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Figure Pathogenesis of progressive multifocal leukoencephalopathy (PML)‏ Pathogenesis of progressive multifocal leukoencephalopathy (PML) Steps 1–3 show.

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Presentation on theme: "Figure Pathogenesis of progressive multifocal leukoencephalopathy (PML)‏ Pathogenesis of progressive multifocal leukoencephalopathy (PML) Steps 1–3 show."— Presentation transcript:

1 Figure Pathogenesis of progressive multifocal leukoencephalopathy (PML)‏
Pathogenesis of progressive multifocal leukoencephalopathy (PML) Steps 1–3 show initiation of JC virus (JCV) infection, and establish latency in kidney that can become persistent in lymphoid organs, notably the bone marrow, in which the viral regulatory region sequences become rearranged from the nonvirulent to a neurovirulent or PML variant. Steps 4–6 involve the biological effects of natalizumab treatment over time, forcing migration of CD 34+ and pre-B cells into the circulation since it prevents homing of these cells in the marrow due to blocking of binding to cell adhesion molecules. At these steps, natalizumab is associated with temporal gene regulation of a number of factors including those that augment JCV replication that may account for high incidence of PML in patients with multiple sclerosis treated with natalizumab for 24 doses or more. Steps 7–10 show progression of JCV to the brain and establishment of PML. The authors thank David Carter, In Tune Communications, Canada, for assembly of the figure. EBV = Epstein-Barr virus. Eugene O. Major, and Avindra Nath Neurol Neuroimmunol Neuroinflamm 2016;3:e235 © 2016 American Academy of Neurology

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