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Viruses can both induce and target RNA silencing, and have evolved a number of strategies to overcome RNA-silencing mediated host defence mechanisms via their multifunctional proteins, some of which can act as suppressors of RNA silencing (VSR), and which are also able to interfere with host miRNA pathways leading to disease induction and symptoms [reviewed in 13].
To counteract the silencing mediated host defence, plant viruses encode various viral RSSs [ 15].
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β-FXIIa is also able to activate the classic complement system pathway via C1r and to a lesser extent C1 s linking haemostasis and complement-mediated host defence [3].
However, emerging evidence implicates some copper transport proteins in macrophage-mediated host defence.
Such effects are likely to be an important component of zinc-mediated host defence.
These proteins are thus likely to play a role in phagocyte-mediated host defence.
Many of the copper transport genes have also been implicated in macrophage-mediated host defence (e.g. CTR1, CTR2, ATP7A, CP).
Hence, zinc may contribute to macrophage-mediated host defence through promoting inflammasome activation, in addition to regulating TLR responses.
It is also possible that inducible copper redistribution contributes to macrophage-mediated host defence by promoting the export of iron (discussed below).
Given the crucial role of this cytokine in control of infectious diseases, such effects are likely to be important for zinc-mediated host defence.
We do not extensively cover strategies utilized by pathogens to defend against zinc- and copper-mediated host defence, since others have reviewed this literature in detail recently [ 2– 4].
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