Autophagy is a catabolic process that refers to the engulfment of intracellular components into double-membraned autophagosomes that eventually fuse with the lysosomes for degradation and recycling of their content. ATG8/LC3-family proteins play a central role in the autophagy process due to their ability to interact with components of the autophagy machinery as well as selective autophagy receptors and adaptor proteins. Such interactions are usually mediated through LC3-interacting region (LIR) motifs. Autophagy has been widely described as a recycling pathway during nutrient starvation or as a quality-control pathway to eliminate damaged organelles. Nevertheless, this mechanism has been adapted to defend cells against intracellular pathogens. Recent years have seen an outburst of studies on autophagy and viral infections. Autophagy may exert a variety of antiviral functions, including the degradation of viral components (known as virophagy or virus xenophagy), the activation of innate immunity by the delivery of viral nucleic acids to the Toll-like receptors, and adaptive immunity through the major histocompatibility complexe II (MCH-II). To date, only the viral Matrix protein M2 of Influenza virus has been experimentally shown to have a LIR motif necessary to hijack the autophagy machinery, leaving open a vast field for investigation. Giving the increasing interest in the elucidation of LIR-dependent function of autophagy-related proteins in viruses, we show in this database all the LIR motifs detected in all viral protein sequences available.
Copyright © Ioannis Nezis lab | University of Warwick
