is little data to link this virus to the pathogenesis of MS.”

“Mechanistic studies like this have a role to play, but they must have a well-defined hypothesis and purpose. For example does herpes virus infection of white blood cells in the lab result in the same defect in NK cells that are seen in MSers? Now that would be a question worth answering? Simple? Not at all. What happens in  the lab is very different to what happens in the body. To study this properly you would need to investigate normal people before and after herpes virus infections. Something we are planning to do in the future in relation to EBV infection.”

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