Raw data_<b>Exaptation of an endogenous viral element contributes to limiting cell fusing agent virus infection in </b><b><i>Aedes albopictus</i></b>

The genome of <i>Aedes spp.</i> mosquitoes host hundreds of non-retroviral endogenous viral elements (nrEVEs), the majority of which are confined in piRNA clusters and produce P-element-induced wimpy testis-interacting RNAs (piRNAs), which were shown to be antiviral. Whether this is a universal mechanism or some nrEVEs have been exapted for antiviral functions as transcribed RNA or translated proteins remains elusive. To delineate the antiviral potential of non-retroviral endogenous viral elements (nrEVEs), we employed the Asian tiger mosquito <i>Aedes albopictus</i> and the Cell fusing agent virus, a constituent of the mosquito virome. Within this context, we identified twenty nrEVEs located outside canonical piRNA clusters and encompassing complete viral open reading frames. By integrating <i>in vitro</i> and <i>in vivo</i> experimental approaches, we provide evidence that one nrEVE, designated Flavi24, is translated in adult mosquitoes and contributes to the suppression of infection by the cognate virus. Our results expand the functions of <i>Ae. albopictus</i> nrEVEs suggesting they can regulate host-virus interactions through various mechanisms.