A Transgenic Flock House Virus Replicon Reveals an RNAi Independent Antiviral Mechanism Acting in Follicular Somatic Cells.

Fiche publication

Date publication

décembre 2018

Journal

G3 (Bethesda, Md.)

Auteurs

Membres identifiés du Cancéropôle Est :
Pr IMLER Jean-Luc , Dr MEIGNIN Carine

Tous les auteurs :
Martins N, Lemoine A, Santiago E, Paro S, Imler JL, Meignin C

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/30530643

Résumé

The small interfering RNA (siRNA) pathway is the main and best studied invertebrate antiviral response. Other poorly characterized protein based antiviral mechanisms also contribute to the control of viral replication in insects. In addition, it remains unclear whether tissue specific factors contribute to RNA and protein-based antiviral immunity mechanisms. In vivo screens to identify such factors are challenging and time consuming. In addition, the scored phenotype is usually limited to survival and/or viral load. Transgenic viral replicons are valuable tools to overcome these limitations and screen for novel antiviral factors. Here we describe transgenic lines encoding a Flock House Virus-derived replicon (FHVΔB2eGFP), expressing GFP as a reporter of viral replication. This replicon is efficiently controlled by the siRNA pathway in most somatic tissues, with GFP fluorescence providing a reliable marker for the activity of antiviral RNAi. Interestingly, in follicular somatic cells (FSC) of ovaries, this replicon is still partially repressed in an siRNA independent manner. We did not detect replicon derived Piwi-interacting RNAs in FSCs and identified 31 differentially expressed genes between restrictive and permissive FSCs. Altogether, our results uncovered a yet unidentified RNAi-independent mechanism controlling FHV replication in FSCs of ovaries and validate the FHVΔB2eGFP replicon as a tool to screen for novel tissue specific antiviral mechanisms.