Immunogenicity analysis of the E. coli expressed structural protein VP1 of persistent infection foot-and-mouth disease virus.

The persistent infection of FMDV in cloven hoofed animals has made the epidemic prevention and control more difficult. VP1 is the main immunogenic protein and first candidate of vaccine development for FMDV prevention. However, the mutation of VP1 in host cell with persistent infection FMDV (PI-FMDV) caused the change of its immunogenicity. Hence, it is imperative to establish the expression system for VP1 of PI-FMDV (PI-VP1) and re-evaluate its immunogenicity. In this study, the PI-VP1 with His-tag was cloned into pET-28a vector. PI-VP1 protein was expressed and purified in E. coli, and further the antiserum of immunized mice was analyzed. Results showed that purified PI-VP1 protein produced a good humoral and cellular immune response after immunizing mice. Furthermore, our study showed that the antiserum could not only neutralize PI-FMDV, but also prevent the adsorption of WT-FMDV. In summarize, our work provides valuable implications for the FMDV vaccines and therapeutics development.

Foot-and-mouth disease virus VP1 promotes viral replication by regulating the expression of chemokines and GBP1.

Foot-and-mouth disease virus (FMDV) is an acute, highly contagious, and economically destructive pathogen of vesicular disease that affects domestic and wild cloven-hoofed animals. The FMDV VP1 protein is an important part of the nucleocapsid and plays a significant role during FMDV infection. However, the signal pathways mediated by VP1 in the life cycle of FMDV and the related mechanisms are not yet fully understood. Here, we performed RNA-seq to compare gene expression profiles between pCAGGS-HA-VP1 transfected PK-15 cells and pCAGGS-HA (empty vector) transfected PK-15 cells. The results showed 5,571 genes with significantly different expression levels, of which 2,981 were up-regulated and 2,590 were down-regulated. GO enrichment analysis showed that 51 GO terms were significantly enriched in cell components including protein complex, membrane and organelle part. KEGG enrichment analysis showed 11 KEGG pathways were significantly enriched which were mainly related to the immune system, infectious viral disease, and signal transduction. Among the up-regulated genes, the chemokines such as CCL5, CXCL8, and CXCL10 in turn promoted FMDV replication. In contrast, GBP1, an interferon-stimulated gene that was suppressed by VP1 and FMDV, could effectively inhibit FMDV replication. Our research provides a comprehensive overview of the response of host cells to VP1 protein and a basis for further research to understand the roles of VP1 in FMDV infection including the genes involved in FMDV replication.