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The Different Tactics of Foot-and-Mouth Disease Virus to Evade Innate Immunity
Gisselle N Medina1,2, Fayna Díaz-San Segundo1,3, Carolina Stenfeldt1,4
1Plum Island Animal Disease Center, United States Department of Agriculture, Agricultural Research Service, Orient, NY, United States.
Abstract:
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) in vivo 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.
Insights
Foot-and-mouth disease virus (FMDV) evades the host immune system by employing numerous strategies to inhibit interferon (IFN) responses. This review details FMDV virulence factors and the host immune response during infection.
Area of Science:
- Virology
- Immunology
- Molecular Biology
Background:
- Foot-and-mouth disease virus (FMDV) triggers a potent immune response, primarily involving type I and type III interferons (IFNs).
- FMDV has developed sophisticated mechanisms to counteract these host antiviral defenses.
Purpose of the Study:
- To summarize and discuss the virulence factors of FMDV.
- To elucidate the host immune footprint characterizing FMDV infection.
Main Methods:
- Review of existing literature on FMDV immune evasion strategies.
- Analysis of host-pathogen interactions in cell culture and natural hosts.
Main Results:
- FMDV inhibits IFN induction transcriptionally and translationally.
- FMDV interferes with protein trafficking, post-translational modifications, autophagy, and stress granule formation.
- FMDV modulates immune cell function both in vitro and in vivo.
Conclusions:
- FMDV utilizes diverse strategies across its genome to overcome host antiviral immunity.
- Understanding these FMDV virulence factors is crucial for characterizing host immune responses during infection.
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