Review highlights GP4's role in PRRSV, focusing on its structure, immune response, and vaccine potential.
Porcine reproductive and respiratory syndrome, a highly contagious disease, poses a severe threat to the global swine industry. Its causative agent, PRRSV, induces reproductive disorders (abortion, stillbirth) in pregnant sows and respiratory disease in piglets. The host immune system is disrupted by PRRSV, and no specific antiviral drugs are currently available. Thus, vaccination is regarded as the primary strategy for PRRS prevention and control. GP4, a key minor structural protein of PRRSV with an estimated molecular weight of 32 kDa, contains four conserved N-glycosylation sites at residues 37, 84, 120 and 130. Critical neutralizing epitopes are harbored in its extracellular domain (amino acids 40–79). PRRSV binding to the host CD163 receptor is mediated by GP4, which also regulates viral assembly and release, and induces protective immune responses. Hence, GP4 is identified as a central target for PRRS vaccine development. In this review, GP4’s structural characteristics, genetic evolution and interaction mechanisms are summarized. Its roles in viral life cycle, virulence, immune evasion and potential applications are discussed, providing a theoretical reference for PRRSV control.
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Zhang et al. (2026) studied this question.
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