Origin and function of anti-interferon type I viral proteins

IF 2.8 3区医学 Q3 VIROLOGY

Virology Pub Date : 2025-02-20 DOI:10.1016/j.virol.2025.110456

Marta Acchioni , Chiara Acchioni , John Hiscott , Marco Sgarbanti

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引用次数: 0

Abstract

Type I interferons (IFN-I) are the most important innate immune cytokines produced by vertebrate host cells following, virus infection. Broadly speaking, detection of infecting viral nucleic acids by pattern recognition receptors (PRR) and subsequent downstream signaling triggers synthesis of a large number of IFN-I-stimulated genes (ISGs), endowed with diverse antiviral effector function. The co-evolution of virus-host interactions over million years has resulted in the emergence of viral strategies that target and inhibit host PRR-mediated detection, signal transduction pathways and IFN-I-mediated stimulation of ISGs. In this review, we illustrate the multiple mechanisms of viral immune evasion and discuss the co-evolution of anti-IFN-I viral proteins by summarizing key examples from recent literature. Due to the large number of anti-IFN-I proteins described, we provide here an evaluation of the prominent examples from different virus families. Understanding the unrelenting evolution of viral evasion strategies will provide mechanistic detail concerning these evolving interactions but will further enhance the development of tailored antiviral approaches.

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来源期刊

Virology 医学-病毒学

CiteScore

6.00

自引率

0.00%

发文量

157

审稿时长

50 days

期刊介绍： Launched in 1955, Virology is a broad and inclusive journal that welcomes submissions on all aspects of virology including plant, animal, microbial and human viruses. The journal publishes basic research as well as pre-clinical and clinical studies of vaccines, anti-viral drugs and their development, anti-viral therapies, and computational studies of virus infections. Any submission that is of broad interest to the community of virologists/vaccinologists and reporting scientifically accurate and valuable research will be considered for publication, including negative findings and multidisciplinary work.Virology is open to reviews, research manuscripts, short communication, registered reports as well as follow-up manuscripts.