Abstract
Autophagy is a biological process that helps cells to recycle obsolete cellular components and which greatly contributes to maintaining cellular integrity in response to environmental stress factors. Autophagy is also among the first lines of cellular defense against invading microorganisms, including viruses. The autophagic destruction of invading pathogens, a process referred to as xenophagy, involves cytosolic autophagy receptors, such as p62/SQSTM1 (Sequestosome 1) or NDP52/CALCOCO2 (Nuclear Dot 52 KDa Protein/Calcium Binding And Coiled-Coil Domain 2), which bind to microbial components and target them towards growing autophagosomes for degradation. However, most, if not all, infectious viruses have evolved molecular tricks to escape from xenophagy. Many viruses even use autophagy, part of the autophagy pathway or some autophagy-associated proteins, to improve their infectious potential. In this regard, the measles virus, responsible for epidemic measles, has a unique interface with autophagy as the virus can induce multiple rounds of autophagy in the course of infection. These successive waves of autophagy result from distinct molecular pathways and seem associated with anti- and/or pro-measles virus consequences. In this review, we describe what the autophagy–measles virus interplay has taught us about both the biology of the virus and the mechanistic orchestration of autophagy.
Highlights
Measles virus (MeV) is a member of the Morbillivirus genus in the Paramyxoviridae family responsible for Measles, a common childhood infectious disease characterized by high fever, respiratory infection and typical macullo papular rash [1]
The infection of epithelial cells with MeV leads to a strong perturbation of the autophagy status of the cells
A few hours later, a second wave of autophagy that depends on viral replication is activated through interaction between
Summary
Measles virus (MeV) is a member of the Morbillivirus genus in the Paramyxoviridae family responsible for Measles, a common childhood infectious disease characterized by high fever, respiratory infection and typical macullo papular rash [1]. Clinical/virulent strains of MeV invade, first, the immune cells using CD150/SLAM (Signaling Lymphocytic Activation Molecule) expressed on dendritic macrophages. F protein leading to membrane fusion and virus genome delivery within the infected cell. Engagement of F induce conformational modification of virus replicates in thetocytosol and fusion spreads byvirus budding from the cell surface infected the F protein leading membrane and genome delivery within the of infected cell.cells. Macroautophagy, hereafter referred to as autophagy, is an intracellular degradation system uninfected cells [7]. In addition to regulating cell homeostasis, the autophagy machinery can be used as a cell defense mechanism against intracellular microbes, such as bacteria or viruses, through their degradation (a process referred to as xenophagy) [9,10]. Due to the crucial roles of the autophagy process in the context of infections and immunity, measles virus–autophagy interplay has been recently investigated, revealing an intricate cross-talk that is reviewed thereafter
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