Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

A New Derivative of Retro-2 Displays Antiviral Activity against Respiratory Syncytial Virus

Adrien Le Rouzic
,
Jenna Fix
,
Robin Vinck
ORCID logo ,
Sandrine Kappler-Gratias
,
Romain Volmer
,
Franck Gallardo
,
Jean-François Eléouët
ORCID logo ,
Mathilde Keck
ORCID logo ,
Jean-Christophe Cintrat
ORCID logo ,
Julien Barbier
ORCID logo ,
Daniel Gillet
* ORCID logo ,
Marie Galloux
* ORCID logo
Version 1 : Received: 26 October 2023 / Approved: 26 October 2023 / Online: 26 October 2023 (16:10:47 CEST)

A peer-reviewed article of this Preprint also exists.

Le Rouzic, A.; Fix, J.; Vinck, R.; Kappler-Gratias, S.; Volmer, R.; Gallardo, F.; Eléouët, J.-F.; Keck, M.; Cintrat, J.-C.; Barbier, J.; Gillet, D.; Galloux, M. A New Derivative of Retro-2 Displays Antiviral Activity against Respiratory Syncytial Virus. Int. J. Mol. Sci. 2024, 25, 415. Le Rouzic, A.; Fix, J.; Vinck, R.; Kappler-Gratias, S.; Volmer, R.; Gallardo, F.; Eléouët, J.-F.; Keck, M.; Cintrat, J.-C.; Barbier, J.; Gillet, D.; Galloux, M. A New Derivative of Retro-2 Displays Antiviral Activity against Respiratory Syncytial Virus. Int. J. Mol. Sci. 2024, 25, 415.

Abstract

Human respiratory syncytial virus (hRSV) is the most common cause of bronchiolitis and pneumonia in new-borns, with all children being infected before the age of two. Reinfections are very common throughout life, and can cause severe respiratory infections in the elderly and immunocompromised adults. Although vaccines and preventive antibodies have recently been licensed for use in specific subpopulations of patients, there is still no therapeutic treatment commonly available for these infections. Here, we investigated the potential antiviral activity of Retro-2.2, a derivative of the cellular retrograde transport inhibitor Retro-2, against hRSV. We show that Retro-2.2 inhibits hRSV replication in cell culture, and impairs the ability of hRSV to form syncytia. Our results suggest that Retro-2.2 treatment affects virus spread by disrupting the trafficking of the viral de novo synthetized F and G glycoproteins to the plasma membrane, leading to a defect in virion morphogenesis. Taken together, our data show that targeting intracellular transport may be an effective strategy against hRSV infection.

Keywords

Respiratory syncytial virus; Retro-2.2; fusion protein; retrograde transport; antiviral

Subject

Biology and Life Sciences, Virology

Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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