% 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{Zimmermann:288506,
      author       = {C. Zimmermann and G. M. Watson and L. Bauersfeld and R.
                      Berry and B. Ciblis and H. Lan and C. Gerke and V. Oberhardt
                      and J. Fuchs and M. Hofmann and C. Freund and J. Rossjohn
                      and F. Momburg$^*$ and H. Hengel and A. Halenius},
      title        = {{D}iverse cytomegalovirus {US}11 antagonism and {MHC}-{A}
                      evasion strategies reveal a tit-for-tat coevolutionary arms
                      race in hominids.},
      journal      = {Proceedings of the National Academy of Sciences of the
                      United States of America},
      volume       = {121},
      number       = {9},
      issn         = {0027-8424},
      address      = {Washington, DC},
      publisher    = {National Acad. of Sciences},
      reportid     = {DKFZ-2024-00379},
      pages        = {e2315985121},
      year         = {2024},
      abstract     = {Recurrent, ancient arms races between viruses and hosts
                      have shaped both host immunological defense strategies as
                      well as viral countermeasures. One such battle is waged by
                      the glycoprotein US11 encoded by the persisting human
                      cytomegalovirus. US11 mediates degradation of major
                      histocompatibility class I (MHC-I) molecules to prevent CD8+
                      T-cell activation. Here, we studied the consequences of the
                      arms race between US11 and primate MHC-A proteins, leading
                      us to uncover a tit-for-tat coevolution and its impact on
                      MHC-A diversification. We found that US11 spurred MHC-A
                      adaptation to evade viral antagonism: In an ancestor of
                      great apes, the MHC-A A2 lineage acquired a Pro184Ala
                      mutation, which confers resistance against the ancestral
                      US11 targeting strategy. In response, US11 deployed a unique
                      low-complexity region (LCR), which exploits the MHC-I
                      peptide loading complex to target the MHC-A2 peptide-binding
                      groove. In addition, the global spread of the human HLA-A*02
                      allelic family prompted US11 to employ a superior LCR
                      strategy with an optimally fitting peptide mimetic that
                      specifically antagonizes HLA-A*02. Thus, despite
                      cytomegaloviruses low pathogenic potential, the increasing
                      commitment of US11 to MHC-A has significantly promoted
                      diversification of MHC-A in hominids.},
      keywords     = {HLA-A (Other) / MHC class I (Other) / coevolution (Other) /
                      cytomegalovirus (Other) / tapasin (Other)},
      cin          = {D120 / D121},
      ddc          = {500},
      cid          = {I:(DE-He78)D120-20160331 / I:(DE-He78)D121-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38377192},
      doi          = {10.1073/pnas.2315985121},
      url          = {https://inrepo02.dkfz.de/record/288506},
}