Genetic characterization and pathogenicity of a novel recombinant PRRSV from lineage 1, 8 and 3 in China failed to infect MARC-145 cells

文献类型： 外文期刊

第一作者： Li, Yang

作者： Li, Yang;Jiao, Dian;Jing, Yang;He, Yuan;Han, Weiguo;Li, Zhiwei;Feng, Yingtong;Xiao, Shuqi;Ma, Zhiqian

作者机构：

关键词： Porcine reproductive and respiratory syndrome; virus (PRRSV); NADC30-like; Recombination; Pathogenicity; Cell tropism

期刊名称：MICROBIAL PATHOGENESIS （ 影响因子：3.848； 五年影响因子：3.957 ）

ISSN： 0882-4010

年卷期： 2022 年 165 卷

页码：

收录情况： SCI

摘要： The diversity of porcine reproductive and respiratory syndrome virus (PRRSV) in China is increasing rapidly along with mutation and recombination. Recombination could occur between inter-and intra-lineage of PRRSV, which accelerated the complexity of pathogenicity and cell tropism of the recombinant strain. In the present study, a novel PRRSV strain named HN-YL1711 was isolated from a pig farm suffering from severe respiratory difficulty in Henan province, China. The whole genomic sequence analysis indicated that the genome of HN-YL1711 was 15018 nt. It shared 86%, 87.3%, 88.1%, 91.1%, 84.2%, and 84.1% nucleotide similarities with PRRSVs VR2332, CH1a, JXA1, NADC30, QYYZ, and GM2, respectively. Based on phylogenetic analysis of Nsp2, ORF5 and complete genomes, HN-YL1711 was classified into lineage 1 of PRRSV. However, seven genomic break points were detected in recombination analysis, which indicated that the HN-YL1711 originated from multiple recombination among NADC30-like (major parent, lineage 1), JXA1-like (minor parent, lineage 8), and QYYZ-like (minor parent, lineage 3) PRRSV. Porcine alveolar macrophages (PAMs), 3D4/21-CD163 and MARC-145 cells were used to explore the viral adaptation of HN-YL1711. The results indicated that it could infect the PAMs but failed to infect MARC-145 cells. Challenge experiments showed that HN-YL1711 exhibits intermediate virulence in pigs, compared with HP-PRRSV JXA1 and LP-PRRSV CH1a. Taken together, our findings suggest that recombination remains an important factor in PRRSV evolution and that recombination further complicates the cell tropism and pathogenicity of PRRSV.

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