Speaker
Description
Although annual epidemics of seasonal influenza affect around 10% of the global population, current treatment options are limited and development of new antivirals is urgently needed. Here, we reveal key kinases required for influenza A virus (IAV) entry as potential novel drug targets. Using SILAC-based quantitative phosphoproteomics we quantified over 3000 IAV-induced phosphorylation changes that occur within minutes of infection. We developed a protocol to identify cellular kinases responsible for these changes and show that inhibition of selected kinases, such as the G protein-coupled receptor kinase 2 (GRK2), leads to decreased IAV replication. Focusing on GRK2 as potential drug target, we found that specific GRK2 inhibitors significantly reduced replication of seasonal and pandemic IAVs in primary human airway cultures and in mice. Ongoing studies using quantitative phosphoproteomics aim to compare the phosphorylation signature induced by different IAV strains, including seasonal human and avian viruses in order to identify additional drug targets with the potential to inhibit a broad spectrum of influenza viruses.
| Choose primary session | Virus host cell interaction |
|---|---|
| Choose secondary Session | Vaccines and antivirals |
