Highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) evades cytotoxic T lymphocyte (CTL) responses through interactions between viral Nsp1α and Nsp4 and β2 M heavy and light chains, respectively, of swine leukocyte antigen class (SLA)-I. However, whether the immunoproteasome (i-proteasome) complex, which is an important component of the antigen delivery pathway that functions by mediating peptide production, is also affected by viral infection is unknown. In this study, we investigated the effects of HP-PRRSV (HuN4-F5) infection on IFN-γ-induced i-proteasome expression using a cell culture system (alveolar macrophages, AMs). We found that this virus inhibited the expression of IFN-γ-induced i-proteasome subunits LMP2, LMP7, and MECL-1 at the mRNA and protein level. In addition, expression levels of the i-proteasome regulatory subunits PSME1 and PSME2 in the HP-PRRSV HuN4-F5-infected group were also significantly decreased compared to those in the uninfected group. However, there was no significant difference in the expression of proteasome subunits PSMB5, PSMB6, and PSMB7 between HP-PRRSV HuN4-F5-infected and uninfected groups. This study provides insight into the mechanisms underlying immune regulation by HP-PRRSV; specifically, this virus affects the antigen-processing machinery by suppressing IFN-γ-induced i-proteasome expression in infected AMs.

高致病性猪繁殖与呼吸综合征病毒（HP-PRRSV）通过猪白细胞抗原类别（SLA）-I的病毒Nsp1α与Nsp4和β2M重链和轻链之间的相互作用逃避了细胞毒性T淋巴细胞（CTL）的反应。然而，尚不清楚免疫蛋白酶体（i-蛋白酶体）复合物是否是病毒介导的，该复合物是通过介导肽产生起作用的抗原传递途径的重要组成部分。在这项研究中，我们调查了使用细胞培养系统（肺泡巨噬细胞，AM）对HP-PRRSV（HuN4-F5）感染对IFN-γ诱导的i-蛋白酶体表达的影响。我们发现，该病毒在mRNA和蛋白质水平上抑制了IFN-γ诱导的i-蛋白酶体亚基LMP2，LMP7和MECL-1的表达。此外，与未感染组相比，HP-PRRSV HuN4-F5感染组中i-蛋白酶体调节亚基PSME1和PSME2的表达水平也显着降低。但是，HP-PRRSV HuN4-F5感染组和未感染组之间蛋白酶体亚基PSMB5，PSMB6和PSMB7的表达没有显着差异。这项研究提供了对HP-PRRSV免疫调节基础机制的见解；具体而言，该病毒通过抑制受感染AM中IFN-γ诱导的i-蛋白酶体表达来影响抗原加工机制。HP-PRRSV HuN4-F5感染和未感染组之间的PSMB7和PSMB7。这项研究提供了对HP-PRRSV免疫调节基础机制的见解；具体而言，该病毒通过抑制受感染AM中IFN-γ诱导的i-蛋白酶体表达来影响抗原加工机制。HP-PRRSV HuN4-F5感染和未感染组之间的PSMB7和PSMB7。这项研究提供了对HP-PRRSV免疫调节基础机制的见解；具体而言，该病毒通过抑制受感染AM中IFN-γ诱导的i-蛋白酶体表达来影响抗原加工机制。