mTORC2 confers neuroprotection and potentiates immunity during virus infection

Rahul K. Suryawanshi, Chandrashekhar D. Patil, Alex Agelidis, Raghuram Koganti, Joshua M. Ames, Lulia Koujah, Tejabhiram Yadavalli, Krishnaraju Madavaraju, Lisa M. Shantz and Deepak Shukla ()
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Rahul K. Suryawanshi: University of Illinois at Chicago
Chandrashekhar D. Patil: University of Illinois at Chicago
Alex Agelidis: University of Illinois at Chicago
Raghuram Koganti: University of Illinois at Chicago
Joshua M. Ames: University of Illinois at Chicago
Lulia Koujah: University of Illinois at Chicago
Tejabhiram Yadavalli: University of Illinois at Chicago
Krishnaraju Madavaraju: University of Illinois at Chicago
Lisa M. Shantz: Pennsylvania State University College of Medicine
Deepak Shukla: University of Illinois at Chicago

Nature Communications, 2021, vol. 12, issue 1, 1-10

Abstract: Abstract Herpes simplex virus type-1 (HSV-1) causes ocular and orofacial infections. In rare cases, HSV-1 can cause encephalitis, which leads to permanent brain injuries, memory loss or even death. Host factors protect humans from viral infections by activating the immune response. However, factors that confer neuroprotection during viral encephalitis are poorly understood. Here we show that mammalian target of rapamycin complex 2 (mTORC2) is essential for the survival of experimental animals after ocular HSV-1 infection in vivo. We find the loss of mTORC2 causes systemic HSV-1 infection due to defective innate and adaptive immune responses, and increased ocular and neuronal cell death that turns lethal for the infected mice. Furthermore, we find that mTORC2 mediated cell survival channels through the inactivation of the proapoptotic factor FoxO3a. Our results demonstrate how mTORC2 potentiates host defenses against viral infections and implicate mTORC2 as a necessary factor for survival of the infected host.

Date: 2021
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DOI: 10.1038/s41467-021-26260-5

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