Tuesday, 12th of November 2013 |
Autophagy is an evolutionarily conserved lysosomal dependent degradative pathway for recycling of long-lived proteins and damaged organelles. Autophagy is also an essential cellular response to fight infection by destroying infectious pathogens trapped within autophagosomes and plays a key role in the induction of both innate and adaptive immune responses. Numerous viruses have evolved strategies to counteract autophagy in order to escape from degradation or/and to inhibit immune signals. The kinetic and molecular pathways involved in the induction of autophagy upon infections might determine if cells would be able to control pathogens or would be invaded by them. In this article, the authors show that measles virus infection induces successive autophagy signallings in cells via distinct molecular pathways. A first autophagy wave is induced by the engagement of the measles virus cellular receptor CD46 and the scaffold protein GOPC. A second wave is initiated after viral replication by the expression of the non-structural measles virus protein C and is sustained overtime within infected cells thanks to the formation of syncytia. This sustained autophagy is exploited by measles virus to limit the death of infected cells and to improve viral particle formation. The authors conclude by describing new molecular pathways by which measles virus hijacks autophagy to promote its infectivity. More details are available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3784470/
Abstract
The interplay between autophagy and intracellular pathogens is intricate as autophagy is an essential cellular response to fight against infections, whereas numerous microbes have developed strategies to escape this process or even exploit it to their own benefit. The fine tuned timing and/or selective molecular pathways involved in the induction of autophagy upon infections could be the cornerstone allowing cells to either control intracellular pathogens, or be invaded by them. We report here that measles virus infection induces successive autophagy signallings in permissive cells, via distinct and uncoupled molecular pathways. Immediately upon infection, attenuated measles virus induces a first transient wave of autophagy, via a pathway involving its cellular receptor CD46 and the scaffold protein GOPC. Soon after infection, a new autophagy signaling is initiated which requires viral replication and the expression of the non-structural measles virus protein C. Strikingly, this second autophagy signaling can be sustained overtime within infected cells, independently of the expression of C, but via a third autophagy input resulting from cell-cell fusion and the formation of syncytia. Whereas this sustained autophagy signaling leads to the autophagy degradation of cellular contents, viral proteins escape from degradation. Furthermore, this autophagy flux is ultimately exploited by measles virus to limit the death of infected cells and to improve viral particle formation. Whereas CD150 dependent virulent strains of measles virus are unable to induce the early CD46/GOPC dependent autophagy wave, they induce and exploit the late and sustained autophagy. Overall, our work describes distinct molecular pathways for an induction of self-beneficial sustained autophagy by measles virus.
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