DI-UMONS : Dépôt institutionnel de l’université de Mons

Recherche transversale
(titres de publication, de périodique et noms de colloque inclus)
2018-11-30 - Colloque/Présentation - poster - Anglais - 1 page(s)

Phuengpornsawan Vicharnee , Tafforeau Lionel , "Deciphering how influenza A virus hijacks the host cellular translation machinery during cell infection" in 2nd Annual meeting of the Namur Research Pole in Infectiology, Namur, Belgique, 2018

  • Codes CREF : Biologie (DI3100)
  • Unités de recherche UMONS : Biologie cellulaire (S815)
  • Instituts UMONS : Institut des Sciences et Technologies de la Santé (Santé), Institut des Biosciences (Biosciences)

Abstract(s) :

(Anglais) Influenza A virus (IAV) causes seasonal and pandemic infections. The IAV genome consists of 8 negative-sense single-stranded RNAs requiring host cells in the translation of the viral proteins, which is essential for the virus replication. Nonstructural protein 1(NS1) which is found in infected cells plays a major role in the virus replication cycle by blocking innate immune system in the infected cells. This leads to the inability of the cells to respond the viral infection properly. In the nucleus, NS1 inhibits the correct processing and the export of cellular mRNA, therefore enhancing the production of viral mRNA. The goal of this project is to identify the functional role of cellular proteins involved in translation that interacts with NS1 during IAV infection. We selected about 50 cellular proteins from human-pathogen interaction database, showing an interaction with NS1 from high-throughput interactome screening based on their translational functions. We carried out a screening using the Gaussia Princeps complementation assay (GPCA) to validate the direct physical interactions between the cellular proteins and NS1. Among the positive interactions, we further confirmed them by co-immunoprecipitation. To characterize the involvement of these NS1 interactors in IAV infection cycle, we will analyze an infectious cycle of IAV upon siRNA-mediated depletion of each of them in A549 cells.