Comptes Rendus Biologies (Apr 2021)

FHL1 is a key player of chikungunya virus tropism and pathogenesis

  • Meertens, Laurent,
  • Hafirassou, Mohamed Lamine,
  • Couderc, Thérèse,
  • Bonnet-Madin, Lucie,
  • Kril, Vasiliya,
  • Kümmerer, Beate M.,
  • Labeau, Athena,
  • Brugier, Alexis,
  • Simon-Loriere, Etienne,
  • Burlaud-Gaillard, Julien,
  • Doyen, Cécile,
  • Pezzi, Laura,
  • Goupil, Thibaud,
  • Rafasse, Sophia,
  • Vidalain, Pierre-Olivier,
  • Legout, Anne Bertrand,
  • Gueneau, Lucie,
  • Juntas-Morales, Raul,
  • Yaou, Rabah Ben,
  • Bonne, Gisèle,
  • de Lamballerie, Xavier,
  • Benkirane, Monsef,
  • Roingeard, Philippe,
  • Delaugerre, Constance,
  • Lecuit, Marc,
  • Amara, Ali

DOI
https://doi.org/10.5802/crbiol.40
Journal volume & issue
Vol. 343, no. 4
pp. 79 – 89

Abstract

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Chikungunya is an infectious disease caused by the chikungunya virus (CHIKV), an alphavirus transmitted to humans by Aedes mosquitoes, and for which there is no licensed vaccine nor antiviral treatments. By using a loss-of-function genetic screen, we have recently identified the FHL1 protein as an essential host factor for CHIKV tropism and pathogenesis. FHL1 is highly expressed in muscles cells and fibroblasts, the main CHIKV-target cells. FHL1 interacts with the viral protein nsP3 and plays a critical role in CHIKV genome amplification. Experiments in vivo performed in FHL1-deficient mice have shown that these animals are resistant to infection and do not develop muscular lesions. Altogether these observations, published in the journal Nature [1], show that FHL1 is a key host factor for CHIKV pathogenesis and identify the interaction between FHL1 and nsP3 as a promising target for the development of new antiviral strategies.

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