Endobiont Viruses Sensed by the Human Host – Beyond Conventional Antiparasitic Therapy
Wide-spread protozoan parasites carry endosymbiotic dsRNA viruses with uncharted implications to the human host. Among them, Trichomonas vaginalis, a parasite adapted to the human genitourinary tract, infects globally ∼250 million each year rendering them more susceptible to devastating pregnancy co...
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| Published in: | PloS one Vol. 7; no. 11; p. e48418 |
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| Main Authors: | , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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United States
Public Library of Science
07.11.2012
Public Library of Science (PLoS) |
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| ISSN: | 1932-6203, 1932-6203 |
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| Abstract | Wide-spread protozoan parasites carry endosymbiotic dsRNA viruses with uncharted implications to the human host. Among them, Trichomonas vaginalis, a parasite adapted to the human genitourinary tract, infects globally ∼250 million each year rendering them more susceptible to devastating pregnancy complications (especially preterm birth), HIV infection and HPV-related cancer. While first-line antibiotic treatment (metronidazole) commonly kills the protozoan pathogen, it fails to improve reproductive outcome. We show that endosymbiotic Trichomonasvirus, highly prevalent in T. vaginalis clinical isolates, is sensed by the human epithelial cells via Toll-like receptor 3, triggering Interferon Regulating Factor -3, interferon type I and proinflammatory cascades previously implicated in preterm birth and HIV-1 susceptibility. Metronidazole treatment amplified these proinflammatory responses. Thus, a new paradigm targeting the protozoan viruses along with the protozoan host may prevent trichomoniasis-attributable inflammatory sequelae. |
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| AbstractList | Wide-spread protozoan parasites carry endosymbiotic dsRNA viruses with uncharted implications to the human host. Among them, Trichomonas vaginalis, a parasite adapted to the human genitourinary tract, infects globally ∼250 million each year rendering them more susceptible to devastating pregnancy complications (especially preterm birth), HIV infection and HPV-related cancer. While first-line antibiotic treatment (metronidazole) commonly kills the protozoan pathogen, it fails to improve reproductive outcome. We show that endosymbiotic Trichomonasvirus, highly prevalent in T. vaginalis clinical isolates, is sensed by the human epithelial cells via Toll-like receptor 3, triggering Interferon Regulating Factor -3, interferon type I and proinflammatory cascades previously implicated in preterm birth and HIV-1 susceptibility. Metronidazole treatment amplified these proinflammatory responses. Thus, a new paradigm targeting the protozoan viruses along with the protozoan host may prevent trichomoniasis-attributable inflammatory sequelae.Wide-spread protozoan parasites carry endosymbiotic dsRNA viruses with uncharted implications to the human host. Among them, Trichomonas vaginalis, a parasite adapted to the human genitourinary tract, infects globally ∼250 million each year rendering them more susceptible to devastating pregnancy complications (especially preterm birth), HIV infection and HPV-related cancer. While first-line antibiotic treatment (metronidazole) commonly kills the protozoan pathogen, it fails to improve reproductive outcome. We show that endosymbiotic Trichomonasvirus, highly prevalent in T. vaginalis clinical isolates, is sensed by the human epithelial cells via Toll-like receptor 3, triggering Interferon Regulating Factor -3, interferon type I and proinflammatory cascades previously implicated in preterm birth and HIV-1 susceptibility. Metronidazole treatment amplified these proinflammatory responses. Thus, a new paradigm targeting the protozoan viruses along with the protozoan host may prevent trichomoniasis-attributable inflammatory sequelae. Wide-spread protozoan parasites carry endosymbiotic dsRNA viruses with uncharted implications to the human host. Among them, Trichomonas vaginalis, a parasite adapted to the human genitourinary tract, infects globally ∼250 million each year rendering them more susceptible to devastating pregnancy complications (especially preterm birth), HIV infection and HPV-related cancer. While first-line antibiotic treatment (metronidazole) commonly kills the protozoan pathogen, it fails to improve reproductive outcome. We show that endosymbiotic Trichomonasvirus, highly prevalent in T. vaginalis clinical isolates, is sensed by the human epithelial cells via Toll-like receptor 3, triggering Interferon Regulating Factor -3, interferon type I and proinflammatory cascades previously implicated in preterm birth and HIV-1 susceptibility. Metronidazole treatment amplified these proinflammatory responses. Thus, a new paradigm targeting the protozoan viruses along with the protozoan host may prevent trichomoniasis-attributable inflammatory sequelae. Wide-spread protozoan parasites carry endosymbiotic dsRNA viruses with uncharted implications to the human host. Among them, Trichomonas vaginalis, a parasite adapted to the human genitourinary tract, infects globally ~250 million each year rendering them more susceptible to devastating pregnancy complications (especially preterm birth), HIV infection and HPV-related cancer. While first-line antibiotic treatment (metronidazole) commonly kills the protozoan pathogen, it fails to improve reproductive outcome. We show that endosymbiotic Trichomonasvirus, highly prevalent in T. vaginalis clinical isolates, is sensed by the human epithelial cells via Toll-like receptor 3, triggering Interferon Regulating Factor -3, interferon type I and proinflammatory cascades previously implicated in preterm birth and HIV-1 susceptibility. Metronidazole treatment amplified these proinflammatory responses. Thus, a new paradigm targeting the protozoan viruses along with the protozoan host may prevent trichomoniasis-attributable inflammatory sequelae. |
| Audience | Academic |
| Author | Nibert, Max L. Takagi, Yuko Hayes, Gary R. Fichorova, Raina N. Singh, Bibhuti N. Murray, Ryan Goodman, Russell P. Chepa-Lotrea, Xenia Kula, Tomasz Yamamoto, Hidemi S. Beach, David H. Buck, Olivia R. Lee, Yujin |
| AuthorAffiliation | 3 Department of Biochemistry and Molecular Biology and Department of Obstetrics and Gynecology, SUNY Upstate Medical University, Syracuse, New York, United States of America 2 Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts, United States of America 4 Department of Microbiology and Immunology, SUNY Upstate Medical University, Syracuse, New York, United States of America 1 Laboratory of Genital Tract Biology, Department of Obstetrics, Gynecology and Reproductive Biology, Harvard Medical School and Brigham and Women’s Hospital, Boston, Massachusetts, United States of America University of Lausanne, Switzerland |
| AuthorAffiliation_xml | – name: 3 Department of Biochemistry and Molecular Biology and Department of Obstetrics and Gynecology, SUNY Upstate Medical University, Syracuse, New York, United States of America – name: 1 Laboratory of Genital Tract Biology, Department of Obstetrics, Gynecology and Reproductive Biology, Harvard Medical School and Brigham and Women’s Hospital, Boston, Massachusetts, United States of America – name: 2 Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts, United States of America – name: University of Lausanne, Switzerland – name: 4 Department of Microbiology and Immunology, SUNY Upstate Medical University, Syracuse, New York, United States of America |
| Author_xml | – sequence: 1 givenname: Raina N. surname: Fichorova fullname: Fichorova, Raina N. – sequence: 2 givenname: Yujin surname: Lee fullname: Lee, Yujin – sequence: 3 givenname: Hidemi S. surname: Yamamoto fullname: Yamamoto, Hidemi S. – sequence: 4 givenname: Yuko surname: Takagi fullname: Takagi, Yuko – sequence: 5 givenname: Gary R. surname: Hayes fullname: Hayes, Gary R. – sequence: 6 givenname: Russell P. surname: Goodman fullname: Goodman, Russell P. – sequence: 7 givenname: Xenia surname: Chepa-Lotrea fullname: Chepa-Lotrea, Xenia – sequence: 8 givenname: Olivia R. surname: Buck fullname: Buck, Olivia R. – sequence: 9 givenname: Ryan surname: Murray fullname: Murray, Ryan – sequence: 10 givenname: Tomasz surname: Kula fullname: Kula, Tomasz – sequence: 11 givenname: David H. surname: Beach fullname: Beach, David H. – sequence: 12 givenname: Bibhuti N. surname: Singh fullname: Singh, Bibhuti N. – sequence: 13 givenname: Max L. surname: Nibert fullname: Nibert, Max L. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23144878$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | COPYRIGHT 2012 Public Library of Science 2012 Fichorova et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2012 Fichorova et al 2012 Fichorova et al |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Competing Interests: The authors have declared that no competing interests exist. Current address: Xenia Chepa-Lotrea: NIH, NIDDK, Liver Disease Branch Immunology, Section, Bethesda, Maryland, United States of America Current address: Northeastern University, Boston, Massachusetts, United States of America Current address: Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, United States of America Performed the experiments: RNF YL HSY ORB XCL. Analyzed the data: RNF YL HSY RM ORB. Wrote the paper: RNF. Conceived and designed the experiments, immunology and cell biology: RNF; virology: MLN. Contributed reagents/materials/analysis tools, LPS and primary TV isolates: BNS DHB GH; virion isolation and RT-PCR: YT TK RPG; TVV dsRNA and RNAse treatments: YT; TV culture: DHB GH XCL RM ORB RNF; TV cloning: RNF; Western blot: ORB; qNPA: HSY; luciferase and immunoassays: YL HSY RM ORB. Reviewed and approved the manuscript: RNF YL HSY YT GH RPG XCL ORB RM TK DHB BNS MLN. Recruited clinical subjects: BNS. |
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| Title | Endobiont Viruses Sensed by the Human Host – Beyond Conventional Antiparasitic Therapy |
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