FHL1 is a key player of chikungunya virus tropism and pathogenesis

Laurent Meertens(Centre National de la Recherche Scientifique), Mohamed Lamine Hafirassou(Centre National de la Recherche Scientifique), Thérèse Couderc(Inserm), Lucie Bonnet‐Madin(Centre National de la Recherche Scientifique), Vasiliya Kril(Centre National de la Recherche Scientifique), Beate M. Kümmerer(University of Bonn), Athéna Labeau(Centre National de la Recherche Scientifique), Alexis Brugier(Centre National de la Recherche Scientifique), Etienne Simon‐Lorière(Institut Pasteur), Julien Burlaud‐Gaillard(Université de Tours), Cécile M. Doyen(Centre National de la Recherche Scientifique), Laura Pezzı(Inserm), Thibaud Goupil(Inserm), Sophia Rafasse(Inserm), Pierre‐Olivier Vidalain(Centre National de la Recherche Scientifique), Anne Bertrand Legout(Inserm), Lucie Gueneau(Inserm), Raúl Juntas‐Morales(Centre Hospitalier Universitaire de Montpellier), Rabah Ben Yaou(Inserm), Gisèle Bonne(Inserm), Xavier de Lamballerie(Inserm), Monsef Benkirane(Centre National de la Recherche Scientifique), Philippe Roingeard(Université de Tours), Constance Delaugerre(Centre National de la Recherche Scientifique), Marc Lecuit(Inserm), Ali Amara(Centre National de la Recherche Scientifique)
Comptes Rendus Biologies
April 21, 2021
Cited by 3Open Access
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Abstract

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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