Monkey virus like MS

Blair TC, Manoharan M, Rawlings-Rhea SD, Tagge I, Kohama SG, Hollister-Smith J, Ferguson B, Woltjer RL, Frederick MC, Pollaro J, Rooney WD, Sherman LS, Bourdette DN, Wong SW.
Immunopathology of Japanese macaque encephalomyelitis is similar to multiple sclerosis. J Neuroimmunol. 2016 Feb 15;291:1-10. 

Japanese macaque encephalomyelitis (JME) is an inflammatory demyelinating disease that occurs spontaneously in a colony of Japanese macaques (JM) at the Oregon National Primate Research Center. Animals with JME display clinical signs resembling multiple sclerosis (MS), and magnetic resonance imaging reveals multiple T2-weighted hyperintensities and gadolinium-enhancing lesions in the central nervous system (CNS). Here we undertook studies to determine if JME possesses features of an immune-mediated disease in the CNS. Comparable to MS, the CNS of animals with JME contain active lesions positive for IL-17, CD4+ T cells with Th1 and Th17 phenotypes, CD8+ T cells, and positive CSF findings.

There is a colony of monkeys in Portland Oregon that get a demyelinating disease. It occurs in about 5% of the monkies and they have found that this is caused by a Herpes-like virus. Is this the ultimate animal model to test out anti-viral strategies

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  • A very important news indeed.
    I bet TNF blockers worsen this disease, anti-cd20 ameliorates it a lot and that IFN, fingo and DMF works in this disease as well.
    I assume that for ProfG and his EBV research this could be simply pivotal.

    • Theoretically we can even say that MS is autoimmune, but really that was the current DMTs, and HTSC itself would cure the disease, would for example CBOs disappear, but it is not what we observe in fact … So the interaction gene -environment seems to be much clearer than simply say that it is a self-imine disease where immune cells attack "randomly" CNS …

  • I read the 2011 study with monkeys Oregon soon as I closed the diagnosis for MS. Really it seems to be an interesting model to study the disease … At that time also wondered if it was the first time I watched this type of infection in monkeys in a "natural" …

  • Yep, for me this news is on par with the ocrelizumab, if not better – we are talking here about a very probably cause not just some drug.

  • It is interesting in that it mimics MS in vivo (CD4+ infiltrates, Th1 and Th17 with high levels of IL-17 production and shows clusters of B-cell infiltrates as well) without artificially inducing the inflammatory processes as in EAE. Also, high levels of IgG in the CSF. Can Ocrelizumab/Rituximab traverse the BBB to address this? The takeaway message is that it occurs spontaneously and should give researchers a better understanding of the pathology.

  • Very interesting indeed. I do hope, though, that this does not lead to Macaques – intelligent primates – in cages in labs.

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