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Porcine reproductive and respiratory syndrome virus (PRRSV) is a small, enveloped, single-stranded positive-sense RNA virus that belongs to the family Arteriviridae and is the causative agent of PRRS in swine (Lunney et al., 2016). The virus primarily targets porcine alveolar macrophages, utilizing host receptors such as CD163 and SIGLEC1 for attachment and internalization (Zhang and Yoo, 2015). Immune system activation occurs when the host recognizes viral antigens, particularly the major envelope glycoprotein 5 (GP5), the membrane protein (M), and the nucleocapsid protein (N), which are critical for inducing neutralizing antibodies and T-cell responses (Du et al., 2017). However, PRRSV is notorious for its ability to evade the host immune system through mechanisms like glycan shielding and the inhibition of type I interferon production, leading to delayed and often ineffective immune clearance (Sun et al., 2018). Vaccines, including modified live virus (MLV) and inactivated versions, aim to prime the immune system against these antigens, but their efficacy is often limited by the high genetic diversity of the virus and the risk of antibody-dependent enhancement (Nan et al., 2017).
Induction of humoral and cellular immune responses through the presentation of viral structural antigens (GP5, M, N) to host lymphocytes to generate neutralizing antibodies and T-cell immunity.
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