**Jonathan Turpin, Etienne Frumence, Philippe Desprès, Wildriss Viranaicken \* and Pascale Krejbich-Trotot \***

PIMIT, Processus Infectieux en Milieu Insulaire Tropical, Université de La Réunion, INSERM UMR 1187, CNRS 9192, IRD 249, Plateforme CYROI, 97490 Sainte-Clotilde, Ile de La Réunion, France;

jonathan.turpin@univ-reunion.fr (J.T.); etiennefrum@gmail.com (E.F.); philippe.despres@univ-reunion.fr (P.D.) **\***wildriss.viranaicken@univ-reunion.fr

 Correspondence: (W.V.); pascale.krejbich@univ-reunion.fr (P.K-T.); Tel.: +33-262938829 (W.V.)

Received: 16 September 2019; Accepted: 26 October 2019; Published: 29 October 2019

**Abstract:** Zika virus (ZIKV) is an emerging human mosquito-transmitted pathogen of global concern, known to be associated with complications such as congenital defects and neurological disorders in adults. ZIKV infection is associated with induction of cell death. However, previous studies sugges<sup>t</sup> that the virally induced apoptosis occurs at a slower rate compared to the course of viral production. In this present study, we investigated the capacity of ZIKV to delay host cell apoptosis. We provide evidence that ZIKV has the ability to interfere with apoptosis whether it is intrinsically or extrinsically induced. In cells expressing viral replicon-type constructions, we show that this control is achieved through replication. Finally, our work highlights an important role for anti-apoptotic Bcl-2 family protein in the ability of ZIKV to control apoptotic pathways, avoiding premature cell death and thereby promoting virus replication in the host-cell.

**Keywords:** Zika virus; apoptosis; viral replication; Bcl-2 protein family
