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J Virol. 2017 Jun 26;91(14). pii: e01081-16. doi: 10.1128/JVI.01081-16. Print 2017 Jul 15.

Collateral Damage during Dengue Virus Infection: Making Sense of DNA by cGAS.

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Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York, USA
Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA.


Early sensing of viral components or infection-induced tissue damage is a prerequisite for the successful control of pathogenic viruses by the host innate immune system. Recent results from our laboratory show how immune cells use the DNA-sensing machinery to detect intracellular damage generated early during infection by an RNA virus, namely, dengue virus (DENV). Conversely, we found that DENV can efficiently dismantle this sensing mechanism by targeting the cyclic GMP-AMP synthase (cGAS) and the stimulator of interferon (IFN) genes (STING), two crucial host factors involved in DNA detection and type I IFN production. These findings highlight the relevance of the DNA-sensing mechanism in the detection and control of infections by RNA viruses. In this review, we discuss how DENV modulates the innate immune DNA-sensing pathway, activated in the context of cellular damage during infection.


DNA sensing; STING; cGAS; damage; dengue virus; innate immunity; interferon; mitochondria; mtDNA

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