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@ARTICLE{Chen:285490,
      author       = {Chen, Yuexuan and Klute, Susanne and Bansal, Anju and
                      Sparrer, Konstantin Maria Johannes and Serra-Moreno, Ruth},
      title        = {{HIV}-1 {V}pr is targeted for degradation by autophagy.},
      journal      = {PLoS pathogens},
      volume       = {22},
      number       = {3},
      issn         = {1553-7366},
      address      = {Lawrence, Kan.},
      publisher    = {PLoS},
      reportid     = {DZNE-2026-00266},
      pages        = {e1014020},
      year         = {2026},
      abstract     = {Autophagy is part of the innate immune arsenal to fight
                      viruses, including HIV-1. We previously reported that HIV-1
                      Gag is targeted for autophagy-mediated degradation. Here, we
                      identify HIV-1 Vpr, an important virulence factor, as an
                      autophagy target in HIV-1 NL4-3, a lab adapted molecular
                      clone. Notably, Vpr proteins from a collection of
                      transmitted/founder viruses (TFVs) were resistant to
                      autophagy. Based on this observation, we identified residues
                      at positions 37, 45, 77, 83-86, 93-94 in NL4-3 Vpr as
                      responsible for its susceptibility to autophagy.
                      Importantly, differences between NL4-3 and TFV Vpr proteins
                      at these positions impact their interaction with the
                      autophagy receptors NDP52, SQSTM1/p62 and TAX1BP1. By
                      engineering NL4-3 molecular clones harboring either
                      autophagy-sensitive or -resistant vpr, we found that in 2D
                      and 3D in vitro systems virus spread was significantly
                      reduced for the virus carrying autophagy-sensitive Vpr. In
                      conclusion, our study identifies Vpr as a novel autophagy
                      target and suggests that Vpr susceptibility to autophagy
                      impacts HIV-1 spread.},
      keywords     = {Autophagy: physiology / Humans / vpr Gene Products, Human
                      Immunodeficiency Virus: metabolism / vpr Gene Products,
                      Human Immunodeficiency Virus: genetics / HIV-1: metabolism /
                      HIV-1: genetics / HIV-1: pathogenicity / HIV Infections:
                      metabolism / HIV Infections: virology / HIV Infections:
                      immunology / HEK293 Cells / Proteolysis / vpr Gene Products,
                      Human Immunodeficiency Virus (NLM Chemicals) / vpr protein,
                      Human immunodeficiency virus 1 (NLM Chemicals)},
      cin          = {AG Sparrer},
      ddc          = {610},
      cid          = {I:(DE-2719)1910003},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41770818},
      pmc          = {pmc:PMC12970978},
      doi          = {10.1371/journal.ppat.1014020},
      url          = {https://pub.dzne.de/record/285490},
}