数字农科院2.0

Porcine reproductive and respiratory syndrome virus nsp4-mediated β2M downregulation contributes to SLA-I decrease and virus infection in vivo and in vitro

文献类型： 外文期刊

作者： Lei Kang;Abdul Wahaab;Pengfei Qi;Yafeng Qiu;Jianchao Wei;Beibei Li;Donghua Shao;Zongjie Li;Ke Liu;Zhiyong Ma;Shuo Su

作者机构：

关键词： CTL;nsp4;Persistent infection;Porcine reproductive and respiratory syndrome virus;SLA-I;β2-microglobulin

期刊名称： Virology

ISSN： 0042-6822

年卷期： 2024 年 595 卷

页码：

收录情况： SCIE（2024版）

摘要： Porcine reproductive and respiratory syndrome virus (PRRSV) infection inhibits swine leukocyte antigen class I (SLA-I) expression in pigs, resulting in inefficient antigen presentation and subsequent low levels of cellular PRRSV-specific immunity as well as persistent viremia. We previously observed that the non-structural protein 4 (nsp4) of PRRSV contributed to inhibition of the β2-microglobulin (β2M) and SLA-I expression in cells. Here, we constructed a series of nsp4 mutants with different combination of amino acid mutations to attenuate the inhibitory effect of nsp4 on β2M and SLA-I expression. Almost all nsp4 mutants exogenously expressed in cells showed an attenuated effect on inhibition of β2M and SLA-I expression, but the recombinant PRRSV harboring these nsp4 mutants failed to be rescued with exception of the rPRRSV-nsp4-mut10 harboring three amino acid mutations. However, infection of rPRRSV-nsp4-mut10 not only enhanced β2M and SLA-I expression in both cells and pigs but also promoted the DCs to active the CD3+CD8+T lymphocytes more efficiently, as compared with its parental PRRSV (rPRRVS-nsp4-wt). These data suggested that the inhibition of nsp4-mediated β2M downregulation improved β2M/SLA-I expression in pigs.

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