Like all pathogens, foot-and-mouth disease virus (FMDV) is recognized by the immune system inducing a heightened immune response mainly mediated by type I and type III IFNs. To overcome the strong antiviral response induced by these cytokines, FMDV has evolved many strategies exploiting each region of its small RNA genome. These include: (a) inhibition of IFN induction at the transcriptional and translational level, (b) inhibition of protein trafficking; (c) blockage of specific post-translational modifications in proteins that regulate innate immune signaling; (d) modulation of autophagy; (e) inhibition of stress granule formation; and (f) modulation of immune cell function. Here, we summarize and discuss FMDV virulence factors and the host immune footprint that characterize infection in cell culture and in the natural hosts.
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| http://dx.doi.org/10.3389/fmicb.2018.02644 | DOI Listing |
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John Brooksby was an outstanding Scottish veterinary virologist who worked at the Pirbright Institute (Pirbright) for 40 years, including 16 as the institute's director. He devised quantitative methods for measuring neutralising antibodies and perfected a complement fixation test for the diagnosis, typing and strain differentiation of foot and mouth disease (FMD), especially when combined with neutralisation. He identified four of the seven types of FMD virus (FMDV) and many subtypes.
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