@article{RasaNoraKrukleHenningetal.2018,
  author    = {Rasa, Santa and Nora-Krukle, Zaiga and Henning, Nina and Eliassen, Eva and Shikova, Evelina and Harrer, Thomas and Scheibenbogen, Carmen and Murovska, Modra and Prusty, Bhupesh K.},
  title     = {Chronic viral infections in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)},
  series = {Journal of Translational Medicine},
  volume    = {16},
  journal   = {Journal of Translational Medicine},
  number    = {268},
  doi       = {10.1186/s12967-018-1644-y},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-224960},
  pages     = {1-25},
  year      = {2018},
  abstract  = {Background and main text: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex and controversial clinical condition without having established causative factors. Increasing numbers of cases during past decade have created awareness among patients as well as healthcare professionals. Chronic viral infection as a cause of ME/CFS has long been debated. However, lack of large studies involving well-designed patient groups and validated experimental set ups have hindered our knowledge about this disease. Moreover, recent developments regarding molecular mechanism of pathogenesis of various infectious agents cast doubts over validity of several of the past studies. Conclusions: This review aims to compile all the studies done so far to investigate various viral agents that could be associated with ME/CFS. Furthermore, we suggest strategies to better design future studies on the role of viral infections in ME/CFS.},
  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}
}