The European Union as a Mediator in Israel-Palestine: Operations Cast Lead and Protective Edge. EU Diplomacy Paper 01/2016

The European Union (EU) has played an important, yet inconsistent role in the Israel-Palestine conflict since the1980 Venice Declaration. This paper analyses how the EU’s role as a mediator has changed more recently in the Israel-Gaza conflict. Specifically, it examines how the ‘Concept on Strengthening EU Mediation and Dialogue Capacities’ adopted in 2009 and the creation of the European External Action Service and the High Representative by the Lisbon Treaty have changed the EU’s resources and strategies as a mediator as well as how these developments improved cooperation and coordination with other mediators. This analysis is done through a comparison of the EU’s role in the Israeli Operation Cast Lead in 2008/2009 and Operation Protective Edge in 2014. It is argued that the aforementioned changes made the EU a more capable mediator and facilitated internal coordination. However, these changes did not create more resources for the EU as a mediator, rather they changed how the EU used its resources.

Influenza A virus ribonucleoproteins modulate host recycling by competing with Rab11 effectors

Influenza A virus assembly is an unclear process, whereby individual virion components form an infectious particle. The segmented nature of the influenza A genome imposes a problem to assembly because it requires packaging of eight distinct RNA particles (vRNPs). It also allows genome mixing from distinct parental strains, events associated with influenza pandemic outbreaks. It is important to public health to understand how segmented genomes assemble, a process that is dependent on the transport of components to assembly sites. Previously, it has been shown that vRNPs are carried by recycling endosome vesicles, resulting in a change of Rab11 distribution. Here, we describe that vRNP binding to recycling endosomes impairs recycling endosome function, by competing for Rab11 binding with family-interacting proteins, and that there is a causal relationship between Rab11 ability to recruit family-interacting proteins and Rab11 redistribution. This competition reduces recycling sorting at an unclear step, resulting in clustering of single- and double-membraned vesicles. These morphological changes in Rab11 membranes are indicative of alterations in protein and lipid homeostasis during infection. Vesicular clustering creates hotspots of the vRNPs that need to interact to form an infectious particle.