Abstract
Autophagy is a major catabolic pathway involved in several important cellular functions including homeostasis, development, differentiation and immunity. Consequently, deregulations of this process have been observed in several pathologies. Autophagy leads to the lysosomal degradation of cellular components after their sequestration in vacuoles called autophagosomes. During nutrient starvation, autophagy degrades randomly cytoplasmic components, but it is now well established that this process can be highly selective thanks to proteins that allow the specific targeting of substrates to autophagosomes. These proteins, called autophagy receptors, are able to bind specific substrates and the members of the "ATG8-like" family (divided in two subfamilies: LC3 and GABARAP in mammals), which are decorating autophagosomes. The role of selective autophagy during viral infection is not extensively studied yet. However, the literature shows that viruses have evolved to block, divert or use this process to promote their replication.
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