% 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{Hodel:177003,
      author       = {F. Hodel and A. Y. Chong and P. Scepanovic and Z. M. Xu and
                      O. Naret and C. W. Thorball and S. Rüeger and P.
                      Marques-Vidal and P. Vollenweider and M. Begemann and H.
                      Ehrenreich and N. Brenner$^*$ and N. Bender$^*$ and T.
                      Waterboer$^*$ and A. J. Mentzer and A. V. S. Hill and C.
                      Hammer and J. Fellay},
      title        = {{H}uman genomics of the humoral immune response against
                      polyomaviruses.},
      journal      = {Virus evolution},
      volume       = {7},
      number       = {2},
      issn         = {2057-1577},
      address      = {Oxford},
      publisher    = {Oxford Univ. Press},
      reportid     = {DKFZ-2021-02236},
      pages        = {veab058},
      year         = {2021},
      abstract     = {Human polyomaviruses are widespread in humans and can cause
                      severe disease in immunocompromised individuals. To identify
                      human genetic determinants of the humoral immune response
                      against polyomaviruses, we performed genome-wide association
                      studies and meta-analyses of qualitative and quantitative
                      immunoglobulin G responses against BK polyomavirus (BKPyV),
                      JC polyomavirus (JCPyV), Merkel cellpolyomavirus (MCPyV), WU
                      polyomavirus (WUPyV), and human polyomavirus 6 (HPyV6) in
                      15,660 individuals of European ancestry from three
                      independent studies. We observed significant associations
                      for all tested viruses: JCPyV, HPyV6, and MCPyV associated
                      with human leukocyte antigen class II variation, BKPyV and
                      JCPyV with variants in FUT2, responsible for secretor
                      status, MCPyV with variants in STING1, involved in
                      interferon induction, and WUPyV with a functional variant in
                      MUC1, previously associated with risk for gastric cancer.
                      These results provide insights into the genetic control of a
                      family of very prevalent human viruses, highlighting genes
                      and pathways that play a modulating role in human humoral
                      immunity.},
      keywords     = {GWAS (Other) / genomics (Other) / human (Other) / infection
                      (Other) / meta-analysis (Other) / polyomavirus (Other)},
      cin          = {F022 / F020},
      ddc          = {610},
      cid          = {I:(DE-He78)F022-20160331 / I:(DE-He78)F020-20160331},
      pnm          = {316 - Infektionen, Entzündung und Krebs (POF4-316)},
      pid          = {G:(DE-HGF)POF4-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34532061},
      pmc          = {pmc:PMC8438875},
      doi          = {10.1093/ve/veab058},
      url          = {https://inrepo02.dkfz.de/record/177003},
}