Sensing of HSV-1 by the cGAS–STING pathway in microglia orchestrates antiviral defence in the CNS

Line S. Reinert, Katarína Lopušná, Henriette Winther, Chenglong Sun, Martin K. Thomsen, Ramya Nandakumar, Trine H. Mogensen, Morten Meyer, Christian Vægter, Jens R. Nyengaard, Katherine A. Fitzgerald and Søren R. Paludan ()
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Line S. Reinert: University of Aarhus
Katarína Lopušná: University of Aarhus
Henriette Winther: University of Aarhus
Chenglong Sun: University of Aarhus
Martin K. Thomsen: University of Aarhus
Ramya Nandakumar: University of Aarhus
Trine H. Mogensen: University of Aarhus
Morten Meyer: Institute of Molecular Medicine, University of Southern Denmark
Christian Vægter: University of Aarhus
Jens R. Nyengaard: University of Aarhus
Katherine A. Fitzgerald: University of Massachusetts Medical School
Søren R. Paludan: University of Aarhus

Nature Communications, 2016, vol. 7, issue 1, 1-12

Abstract: Abstract Herpes simplex encephalitis (HSE) is the most common form of acute viral encephalitis in industrialized countries. Type I interferon (IFN) is important for control of herpes simplex virus (HSV-1) in the central nervous system (CNS). Here we show that microglia are the main source of HSV-induced type I IFN expression in CNS cells and these cytokines are induced in a cGAS–STING-dependent manner. Consistently, mice defective in cGAS or STING are highly susceptible to acute HSE. Although STING is redundant for cell-autonomous antiviral resistance in astrocytes and neurons, viral replication is strongly increased in neurons in STING-deficient mice. Interestingly, HSV-infected microglia confer STING-dependent antiviral activities in neurons and prime type I IFN production in astrocytes through the TLR3 pathway. Thus, sensing of HSV-1 infection in the CNS by microglia through the cGAS–STING pathway orchestrates an antiviral program that includes type I IFNs and immune-priming of other cell types.

Date: 2016
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DOI: 10.1038/ncomms13348

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