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Porcine reproductive and respiratory syndrome virus (PRRSV) is a highly contagious, enveloped, single-stranded positive-sense RNA virus belonging to the family Arteriviridae (Snijder et al., 2013). The CH-1a strain is historically significant as the first PRRSV strain isolated in China in 1996, representing the North American genotype (Type 2) (Kuang et al., 2009). The virus primarily targets porcine alveolar macrophages, leading to severe reproductive failure in pregnant sows and respiratory distress in growing pigs, which causes substantial economic losses globally (Lunney et al., 2016). PRRSV is characterized by its high genetic variability and its ability to modulate the host's innate immune response, particularly by suppressing type I interferon production (Nan et al., 2017). Therapeutic strategies focus on the use of viral antigens in modified live or inactivated vaccines to elicit protective immunity, although the virus's capacity for rapid evolution and recombination remains a major challenge for vaccine efficacy (Du et al., 2017).
Vaccines utilize viral antigens to induce humoral and cellular immune responses, while antivirals typically inhibit viral RNA synthesis or entry into host macrophages.
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