**5. Conclusions**

In conclusion, we took advantage of a model of persistent CVB4 E2 infection to describe the emergence of fluoxetine-resistant variants. In these variants, mutations in the 2C viral protein have been identified and deserve further investigation.

**Author Contributions:** Conceptualization, E.K.A. and D.H.; methodology, E.K.A., A.B., and D.C.; data analysis, E.K.A., F.S., and I.E.; writing—original draft preparation, E.K.A.; writing—review and editing, I.E., D.H.; supervision, D.H.; funding acquisition, D.H.

**Funding:** This work was supported by Ministère de l'Education Nationale de la Recherche et de la Technologie, Université Lille 2 (Equipe d'accueil 3610), and Centre Hospitalier Régional et Universitaire de Lille, and by EU FP7 (GA-261441-PEVNET: Persistent virus infection as a cause of pathogenic inflammation in type 1 diabetes—an innovative research program of biobanks and expertise).

**Acknowledgments:** The authors thank the team of Laboratoire de Virologie EA3610, Université Lille, Faculté de médecine, and CHU de Lille. The authors thank Jennifer Varghese for reading the manuscript.

**Conflicts of Interest:** The authors declare no conflict of interest. The funder had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.
