| Literature DB >> 28346446 |
Sebastian Aguirre1, Priya Luthra1, Maria T Sanchez-Aparicio1,2, Ana M Maestre1, Jenish Patel1,2,3, Francise Lamothe1, Anthony C Fredericks1,3, Shashank Tripathi1,2, Tongtong Zhu1,3, Jessica Pintado-Silva1,3, Laurence G Webb1,3, Dabeiba Bernal-Rubio1, Alexander Solovyov4, Benjamin Greenbaum4, Viviana Simon1,2,5, Christopher F Basler1, Lubbertus C F Mulder1,2, Adolfo García-Sastre1,2,5, Ana Fernandez-Sesma1,3,5.
Abstract
During the last few decades, the global incidence of dengue virus (DENV) has increased dramatically, and it is now endemic in more than 100 countries. To establish a productive infection in humans, DENV uses different strategies to inhibit or avoid the host innate immune system. Several DENV proteins have been shown to strategically target crucial components of the type I interferon system. Here, we report that the DENV NS2B protease cofactor targets the DNA sensor cyclic GMP-AMP synthase (cGAS) for lysosomal degradation to avoid the detection of mitochondrial DNA during infection. Such degradation subsequently results in the inhibition of type I interferon production in the infected cell. Our data demonstrate a mechanism by which cGAS senses cellular damage upon DENV infection.Entities:
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Year: 2017 PMID： 28346446 PMCID： PMC7457382 DOI： 10.1038/nmicrobiol.2017.37
Source DB: PubMed Journal: Nat Microbiol ISSN： 2058-5276 Impact factor: 17.745