Mechanistic Target of Rapamycin Signaling Activation Antagonizes Autophagy To Facilitate Zika Virus Replication

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  • Bikash R. Sahoo
    School of Veterinary Medicine and Biomedical Sciences, University of Nebraska–Lincoln, Lincoln, Nebraska, USA
  • Aryamav Pattnaik
    School of Veterinary Medicine and Biomedical Sciences, University of Nebraska–Lincoln, Lincoln, Nebraska, USA
  • Arun S. Annamalai
    School of Veterinary Medicine and Biomedical Sciences, University of Nebraska–Lincoln, Lincoln, Nebraska, USA
  • Rodrigo Franco
    School of Veterinary Medicine and Biomedical Sciences, University of Nebraska–Lincoln, Lincoln, Nebraska, USA
  • Asit K. Pattnaik
    School of Veterinary Medicine and Biomedical Sciences, University of Nebraska–Lincoln, Lincoln, Nebraska, USA
  • Susana López
    editor

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<jats:p>The re-emergence of Zika virus (ZIKV) and its association with neurological complications necessitates studies on the molecular mechanisms that regulate ZIKV pathogenesis. The mTOR signaling cascade is tightly regulated and central to normal neuronal development and survival. Disruption of mTOR signaling can result in neurological abnormalities. In the studies reported here, we demonstrate for the first time that ZIKV infection results in activation of both mTORC1 and mTORC2 to promote virus replication. Although autophagy is activated early in infection to counter virus replication, it is subsequently suppressed by mTOR. These results reveal critical roles of mTOR signaling and autophagy in ZIKV infection and point to a possible mechanism underlying ZIKV-induced pathogenesis. Elucidating the role of mTOR signaling in ZIKV infection will provide insights into the mechanisms of ZIKV-induced neurological complications and potential targets for therapeutic approaches.</jats:p>

Journal

  • Journal of Virology

    Journal of Virology 94 (22), 2020-10-27

    American Society for Microbiology

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