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© Therese Couderc, Marc Lecuit
Publication : Comptes rendus biologies

FHL1 is a key player of chikungunya virus tropism and pathogenesis.

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Comptes rendus biologies - 21 Apr 2021

Meertens L, Hafirassou ML, Couderc T, Bonnet-Madin L, Kril V, Kümmerer BM, Labeau A, Brugier A, Simon-Loriere E, Burlaud-Gaillard J, Doyen C, Pezzi L, Goupil T, Rafasse S, Vidalain PO, Legout AB, Gueneau L, Juntas-Morales R, Yaou RB, Bonne G, de Lamballerie X, Benkirane M, Roingeard P, Delaugerre C, Lecuit M, Amara A,

Link to Pubmed [PMID] – 33988325

Link to DOI – 10.5802/crbiol.40

C R Biol 2021 Apr; 343(4): 79-89

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.Le chikungunya est une maladie infectieuse causée par le virus chikungunya (CHIKV), un alphavirus transmis à l’Homme par les moustiques Aedes et contre lequel il n’existe ni vaccin, ni traitements antiviraux. En utilisant une approche de crible génétique par perte de fonction, nous avons récemment identifié la protéine FHL1 comme un facteur cellulaire essentiel pour le tropisme et la pathogénèse du CHIKV. FHL1 est une molécule présente majoritairement dans les cellules musculaires et les fibroblastes, les cibles privilégiées de CHIKV. FHL1 interagit avec la protéine virale nsP3 et joue un rôle décisif dans le mécanisme d’amplification du génome de CHIKV. Des expériences in vivo chez des souris déficientes pour FHL1 ont montré que ces animaux sont résistants à l’infection et ne développent pas de lésions musculaires. L’ensemble de ces observations publiées dans la revue Nature [1] montrent que FHL1 est un facteur cellulaire clé pour la pathogénèse de CHIKV et identifient l’interaction entre FHL1 et nsp3 comme une cible prometteuse pour le développement de nouvelles stratégies antivirales.

https://pubmed.ncbi.nlm.nih.gov/33988325