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@ARTICLE{Hasche:179371,
      author       = {D. Hasche$^*$ and M. Ahmels$^*$ and I.
                      Braspenning-Wesch$^*$ and S. Stephan$^*$ and R. Cao$^*$ and
                      G. Schmidt$^*$ and M. Müller$^*$ and F. Rösl$^*$},
      title        = {{I}soforms of the {P}apillomavirus {M}ajor {C}apsid
                      {P}rotein {D}iffer in {T}heir {A}bility to {B}lock {V}iral
                      {S}pread and {T}umor {F}ormation.},
      journal      = {Frontiers in immunology},
      volume       = {13},
      issn         = {1664-3224},
      address      = {Lausanne},
      publisher    = {Frontiers Media},
      reportid     = {DKFZ-2022-00622},
      pages        = {811094},
      year         = {2022},
      note         = {#EA:F030#LA:F030#},
      abstract     = {Notably, the majority of papillomaviruses associated with a
                      high cancer risk have the potential to translate different
                      isoforms of the L1 major capsid protein. In an infection
                      model, the cutaneous Mastomys natalensis papillomavirus
                      (MnPV) circumvents the humoral immune response of its
                      natural host by first expressing a 30 amino acid extended L1
                      isoform (L1LONG). Although inducing a robust seroconversion,
                      the raised antibodies are not neutralizing in vitro. In
                      contrast, neutralizing antibodies induced by the
                      capsid-forming isoform (L1SHORT) appear delayed by several
                      months. We now provide evidence that, although L1LONG
                      vaccination showed a strong seroconversion, these antibodies
                      were not protective. As a consequence, virus-free animals
                      subsequently infected with MnPV still accumulated high
                      numbers of transcriptionally active viral genomes,
                      ultimately leading to skin tumor formation. In contrast,
                      vaccination with L1SHORT was completely protective. This
                      shows that papillomavirus L1LONG expression is a unique
                      strategy to escape from antiviral immune surveillance.},
      keywords     = {Mastomys coucha (Other) / NMSC (non-melanoma skin cancer)
                      (Other) / cutaneous papillomaviruses (Other) / immune escape
                      mechanism (Other) / major capsid protein (L1) (Other) /
                      neutralizing antibodies (Other) / vaccination (Other) /
                      viral infection (Other)},
      cin          = {F030 / W210 / F035},
      ddc          = {610},
      cid          = {I:(DE-He78)F030-20160331 / I:(DE-He78)W210-20160331 /
                      I:(DE-He78)F035-20160331},
      pnm          = {316 - Infektionen, Entzündung und Krebs (POF4-316)},
      pid          = {G:(DE-HGF)POF4-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35359995},
      pmc          = {pmc:PMC8964102},
      doi          = {10.3389/fimmu.2022.811094},
      url          = {https://inrepo02.dkfz.de/record/179371},
}