International Journal of Molecular Veterinary Research, 2025, Vol.15, No.1, 32-42 http://animalscipublisher.com/index.php/ijmvr 35 4 Host Immune Response and Immunoregulation in PRRSV Infection 4.1 Innate immune response and inhibition of interferon pathways PRRSV is capable of evading and inhibiting the host's innate immune system through various mechanisms, notably inhibiting type I interferon (IFN) response. The virus inhibits pattern recognition receptor-mediated signaling pathways including RIG-I-like receptors and MDA5 by viral protein such as Nsp5, which degrades critical signaling molecules through ER-phagy, and through autophagic degradation of MDA5 by P62 and CCT2 pathways. This results in ineffective IFN production and ablated antiviral state in infected macrophages. PRRSV also co-opts key central immune regulators like MALT1 to neutralize antiviral RNases, additionally repressing innate reactions. While some innate immune modules are induced at an early stage after infection, the response overall is moderate and slow, causing persistence of the virus and vulnerability to secondary infection (Bocard et al., 2021; Chaudhari et al., 2021) (Figure 1). 4.2 Features of adaptive immune responses The adaptive immune response against PRRSV is characterized by slow and weak induction of neutralizing antibody and T-cell responses. The humoral immunity is characterized by early, late and low-level production of neutralizing antibodies and production of non-neutralizing antibodies. The cellular immunity, particularly the CD8+ T cell response, is delayed with effector and cytolytic gene expression occurring weeks after infection. Regulatory T cells are triggered, and antigen presentation is blocked, additionally undermining the adaptive response. PRRSV genetic diversity and extensive viral protein glycosylation lead to epitope shielding and immune evasion, making sterilizing immunity impossible and vaccine design challenging (Bocard et al., 2021; Lagumdzic et al., 2023). 4.3 Immunosuppression and reprogramming of the immune system induced by prrsv infection PRRSV infection induces profound immunosuppression and remodeling of the host immune response. The virus promotes negative immune response regulators and markers of T-cell exhaustion (e.g., PD-L1, IL-10, NF-κB inhibitors) in infected macrophages to promote an immunosuppressive microenvironment. Upregulation of cytokine expression, including upregulated IL-10 and downregulated IL-4, as well as induction of regulatory T cells also lead to impaired immune clearance and increased co-infection susceptibility. PRRSV modulation of host microRNAs and non-coding RNAs also affects immune cell function and apoptosis to augment immunosuppression and chronic infection (Bocard et al., 2021; Chaudhari et al., 2021; Du et al., 2025). 4.4 Relationship Between Immune Response Differences and Viral Persistence Differences in the host immune response, including the level and timing of innate and adaptive immunity, are related directly to PRRSV persistence. Abrogated and delayed IFN and T-cell responses and induction of immune checkpoint molecules and regulatory pathways allow the virus to sustain persistence in lymphoid tissues for months. Higher pathogenic PRRSV strains induce greater IFN and inflammatory responses but possibly also greater immune dysregulation and tissue damage. The inability to generate rapid, robust, and coordinated immune responses is among the most critical determinants of the establishment of persistent infection and failure to evoke sterilizing immunity (Bocard et al., 2021; Chaudhari et al., 2021; Zhang et al., 2024) (Figure 2). 5 Advances in Molecular Diagnostic Techniques for PRRSV 5.1 Traditional diagnostic methods The conventional methods of detecting PRRSV are virus isolation, ELISA, and immunofluorescence assays. The gold standard is virus isolation, which involves the cultivation of PRRSV in permissive cells such as porcine alveolar macrophages or MARC-145 cells. While extremely specific, it is labor-intensive (1-2 weeks), and will not work with low-titer field samples. ELISA is used for the serological surveillance because it is the method of high-throughput detection of PRRSV-specific antibodies. ELISA, however, cannot distinguish between antibodies resulting from infection and those resulting from vaccination, and sensitivity also varies based on commercial kits. Immunofluorescence assays (IFA) and immunoperoxidase monolayer assays (IPMA) similarly detect antigens but are technology and expertise-intensive (Chae et al., 2023).
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