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

Figures

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  Figure 1. Porcine Rotavirus (PoRV) invasion and replication: PoRV attaches to sialic acid (SA) or histo-blood group antigens (HBGAs) on the host cell surface, interacts with integrins and Hsc70 receptors, and mediates the endocytosis pathway via dynamin and cholesterol-dependent lattice proteins. DLP are released into the cytoplasm, where they undergo mRNA transcription, DLP bind to NSP4 and bud out into the ER, where transient membranes are removed and the TLP mature as the VP4 and VP7 proteins are assembled. The progeny virions are released from the cell via cell lysis or a Golgi-independent non-classical vesicular transport mechanism in polarized epithelial cells.

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  Figure 2. Pattern recognition receptor (PRR) signaling pathways and PoRV immune evasion mechanisms: During infection, host pattern recognition receptors (RIG-I/MDA-5, TLR3/7) recognize viral RNA to activate IFN production and the JAK–STAT signaling pathway, inducing antiviral states and immune regulatory responses. PoRV counteracts these defense mechanisms by degrading key signaling molecules through viral proteins (e.g., NSP1, VP3), thereby disrupting interferon synthesis and response pathways.

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  Figure 3. Immune response triggered by PoRV infection: PoRV invasion and replication disrupt epithelial integrity, triggering cytokine release (e.g., IL-8, IL-15) to recruit and activate dendritic cells (DCs) and macrophages. Activated antigen-presenting cells secrete proinflammatory mediators (TNF-α, IL-6, IL-1β) and type I interferons (IFN-α/β). Dendritic cells initiate primary T cell activation through multiple cytokines, driving the differentiation of CD4 + helper T cells and CD8 + cytotoxic T lymphocytes. CD4 + T cells assist B cell activation via cytokines like IFN-γ to produce immunoglobulins. Concurrently, protective pathways such as the TLR5/IL-22 axis are activated to enhance epithelial barrier repair.

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  Figure 4. PoRV VP3 protein disrupts the RNase L antiviral pathway.

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  Figure 5. Comparison of gut microbiota-mediated defense mechanisms against PoRV infection: PoRV infection disrupts epithelial barrier function and induces inflammatory cytokine secretion. Probiotics enhance barrier integrity through competitive exclusion and immunomodulation, thereby limiting PoRV invasion and pathogenic effects. SFB exerts protective effects via non-immune mechanisms by directly promoting epithelial cell renewal and migration, accelerating the physical shedding of susceptible intestinal cells.