Canonical and Non-Canonical Autophagy in HIV-1 Replication Cycle
AbstractAutophagy 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
Scifeed alert for new publicationsNever miss any articles matching your research from any publisher
- Get alerts for new papers matching your research
- Find out the new papers from selected authors
- Updated daily for 49'000+ journals and 6000+ publishers
- Define your Scifeed now
Leymarie, O.; Lepont, L.; Berlioz-Torrent, C. Canonical and Non-Canonical Autophagy in HIV-1 Replication Cycle. Viruses 2017, 9, 270.
Leymarie O, Lepont L, Berlioz-Torrent C. Canonical and Non-Canonical Autophagy in HIV-1 Replication Cycle. Viruses. 2017; 9(10):270.Chicago/Turabian Style
Leymarie, Olivier; Lepont, Leslie; Berlioz-Torrent, Clarisse. 2017. "Canonical and Non-Canonical Autophagy in HIV-1 Replication Cycle." Viruses 9, no. 10: 270.
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.