关键词: Emerging viruses IAV SARS-CoV-2 antagonism host antiviral innate immunity interferon production interferon responses

Mesh : Humans Immunity, Innate SARS-CoV-2 / immunology Host-Pathogen Interactions / immunology Virus Diseases / immunology virology COVID-19 / immunology virology Animals Communicable Diseases, Emerging / virology immunology

来  源:   DOI:10.1080/22221751.2024.2341144   PDF(Pubmed)

Abstract:
The public\'s health is gravely at risk due to the current global outbreak of emerging viruses, specifically SARS-CoV-2 and MPXV. Recent studies have shown that SARS-CoV-2 mutants (such as Omicron) exhibit a higher capability to antagonize the host innate immunity, increasing their human adaptability and transmissibility. Furthermore, current studies on the strategies for MPXV to antagonize the host innate immunity are still in the initial stages. These multiple threats from emerging viruses make it urgent to study emerging virus-host interactions, especially the viral antagonism of host antiviral innate immunity. Given this, we selected several representative viruses that significantly threatened human public health and interpreted the multiple strategies for these viruses to antagonize the host antiviral innate immunity, hoping to provide ideas for molecular mechanism research that emerging viruses antagonize the host antiviral innate immunity and accelerate the research progress. The IAV, SARS-CoV-2, SARS-CoV, MERS-CoV, EBOV, DENV, ZIKV, and HIV are some of the typical viruses. Studies have shown that viruses could antagonize the host antiviral innate immunity by directly or indirectly blocking antiviral innate immune signaling pathways. Proviral host factors, host restriction factors, and ncRNAs (microRNAs, lncRNAs, circRNAs, and vtRNAs) are essential in indirectly blocking antiviral innate immune signaling pathways. Furthermore, via controlling apoptosis, ER stress, stress granule formation, and metabolic pathways, viruses may antagonize it. These regulatory mechanisms include transcriptional regulation, post-translational regulation, preventing complex formation, impeding nuclear translocation, cleavage, degradation, and epigenetic regulation.
摘要:
由于当前全球爆发的新兴病毒,公众的健康处于严重危险之中,特别是SARS-CoV-2和MPXV。最近的研究表明,SARS-CoV-2突变体(如Omicron)表现出更高的拮抗宿主先天免疫的能力,增加它们对人类的适应性和可传播性。此外,目前关于MPXV拮抗宿主先天性免疫的策略研究仍处于起步阶段。这些来自新兴病毒的多重威胁使得研究新兴病毒与宿主的相互作用成为当务之急,尤其是病毒对宿主抗病毒先天免疫的拮抗作用。鉴于此,我们选择了几种显著威胁人类公共健康的代表性病毒,并解释了这些病毒拮抗宿主抗病毒先天性免疫的多种策略,希望为新兴病毒拮抗宿主抗病毒先天免疫的分子机制研究提供思路,加速研究进展。IAV,SARS-CoV-2,SARS-CoV,MERS-CoV,EBOV,DENV,ZIKV,艾滋病毒是一些典型的病毒。研究表明,病毒可以通过直接或间接阻断抗病毒先天性免疫信号通路来拮抗宿主抗病毒先天性免疫。前病毒宿主因子,宿主限制因素,和ncRNAs(microRNAs,lncRNAs,circRNAs,和vtRNA)在间接阻断抗病毒先天免疫信号通路中至关重要。此外,通过控制细胞凋亡,ER压力,应力颗粒形成,和代谢途径,病毒可能会拮抗它。这些调控机制包括转录调控,翻译后调节,防止复合物形成,阻碍核移位,乳沟,降解,和表观遗传调控。
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