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OPTN is a host intrinsic restriction factor against neuroinvasive HSV-1 infection, 2021, Joshua Ames

Discussion in 'Health News and Research unrelated to ME/CFS' started by Mij, Sep 13, 2021.

  1. Mij

    Mij Senior Member (Voting Rights)

    Fast-replicating neurotropic herpesviruses exemplified by herpes simplex virus-1 (HSV-1) naturally infect the central nervous system (CNS). However, most individuals intrinsically suppress the virus during a primary infection and preclude it from significantly damaging the CNS. Optineurin (OPTN) is a conserved autophagy receptor with little understanding of its role in neurotropic viral infections. We show that OPTN selectively targets HSV-1 tegument protein, VP16, and the fusion glycoprotein, gB, to degradation by autophagy. OPTN-deficient mice challenged with HSV-1 show significant cognitive decline and susceptibility to lethal CNS infection. OPTN deficiency unveils severe consequences for recruitment of adaptive immunity and suppression of neuronal necroptosis. Ocular HSV-1 infection is lethal without OPTN and is rescued using a necroptosis inhibitor. These results place OPTN at the crux of neuronal survival from potentially lethal CNS viral infections.


    The autophagy receptor optineurin degrades VP16, restricts HSV-1 spread, and is neuroprotective.
    Last edited by a moderator: Sep 13, 2021

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