Porcine Rotavirus: pathogenic mechanisms, host immune responses, and progress toward control

Porcine Rotavirus (PoRV), a major pathogen causing diarrhea in piglets and significant economic losses, exhibits high genotypic diversity and poses a risk of cross-species transmission. PoRV infection is initiated by the interaction of its outer capsid proteins, VP4 and VP7, with multiple host cell receptors (e.g., sialic acids, integrins), triggering complex processes of endocytosis and membrane penetration that ultimately lead to enterocyte dysfunction and diarrhea. Diverse immune evasion strategies have been evolved by PoRV, among which the host interferon responses and cellular protein synthesis are both suppressed by nonstructural proteins including NSP1 and NSP3. Host defense relies on innate immunity (e.g., RIG-I/MDA-5 and TLR3 signaling pathways) and adaptive immunity centered on virus-specific T cells. Epidemiological surveillance indicates the dominance of RVA genotypes in swine populations worldwide. Furthermore, genetic reassortment events between porcine and human strains underscore a significant zoonotic transmission risk, which poses a significant challenge to public health and compromises the efficacy of existing vaccines. Current control measures rely on biosecurity management and vaccination to enhance maternal antibody transfer. However, given the high genetic variability of the virus, the development of novel broad-spectrum vaccine platforms, such as those based on virus-like particles (VLPs) or multi-epitope antigens, is urgently needed. In this review, current research progress is systematically integrated to advance the understanding of PoRV-host interactions and provide evidence-based guidance for the development of effective control strategies.