Zhang Liujun, Feng Xing, Chen Weizhen, Wang Bo, He Shaojun, Fan Hongjie, Liu Deyi
College of Animal Science, Anhui Science and Technology University, Chuzhou, China.
Front Vet Sci. 2024 Jun 19;11:1420466. doi: 10.3389/fvets.2024.1420466. eCollection 2024.
Porcine reproductive and respiratory syndrome (PRRS) caused by the PRRS virus (PRRSV) has been harming the pig industry worldwide for nearly 40 years. Although scientific researchers have made substantial efforts to explore PRRSV pathogenesis, the immune factors influencing PRRSV infection still need to be better understood. Infectious virus-antibody immune complexes (ICs) formed by PRRSV and sub-or non-neutralizing antibodies specific for PRRSV may significantly promote the development of PRRS by enhancing PRRSV replication through antibody-dependent enhancement. However, nothing is known about whether PRRSV infection is affected by non-infectious ICs (NICs) formed by non-pathogenic/infectious antigens and corresponding specific antibodies. Here, we found that PRRSV significantly induced the transcripts and proteins of interferon-α (IFN-α), IFN-β, IFN-γ, IFN-λ1, and tumor necrosis factor-α (TNF-α) primary porcine alveolar macrophages (PAMs) in the early stage of infection. Our results showed that NICs formed by rabbit-negative IgG (RNI) and pig anti-RNI specific IgG significantly reduced the transcripts and proteins of IFN-α, IFN-β, IFN-γ, IFN-λ1, and TNF-α PAMs and significantly elevated the transcripts and proteins of interleukine-10 (IL-10) and transforming growth factor-β1 (TGF-β1) PAMs. NICs-mediated PRRSV infection showed that NICs not only significantly decreased the induction of IFN-α, IFN-β, IFN-γ, IFN-λ1, and TNF-α by PRRSV but also significantly increased the induction of IL-10 and TGF-β1 by PRRSV and considerably enhanced PRRSV replication PAMs. Our data suggested that NICs could downregulate the production of antiviral cytokines (IFN-α/β/γ/λ1 and TNF-α) during PRRSV infection and facilitated PRRSV proliferation in its host cells by inhibiting innate antiviral immune response. This study elucidated one novel immune response to PRRSV infection, which would enhance our understanding of the pathogenesis of PRRSV.
由猪繁殖与呼吸综合征病毒（PRRSV）引起的猪繁殖与呼吸综合征（PRRS）在全球范围内危害养猪业已近40年。尽管科研人员为探索PRRSV发病机制付出了巨大努力，但影响PRRSV感染的免疫因素仍有待深入了解。PRRSV与PRRSV特异性亚中和或非中和抗体形成的感染性病毒-抗体免疫复合物（ICs）可能通过抗体依赖性增强作用促进PRRSV复制，从而显著推动PRRS的发展。然而，对于PRRSV感染是否受非致病性/感染性抗原与相应特异性抗体形成的非感染性ICs（NICs）影响，目前尚无定论。在此，我们发现PRRSV在感染早期能显著诱导原代猪肺泡巨噬细胞（PAMs）中干扰素-α（IFN-α）、IFN-β、IFN-γ、IFN-λ1和肿瘤坏死因子-α（TNF-α）的转录本和蛋白表达。我们的结果表明，兔阴性IgG（RNI）与猪抗RNI特异性IgG形成的NICs显著降低了PAMs中IFN-α、IFN-β、IFN-γ、IFN-λ1和TNF-α的转录本和蛋白表达，并显著提高了PAMs中白细胞介素-10（IL-10）和转化生长因子-β1（TGF-β1）的转录本和蛋白表达。NICs介导的PRRSV感染表明，NICs不仅显著降低了PRRSV对IFN-α、IFN-β、IFN-γ、IFN-λ1和TNF-α的诱导作用，还显著增加了PRRSV对IL-10和TGF-β1的诱导作用，并大大增强了PRRSV在PAMs中的复制。我们的数据表明，NICs可在PRRSV感染期间下调抗病毒细胞因子（IFN-α/β/γ/λ1和TNF-α）的产生，并通过抑制先天性抗病毒免疫反应促进PRRSV在其宿主细胞中的增殖。本研究阐明了一种针对PRRSV感染的新型免疫反应，这将增进我们对PRRSV发病机制的理解。
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