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Foot-and-mouth disease virus (FMDV) continues to be a significant economic problem worldwide. Control of the disease involves the use of killed-virus vaccines, a control measure developed decades ago. After natural infection, the primary site of replication of FMDV is the pharyngeal area, suggesting that a mucosal immune response is the most effective. Humoral immunity to killed-virus vaccination induces antibodies that can prevent the clinical disease but not local infection. Determining whether infection or vaccination stimulates IgA-mediated local immunity depends on the method of analysis. Different assays have been described to analyze the quality of antibody responses of cattle and swine to FMDV, including indirect double-antibody sandwich enzyme-linked immunosorbent assay (IDAS-ELISA) and antibody capture assay-ELISA (ACA-ELISA). We tested these assays on swine and show that vaccinated animals had FMDV-specific IgM and IgG but no IgA in either serum or saliva. After the infection, both assays detected FMDV-specific IgM, IgG, and IgA in serum. Notably, serum IgA was more readily detected using the ACA-ELISA, whereas IgA was not detected in saliva with this assay. FMDV-specific IgA antibodies were detected in saliva samples using the IDAS-ELISA. These data show that parenterally administered, killed-virus vaccine does not induce a mucosal antibody response to FMDV and illuminates limitations and appropriate applications of the two ELISAs used to measure FMDV-specific responses. Further, the presence of the IgA antivirus in serum correlates with the presence of such antibodies in saliva.

Viruses have evolved multiple mechanisms to evade the innate immune response, particularly the actions of interferons (IFNs). We have previously reported that exposure of dendritic cells (DCs) to foot-and-mouth disease virus (FMDV) in vitro yields no infection and induces a strong type I IFN (IFN-alpha and IFN-beta) response, indicating that DCs may play a critical role in the innate response to the virus. In vivo, FMDV induces lymphopenia and reduced T-cell proliferative responses to mitogen, viral effects that may contribute to evasion of early immune responses. In this study we analyzed the in vivo effects of FMDV infection on the IFN-alpha response of two populations of dendritic cells. During the acute phase of infection of swine, production of IFN-alpha from monocyte-derived DCs (MoDCs) and skin-derived DCs (skin DCs) is inhibited. This effect occurs concurrently with rising viral titers in the blood; however, these cells are not productively infected. Interestingly, there are no changes in the capability of these DCs to take up particles and process antigens, indicating that antigen-presenting cell function is normal. These data indicate that inhibition of the IFN-alpha response of dendritic cell populations from blood and skin by FMDV enhances viral pathogenesis in infected animals.

Foot and mouth disease virus (FMDV) is a picornavirus that causes an acute vesicular disease of cloven-hoofed animals. This virus continues to be a threat to livestock worldwide with outbreaks causing severe economic losses. The present study shows an analysis of immune system phenotype and function during the acute phase of FMDV infection in swine. In the first days of infection, a significant lymphopenia is observed that involves all T cell subsets, CD4(+), CD8(+), and CD4(+)/CD8(+). This marked lymphopenia is not a result of active infection of PBMC with the virus. Further, the response of residual peripheral blood T cells to the mitogen, Concanavalin A (ConA) is significantly reduced and occasionally eliminated. Animals usually resolve clinical signs of disease and develop antigen specific T cell responses to the virus and recover ConA reactivity. These characteristics of acute phase infection likely play an important role in viral pathogenesis, propagation and shedding of viral particles and may be targeted as a way of improving vaccine formulations.