% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Klute:280042,
      author       = {Klute, Susanne and Nchioua, Rayhane and Cordsmeier, Arne
                      and Vishwakarma, Jyoti and Koepke, Lennart and Alshammary,
                      Hala and Jung, Christoph and Hirschenberger, Maximilian and
                      Hoenigsperger, Helene and Fischer, Jana-Romana and
                      Sivarajan, Rinu and Zech, Fabian and Stenger, Steffen and
                      Serra-Moreno, Ruth and Gonzalez-Reiche, Ana Silvia and
                      Sordillo, Emilia Mia and van Bakel, Harm and Simon, Viviana
                      and Kirchhoff, Frank and Jacob, Timo and Kmiec, Dorota and
                      Pichlmair, Andreas and Ensser, Armin and Sparrer, Konstantin
                      Maria Johannes},
      title        = {{M}utation {T}9{I} in {E}nvelope confers autophagy
                      resistance to {SARS}-{C}o{V}-2 {O}micron.},
      journal      = {iScience},
      volume       = {28},
      number       = {7},
      issn         = {2589-0042},
      address      = {St. Louis},
      publisher    = {Elsevier},
      reportid     = {DZNE-2025-00881},
      pages        = {112974},
      year         = {2025},
      abstract     = {Omicron has emerged as the most successful variant of
                      SARS-CoV-2. In addition to mutations in Spike that mediate
                      humoral immune escape, the Omicron-specific Envelope (E) T9I
                      mutation has been associated with increased transmission
                      fitness. However, the underlying mechanism remained unclear.
                      Here, we demonstrate that the E T9I mutation confers
                      resistance to autophagy. Rare Omicron patient isolates
                      encoding the ancestral E T9 remain sensitive to autophagy.
                      Conversely, introducing the E T9I mutation in recombinant
                      2020 SARS-CoV-2 renders it resistant to autophagy. Our data
                      indicate that the E T9I mutation protects virions against
                      lysosomal degradation. At the molecular level, the T9I
                      mutation increases the localization of E at autophagic
                      vesicles and promotes interaction with autophagy-associated
                      proteins SNX12, STX12, TMEM87B, and ABCG2. Our results show
                      that the E T9I mutation renders incoming virions resistant
                      to autophagy, suggesting that evasion of this antiviral
                      mechanism contributes to the efficient spread of Omicron.},
      keywords     = {Biological sciences (Other) / Cell biology (Other) /
                      Microbiology (Other) / Natural sciences (Other)},
      cin          = {AG Sparrer},
      ddc          = {050},
      cid          = {I:(DE-2719)1910003},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40687831},
      pmc          = {pmc:PMC12272759},
      doi          = {10.1016/j.isci.2025.112974},
      url          = {https://pub.dzne.de/record/280042},
}