Abstract: The pathogenicity of porcine reproductive and respiratory syndrome virus (PRRSV) is usually not explained by one gene alone. It is shaped by several viral genes under a specific genomic background. Available studies show that virulence is linked with replication and transcription control, suppression of innate immunity, receptor usage, virion assembly, and recombination. Nsp9, nsp10, and nsp11 are important components of the replicase system. Nsp1α/β, nsp4, and nsp5 often support replication by weakening host antiviral signaling. Nsp2 is highly variable and is associated with assembly, inflammatory responses, and host reprogramming. Structural proteins such as GP2a/GP4, GP5/M, and N affect entry, particlestability, transmission adaptation, and host recognition. Because recombination, lineage replacement, and vaccine-related recombination are common in PRRSV, a single mutation or deletion does not always predict virulence. PRRSV pathogenicity should be evaluated together with replication efficiency, immune evasion, tissue tropism, and whole-genome background. Future work needs broader genome surveillance, functional tests in comparable genetic backgrounds, and targeted intervention of key virulence modules.