Catch Me If You Can: The Link between Autophagy and Viruses
Author(s) -
Nicholas J. Lennemann,
Carolyn B. Coyne
Publication year - 2015
Publication title -
plos pathogens
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.719
H-Index - 206
eISSN - 1553-7374
pISSN - 1553-7366
DOI - 10.1371/journal.ppat.1004685
Subject(s) - autophagy , link (geometry) , biology , microbiology and biotechnology , virology , computer science , genetics , computer network , apoptosis
Autophagy is a process that mediates the degradation of cytoplasmic material, such as damaged organelles and protein aggregates, to maintain cellular homeostasis (Fig. 1) [1]. The autophagic pathway begins with the sequestration of organelles and portions of the cytoplasm via a double-membrane termed the isolation membrane (or phagophore), which can be derived from several cellular compartments (including the endoplasmic reticulum [ER], Golgi complex, ERGolgi intermediate compartment [ERGIC], mitochondria, or ER-mitochondria associated membranes [MAMs], as well as the plasma membrane) [2]. The isolation membrane expands to completely envelop the isolated contents in a double-membrane vesicle called the autophagosome, which then undergoes maturation through fusion with lysosomes to form autolyosomes [3]. A hallmark of canonical autophagy (or “macroautophagy”) is autophagic flux, in which lysosomal enzymes degrade the contents within the autolysome. Alternatively, early/late endosomes can fuse with autophagosomes, forming amphisomes that can then mature to autolysosomes, in which both endosomal and autophagosomal contents are degraded.
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