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Leaky Scanning

Leaky Scanning

During most eukaryotic translation processes, the small 40S ribosome subunit scans an mRNA from its 5' end until it encounters the first start AUG codon. The large 60S ribosomal subunit then joins the smaller one to initiate protein synthesis. The location of the translation initiation is largely determined by the nucleotides near the start codon as there may be multiple translation initiation sites present on the mRNA. Marilyn Kozak discovered that the sequence RCCAUGG (where R...

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Updated: Jun 6, 2025

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production

Published on: March 2, 2014

How Does African Swine Fever Virus Evade the cGAS-STING Pathway?

Can Lin^1,2,3,4, Chenyang Zhang^1,2,3,4, Nanhua Chen^1,2,3,4

¹College of Veterinary Medicine, Yangzhou University, Yangzhou 225009, China.

Pathogens (Basel, Switzerland)

|November 27, 2024

Summary

African swine fever virus (ASFV) evades host immunity by inhibiting the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway. ASFV proteins target key components like cGAS, STING, TBK1, IKKε, IRF3, and NF-κB to suppress antiviral responses.

Keywords:

African swine fever virus DNA sensing STING cGAS innate immunity

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Area of Science:

Virology
Immunology
Molecular Biology

Background:

African swine fever (ASF) is a highly infectious viral disease causing significant economic losses in the swine industry.
Understanding ASFV pathogenesis and immune evasion is crucial for developing effective vaccines.
The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway is vital for innate antiviral immunity, particularly against DNA viruses.

Purpose of the Study:

To elucidate the mechanisms by which ASFV proteins interfere with the cGAS-STING signaling pathway.
To identify specific ASFV proteins that target different components of the type I interferon response.
To provide insights into ASFV immune evasion strategies for vaccine development.

Main Methods:

Bioinformatic analysis of ASFV proteins and their potential interactions with host immune pathways.
Literature review of known ASFV proteins and their characterized functions.
Analysis of published data on the cGAS-STING pathway and its components (cGAS, STING, TBK1, IKKε, IRF3, NF-κB).

Main Results:

ASFV encodes multiple proteins that antagonize the cGAS-STING pathway to inhibit type I interferon production.
Specific proteins like QP383R, EP364R, C129R, and B175L target cGAS, cGAMP, and STING.
Other viral proteins interfere with downstream signaling molecules including TBK1, IKKε, IRF3, and NF-κB, thereby suppressing the antiviral immune response.

Conclusions:

ASFV employs a multi-pronged strategy to evade innate immunity by targeting the cGAS-STING pathway at various levels.
The identified viral proteins offer potential targets for therapeutic interventions and vaccine design against ASF.
Further research into these interactions can lead to a better understanding of ASFV pathogenesis and host-pathogen interactions.