@article{RudelPrustySiegletal.2013,
  author    = {Rudel, Thomas and Prusty, Bhupesh K. and Siegl, Christine and Hauck, Petra and Hain, Johannes and Korhonen, Suvi J. and Hiltunen-Back, Eija and Poulakkainen, Mirja},
  title     = {Chlamydia trachomatis Infection Induces Replication of Latent HHV-6},
  series = {PLoS ONE},
  journal   = {PLoS ONE},
  doi       = {10.1371/journal.pone.0061400},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-96731},
  year      = {2013},
  abstract  = {Human herpesvirus-6 (HHV-6) exists in latent form either as a nuclear episome or integrated into human chromosomes in more than 90\% of healthy individuals without causing clinical symptoms. Immunosuppression and stress conditions can reactivate HHV-6 replication, associated with clinical complications and even death. We have previously shown that co-infection of Chlamydia trachomatis and HHV-6 promotes chlamydial persistence and increases viral uptake in an in vitro cell culture model. Here we investigated C. trachomatis-induced HHV-6 activation in cell lines and fresh blood samples from patients having Chromosomally integrated HHV-6 (CiHHV-6). We observed activation of latent HHV-6 DNA replication in CiHHV-6 cell lines and fresh blood cells without formation of viral particles. Interestingly, we detected HHV-6 DNA in blood as well as cervical swabs from C. trachomatis-infected women. Low virus titers correlated with high C. trachomatis load and vice versa, demonstrating a potentially significant interaction of these pathogens in blood cells and in the cervix of infected patients. Our data suggest a thus far underestimated interference of HHV-6 and C. trachomatis with a likely impact on the disease outcome as consequence of co-infection.},
  language  = {en}
}
@article{PrustyChowdhuryGulveetal.2018,
  author    = {Prusty, Bhupesh K. and Chowdhury, Suvagata R. and Gulve, Nitish and Rudel, Thomas},
  title     = {Peptidase Inhibitor 15 (PI15) Regulates Chlamydial CPAF Activity},
  series = {Frontiers in Cellular and Infection Microbiology},
  volume    = {8},
  journal   = {Frontiers in Cellular and Infection Microbiology},
  number    = {183},
  issn      = {2235-2988},
  doi       = {10.3389/fcimb.2018.00183},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-196918},
  year      = {2018},
  abstract  = {Obligate intracellular pathogenic Chlamydia trachomatis express several serine proteases whose roles in chlamydial development and pathogenicity are not completely understood. The chlamydial protease CPAF is expressed during the replicative phase of the chlamydial developmental cycle and is secreted into the lumen of the Chlamydia-containing vacuole called inclusion. How the secreted protease is activated in the inclusion lumen is currently not fully understood. We have identified human serine peptidase inhibitor PI15 as a potential host factor involved in the regulation of CPAF activation. Silencing expression as well as over expression of PI15 affected normal development of Chlamydia. PI15 was transported into the chlamydial inclusion lumen where it co-localized with CPAF aggregates. We show that PI15 binds to the CPAF zymogen and potentially induces CPAF protease activity at low concentrations. However, at high concentrations PI15 inhibits CPAF activity possibly by blocking its protease domain. Our findings shed light on a new aspect of chlamydial host co-evolution which involves the recruitment of host cell proteins into the inclusion to control the activation of bacterial proteases like CPAF that are important for the normal development of Chlamydia.},
  language  = {en}
}