PRRSV致病基因研究进展OA
Research progress in pathogenic genes of PRRSV
猪繁殖与呼吸综合征病毒(PRRSV)的致病性并非由某个基因单独造成的,而是在全基因组背景下由多个基因共同影响.研究表明,病毒毒力与复制转录调控、先天免疫抑制、受体识别利用及基因重组等关键生物学过程密切相关.非结构蛋白nsp9、nsp10和nsp11构成复制酶系统核心功能单元,是病毒复制的关键组分;nsp1α/β、nsp4和nsp5可通过抑制宿主抗病毒信号为病毒复制创造条件.nsp2是变异程度最高的蛋白之一,不仅参与基因重组和病毒装配,也与炎症反应增强、宿主生理状态改变直接相关.GP2a/GP4、GP5/M及N等结构蛋白,主要调控病毒入侵、病毒粒子稳定性、传播适应性及宿主识别等环节.受基因重组、谱系更替和疫苗株相关重组等因素影响,单一基因位点很难直接对应毒力表型强弱.因此,PRRSV致病性需整合复制效率、免疫逃逸、组织嗜性及全基因组背景开展综合分析.未来研究方向可聚焦于PRRSV强化全基因组分子检测,构建同源遗传背景,开展精准功能验证,并围绕核心毒力调控模块开展靶向干预研究.
The pathogenicity of porcine reproductive and respiratory syndrome virus(PRRSV)is usually not explained by one gene alone.It is shaped by several viral genes under a specific genomic background.Available studies show that virulence is linked with replication and transcription control,suppression of innate immunity,receptor usage,virion assembly,and recombination.Nsp9,nsp10,and nsp11 are important components of the replicase system.Nsp1 a/β,nsp4,and nsp5 often support replication by weakening host antiviral signaling.Nsp2 is highly variable and is associated with assembly,inflammatory responses,and host reprogramming.Structural proteins such as GP2a/GP4,GP5/M,and N affect entry,particle stability,transmission adaptation,and host recognition.Because recombination,lineage replacement,and vaccine-related recombination are common in PRRSV,a single mutation or deletion does not always predict virulence.PRRSV pathogenicity should be evaluated together with replication efficiency,immune evasion,tissue tropism,and whole-genome background.Future work needs broader genome surveillance,functional tests in comparable genetic backgrounds,and targeted intervention of key virulence modules.
李林;许光勇;董虹
北京农学院兽医学(中医药)北京市重点实验室,北京 102206北京中育种猪有限责任公司,北京 100194北京农学院兽医学(中医药)北京市重点实验室,北京 102206
农业科技
猪繁殖与呼吸综合征病毒(PRRSV)致病基因毒力决定免疫逃逸重组
PRRSVpathogenic genesvirulence determinantsimmune evasionrecombination
《中国猪业》 2026 (2)
23-30,8
国家自然科学基金项目(32373058)北京市家畜创新团队项目(BAIC05-2026)
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