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Viral pathogenesis

Enabling HCV's need for fat

Nature Reviews Microbiology volume 11, page 432 (2013)Cite this article

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Following on from previous work, the authors noted that depletion of IKKα (part of the IKK complex, which regulates the antiviral NF-κB signalling pathway) markedly impaired viral particle production and secretion, and specifically assembly. Viral particle assembly is known to involve association of the HCV core protein with host lipid droplets; the authors observed that lipid droplet numbers increased following HCV infection and that depletion of IKKα abrogated this effect. Notably, silencing other NF-κB pathway components had no effect on lipid droplet formation and HCV assembly, indicating that IKKα-mediated induction of lipid droplet synthesis is NF-κB independent.

So, how does HCV activate IKKα? First, the authors identified the HCV 3′ UTR as the component that triggers IKKα-dependent signalling and consequent lipid droplet production. The 3′ UTR was shown to be specifically recognized by the host DexDH/H helicase DDX3X, a putative pathogen recognition receptor, which redistributed in the cytoplasm and colocalized with the 3′ UTR and IKKα. Importantly, the interaction between IKKα and DDX3X resulted in IKKα phosphorylation (and therefore activation) and translocation to the nucleus.

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References

  1. Li, Q. et al. Hepatitis C virus infection activates an innate pathway involving IKK-α in lipogenesis and viral assembly. Nature Med. 26 May 2013 (10.1038/nm.3190)

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Authors
  1. Rachel David
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David, R. Enabling HCV's need for fat. Nat Rev Microbiol 11, 432 (2013). https://doi.org/10.1038/nrmicro3054

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