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Viruses 2017, 9(10), 270;

Canonical and Non-Canonical Autophagy in HIV-1 Replication Cycle

Inserm, U1016, Institut Cochin, 75014 Paris, France
CNRS, UMR8104, 75014 Paris, France
University Paris Descartes, Sorbonne Paris Cité, 75006 Paris, France
Institut Cochin, Department Infection, Immunity, Inflammation, 75014 Paris, France
Author to whom correspondence should be addressed.
Received: 22 July 2017 / Revised: 19 September 2017 / Accepted: 21 September 2017 / Published: 23 September 2017
(This article belongs to the Special Issue Viruses and Autophagy)
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Autophagy is a lysosomal-dependent degradative process essential for maintaining cellular homeostasis, and is a key player in innate and adaptive immune responses to intracellular pathogens such as human immunodeficiency virus type 1 (HIV-1). In HIV-1 target cells, autophagy mechanisms can (i) selectively direct viral proteins and viruses for degradation; (ii) participate in the processing and presentation of viral-derived antigens through major histocompatibility complexes; and (iii) contribute to interferon production in response to HIV-1 infection. As a consequence, HIV-1 has evolved different strategies to finely regulate the autophagy pathway to favor its replication and dissemination. HIV-1 notably encodes accessory genes encoding Tat, Nef and Vpu proteins, which are able to perturb and hijack canonical and non-canonical autophagy mechanisms. This review outlines the current knowledge on the complex interplay between autophagy and HIV-1 replication cycle, providing an overview of the autophagy-mediated molecular processes deployed both by infected cells to combat the virus and by HIV-1 to evade antiviral response. View Full-Text
Keywords: HIV-1; autophagy; LC3-associated phagocytosis; Env; Tat; Nef; Vpu; LC3 HIV-1; autophagy; LC3-associated phagocytosis; Env; Tat; Nef; Vpu; LC3

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Leymarie, O.; Lepont, L.; Berlioz-Torrent, C. Canonical and Non-Canonical Autophagy in HIV-1 Replication Cycle. Viruses 2017, 9, 270.

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