MOE Joint International Research Laboratory of Animal Health and Food Safety, Engineering Laboratory of Animal Immunity of Jiangsu Province, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, People's Republic of China.
College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, People's Republic of China.
Emerg Microbes Infect. 2024 Dec;13(1):2341144. doi: 10.1080/22221751.2024.2341144. Epub 2024 Jun 18.
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.
由于当前全球新兴病毒的爆发，特别是 SARS-CoV-2 和 MPXV，公众的健康受到严重威胁。最近的研究表明，SARS-CoV-2 突变体（如奥密克戎）表现出更高的拮抗宿主固有免疫的能力，增加了它们在人类中的适应性和传染性。此外，目前对 MPXV 拮抗宿主固有免疫的策略的研究仍处于初始阶段。这些新兴病毒的多重威胁使得研究新兴病毒-宿主相互作用变得紧迫，特别是病毒对宿主抗病毒固有免疫的拮抗作用。有鉴于此，我们选择了几种对人类公共健康构成重大威胁的代表性病毒，并解释了这些病毒拮抗宿主抗病毒固有免疫的多种策略，希望为新兴病毒拮抗宿主抗病毒固有免疫的分子机制研究提供思路，并加速研究进展。流感病毒（IAV）、严重急性呼吸综合征冠状病毒 2（SARS-CoV-2）、严重急性呼吸综合征冠状病毒（SARS-CoV）、中东呼吸综合征冠状病毒（MERS-CoV）、埃博拉病毒（EBOV）、登革热病毒（DENV）、寨卡病毒（ZIKV）和人类免疫缺陷病毒（HIV）等是一些典型的病毒。研究表明，病毒可以通过直接或间接阻断抗病毒固有免疫信号通路来拮抗宿主抗病毒固有免疫。病毒前导宿主因子、宿主限制因子和 ncRNAs（microRNAs、lncRNAs、circRNAs 和 vtRNAs）在间接阻断抗病毒固有免疫信号通路中起重要作用。此外，病毒可能通过控制细胞凋亡、内质网应激、应激颗粒形成和代谢途径来拮抗固有免疫。这些调控机制包括转录调控、翻译后调控、阻止复合物形成、阻碍核转位、切割、降解和表观遗传调控。
