基于RNAi的抗病毒免疫

doi:10.16288/j.yczz.25-077

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Hereditas(Beijing) ›› 2025, Vol. 47 ›› Issue (8): 876-884.doi: 10.16288/j.yczz.25-077

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RNAi-based antiviral immunity

Deyu Xu¹^,²(), Xi Zhou¹^,²(), Yujie Ren²()

1. School of Life Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China，Hefei 230027, China
2. State Key Laboratory of Virology and Biosafety, Wuhan Institute of Virology, Chinese Academy of Sciences，Wuhan 430072, China

Received:2025-03-18 Revised:2025-06-24 Online:2025-08-20 Published:2025-07-04
Contact: Xi Zhou, Yujie Ren E-mail:xudeyu@mail.ustc.edu.cn;zhouxi@wh.iov.cn;renyujie@wh.iov.cn
Supported by:
National Natural Science Foundation of China(82472274)

Abstract

Abstract:

RNA interference (RNAi) is a gene silencing mechanism mediated by small RNAs derived from double-stranded RNA (dsRNA), capable of silencing specific genes. Following viral invasion, the dsRNA produced during viral replication is cleaved by the host cell’s Dicer protein, generating virus-derived small interfering RNAs (virus-derived small interference RNAs, vsiRNA). These vsiRNAs then guide the cleavage and degradation of viral RNA via the RNAi pathway, exerting an antiviral effect. Therefore, RNAi is also recognized as an efficient antiviral immune pathway during viral infection. However, through long-term evolution, viruses have developed various strategies to counteract RNAi. For instance, they encode specific viral suppressors of RNAi (VSRs) that target and antagonize key molecules in this pathway. Research indicates that designing drugs to specifically target VSRs can “unlock” the antiviral function of RNAi within host cells, demonstrating highly potent and relatively broad-spectrum antiviral activity. Furthermore, viral infection can also be regulated by host- or virus-derived microRNAs (miRNAs). The role of miRNAs in viral infection provides new targets for antiviral therapy. In this review, we summarize the mechanism of RNAi in antiviral immunity, recent research advances, and its application prospects in antiviral therapy, aiming to provide theoretical support for antiviral immunity research and treatment.

Key words: siRNA, miRNA, antiviral, VSR

Deyu Xu, Xi Zhou, Yujie Ren. RNAi-based antiviral immunity[J]. Hereditas(Beijing), 2025, 47(8): 876-884.

Figures/Tables 2

Fig. 1

Table 1

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VSR分类	作用机制	举例	相关病毒宿主	参考文献
Dicer靶向	与Dicer-2结合，作用于其RNase III结构域，抑制该结构域对双链RNA的切割活性，使得dsRNA无法被有效切割为siRNA	武汉野田村病毒(Wuhan Nodavirus，WhNV)的B2蛋白、DENV的NS4B蛋白等	蚊虫(Culicidae)、猪(Sus scrofa domesticus)、人(Homo sapiens)	[40,41]
dsRNA靶向	与dsRNA结合，抑制Dicer对dsRNA切割加工成vsiRNA的过程	猫疱疹病毒(feline herpesvirus，FHV)、NoV和WhNV的B2蛋白、A型流感病毒(influenza A virus，IAV)的非结构蛋白NS1、EV71的3A蛋白等	家猫(Felis catus)、蚊虫、猪、野生水禽、家禽、人	[2,42,43]
vsiRNA靶向	与vsiRNA结合，使其无法正常组装进RISC，或者干扰RISC的正常功能，使得vsiRNA无法发挥其正常功能	番茄丛生矮化病毒(tomato bushy stunt virus，TBSV)的P19、柯萨奇病毒B3(coxsackievirus B3，CVB3)的13A、风疹病毒(Rubella virus，RUV)的Capsid等	烟草(Nicotiana tabacum)、番茄(Solanum lycopersicum)等茄科植物；人	[44~46]
AGO靶向	抑制AGO2的切割活性，使得RISC无法靶向切割病毒mRNA	黑腹果蝇诺拉病毒(Drosophila melanogaster Nora virus，DmelNV)的病毒蛋白1(VP1)、蟋蟀麻痹病毒(cripavirus，CrPV)1A蛋白	黑腹果蝇(Drosophila melanogaster)、蟋蟀(Gryllulus)等	[47,48]

RNAi-based antiviral immunity

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