@article{KosterGurumurthyKumaretal.2022,
  author    = {Koster, Stefanie and Gurumurthy, Rajendra Kumar and Kumar, Naveen and Prakash, Pon Ganish and Dhanraj, Jayabhuvaneshwari and Bayer, Sofia and Berger, Hilmar and Kurian, Shilpa Mary and Drabkina, Marina and Mollenkopf, Hans-Joachim and Goosmann, Christian and Brinkmann, Volker and Nagel, Zachary and Mangler, Mandy and Meyer, Thomas F. and Chumduri, Cindrilla},
  title     = {Modelling Chlamydia and HPV co-infection in patient-derived ectocervix organoids reveals distinct cellular reprogramming},
  series = {Nature Communications},
  volume    = {13},
  journal   = {Nature Communications},
  number    = {1},
  doi       = {10.1038/s41467-022-28569-1},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-301349},
  year      = {2022},
  abstract  = {Coinfections with pathogenic microbes continually confront cervical mucosa, yet their implications in pathogenesis remain unclear. Lack of in-vitro models recapitulating cervical epithelium has been a bottleneck to study coinfections. Using patient-derived ectocervical organoids, we systematically modeled individual and coinfection dynamics of Human papillomavirus (HPV)16 E6E7 and Chlamydia, associated with carcinogenesis. The ectocervical stem cells were genetically manipulated to introduce E6E7 oncogenes to mimic HPV16 integration. Organoids from these stem cells develop the characteristics of precancerous lesions while retaining the self-renewal capacity and organize into mature stratified epithelium similar to healthy organoids. HPV16 E6E7 interferes with Chlamydia development and induces persistence. Unique transcriptional and post-translational responses induced by Chlamydia and HPV lead to distinct reprogramming of host cell processes. Strikingly, Chlamydia impedes HPV-induced mechanisms that maintain cellular and genome integrity, including mismatch repair in the stem cells. Together, our study employing organoids demonstrates the hazard of multiple infections and the unique cellular microenvironment they create, potentially contributing to neoplastic progression.},
  language  = {en}
}
@article{SinghVermaAkhoonetal.2016,
  author    = {Singh, Krishna P. and Verma, Neeraj and Akhoon, Bashir A . and Bhatt, Vishal and Gupta, Shishir K. and Gupta, Shailendra K. and Smita, Suchi},
  title     = {Sequence-based approach for rapid identification of cross-clade CD8+ T-cell vaccine candidates from all high-risk HPV strains},
  series = {3 Biotech},
  volume    = {6},
  journal   = {3 Biotech},
  doi       = {10.1007/s13205-015-0352-z},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-191056},
  pages     = {10},
  year      = {2016},
  abstract  = {Human papilloma virus (HPV) is the primary etiological agent responsible for cervical cancer in women. Although in total 16 high-risk HPV strains have been identified so far. Currently available commercial vaccines are designed by targeting mainly HPV16 and HPV18 viral strains as these are the most common strains associated with cervical cancer. Because of the high level of antigenic specificity of HPV capsid antigens, the currently available vaccines are not suitable to provide cross-protection from all other high-risk HPV strains. Due to increasing reports of cervical cancer cases from other HPV high-risk strains other than HPV16 and 18, it is crucial to design vaccine that generate reasonable CD8+ T-cell responses for possibly all the high-risk strains. With this aim, we have developed a computational workflow to identify conserved cross-clade CD8+ T-cell HPV vaccine candidates by considering E1, E2, E6 and E7 proteins from all the high-risk HPV strains. We have identified a set of 14 immunogenic conserved peptide fragments that are supposed to provide protection against infection from any of the high-risk HPV strains across globe.},
  language  = {en}
}