Cell mediated innate responses of cattle and swine are diverse during foot-and-mouth disease virus (FMDV) infection: A unique landscape of innate immunity

Abstract

Pathogens in general and pathogenic viruses in particular have evolved a myriad of mechanisms to escape the immune response of mammalian species. Viruses that cause acute disease tend to bear characteristics that make them very contagious, as survival does not derive from chronicity of infection, but spread of disease throughout the herd. Foot-and-mouth disease virus (FMDV) is one of the most contagious viruses known. Upon infection of susceptible species, cloven-hoofed animals, the virus proliferates rapidly and causes a vesicular disease within 2-4 days. Disease symptoms resolve by 10 days to 2 weeks and in most cases, virus can no longer be detected. Periods of fever and viremia are usually brief, 1-3 days. In vivo control of virus infection and clearance of the virus during and following acute infection is of particular interest. The interaction of this virus with cells mediating the early, innate immune response has been analyzed in a number of recent studies. In most reports, the virus has a distinct inhibitory effect on the response of cells early in infection. Here we review these new data and discuss the dynamics of the interaction of virus with different cell types mediating the immune response to infection.

Foot-and-mouth disease virus structural protein VP3 degrades Janus kinase 1 to inhibit IFN-γ signal transduction pathways

“…2 FMDV induces a variety of host innate immune responses, which likely contributes to viral pathogenesis and/or influence the final outcome of viral infection in vitro and in vivo. 3 The innate immune response of the host is the first line of defense against viral infection until specific protection is established by the adaptive immune system. However, FMDV has evolved to counteract the host innate immune response.…”

Foot-and-mouth disease virus infection of dendritic cells triggers phosphorylation of ERK1/2 inducing class I presentation and apoptosis

“…It is known that FMDV interacts with DCs both in mice and in natural host [27,28]. However, the mechanisms involved in this interaction, are not well known.…”

Interplay of foot and mouth disease virus with cell‐mediated and humoral immunity of host

“…Bovine NK cells, like those of other species, have CD335 (natural cytotoxicity receptors), exhibit production of IFN‐γ, lyses of sensitive targets, and appear to have CD335 + /CD2 +/− /CD8 +/− /CD3 − phenotype. It has been shown that the NK cells isolated from cattle, infected with FMDV, have a high cytotoxicity level against the cells of bovine origin in vitro …”

“…Dendritic cells are responsible for scanning for antigens (including vaccine antigen) in the margins and directing them to the regions of lymph nodes concentrated with T cells to initiate immune responses. The maturation of APCs results in uptake of amplified antigen and presentation of viral peptides via MHC classes I and II molecules . These antigenic peptides on the surface of macrophages lead to the stimulation and maintenance of T cell response against FMD virus.…”

“…This increased expression of TLR4 coincides with the concurrent increase in mRNA levels of type I IFNs. This was unexpected because an RNA virus–like FMDV should offer ligands for TLR3 (which recognizes dsRNA, a replication intermediate in many RNA viruses) rather than TLR4, which causes transduction of signals after recognizing lipopolysaccharides from gram‐positive bacteria …”