Key result
Viruses evade cGAS-STING immunity and promote replication using post-translational modifications, viral proteins, and non-coding RNAs.
Why the study?
Viruses have evolved numerous strategies to hinder the cGAS-STING signal transduction and promote immune evasion, prompting the need to outline these regulatory mechanisms to inspire new targets and clinical antiviral treatments.
This review summarizes how viruses evade the cGAS-STING innate immune pathway, highlighting potential targets for novel antiviral treatments.
Suggests antiviral targets in cGAS-STING pathway; leaves open prospective validation before clinical translation.
Virus infection has been consistently threatening public health. The cyclic GMP-AMP synthase (cGAS)-Stimulator of Interferon Genes (STING) pathway is a critical defender to sense various pathogens and trigger innate immunity of mammalian cells. cGAS recognizes the pathogenic DNA in the cytosol and then synthesizes 2'3'-cyclic GMP-AMP (2'3'cGAMP). As the second messenger, cGAMP activates STING and induces the following cascade to produce type I interferon (IFN-I) to protect against infections. However, viruses have evolved numerous strategies to hinder the cGAS-STING signal transduction, promoting their immune evasion. Here we outline the current status of the viral evasion mechanism underlying the regulation of the cGAS-STING pathway, focusing on how post-transcriptional modifications, viral proteins, and non-coding RNAs involve innate immunity during viral infection, attempting to inspire new targets discovery and uncover potential clinical antiviral treatments.
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Hu et al. (2021) conducted a review in Viral infection. cGAS-STING pathway regulation was evaluated. Viruses utilize post-translational modifications, viral proteins, and non-coding RNAs to evade the cGAS-STING innate immune pathway and promote viral replication.
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