Porcine reproductive and respiratory syndrome virus (PRRSV) is a significant threat to the global swine industry. Porcine sialoadhesin (poSn) has been previously shown to mediate PRRSV attachment and internalization. In the current study, we report its unidentified role in antagonism of type I interferon (IFN) production during PRRSV infection. We determined that poSn facilitated PRRSV infection via inhibition of type I IFN transcription. Mechanistically, poSn interacted with a 12 kDa DNAX-activation protein (DAP12), which was dependent on residues 51-57 within DAP12 transmembrane domain (TMD). PRRSV exploited the poSn-DAP12 pathway to attenuate activation of nuclear factor-kappa B (NF-κB). More importantly, the poSn-DAP12 pathway was involved in inhibiting poly (I:C)-triggered IFN production. All these results reveal a novel role of poSn in suppressing host antiviral responses, which deepens our understanding of PRRSV pathogenesis.

中文翻译：

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猪唾液酸粘附素抑制I型干扰素产生，以支持猪生殖和呼吸综合征病毒感染。

猪繁殖与呼吸综合症病毒（PRRSV）对全球养猪业构成重大威胁。先前已显示猪唾液酸粘附素（poSn）介导PRRSV的附着和内在化。在当前的研究中，我们报告了其在PRRSV感染过程中对I型干扰素（IFN）产生拮抗作用中的未知作用。我们确定poSn通过抑制I型IFN转录促进PRRSV感染。从机理上讲，poSn与12 kDa DNAX激活蛋白（DAP12）相互作用，该蛋白依赖于DAP12跨膜结构域（TMD）中的51-57位残基。PRRSV利用poSn-DAP12途径来减弱核因子-κB（NF-κB）的激活。更重要的是，poSn-DAP12途径参与了抑制多聚（I：C）触发的IFN产生。