Hantavirus-infection confers resistance to cytotoxic lymphocyte-mediated apoptosis.

Hantaviruses cause hemorrhagic fever with renal syndrome (HFRS) and hantavirus cardio-pulmonary syndrome (HCPS; also called hantavirus pulmonary syndrome (HPS)), both human diseases with high case-fatality rates. Endothelial cells are the main targets for hantaviruses. An intriguing observation in p...

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Autores principales: Shawon Gupta, Monika Braun, Nicole D Tischler, Malin Stoltz, Karin B Sundström, Niklas K Björkström, Hans-Gustaf Ljunggren, Jonas Klingström
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Publicado: Public Library of Science (PLoS) 2013
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Acceso en línea:https://doaj.org/article/1b22078f2aa1413caf87523ca18aa9f1
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spelling oai:doaj.org-article:1b22078f2aa1413caf87523ca18aa9f12021-11-18T06:05:51ZHantavirus-infection confers resistance to cytotoxic lymphocyte-mediated apoptosis.1553-73661553-737410.1371/journal.ppat.1003272https://doaj.org/article/1b22078f2aa1413caf87523ca18aa9f12013-03-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23555267/pdf/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Hantaviruses cause hemorrhagic fever with renal syndrome (HFRS) and hantavirus cardio-pulmonary syndrome (HCPS; also called hantavirus pulmonary syndrome (HPS)), both human diseases with high case-fatality rates. Endothelial cells are the main targets for hantaviruses. An intriguing observation in patients with HFRS and HCPS is that on one hand the virus infection leads to strong activation of CD8 T cells and NK cells, on the other hand no obvious destruction of infected endothelial cells is observed. Here, we provide an explanation for this dichotomy by showing that hantavirus-infected endothelial cells are protected from cytotoxic lymphocyte-mediated induction of apoptosis. When dissecting potential mechanisms behind this phenomenon, we discovered that the hantavirus nucleocapsid protein inhibits the enzymatic activity of both granzyme B and caspase 3. This provides a tentative explanation for the hantavirus-mediated block of cytotoxic granule-mediated apoptosis-induction, and hence the protection of infected cells from cytotoxic lymphocytes. These findings may explain why infected endothelial cells in hantavirus-infected patients are not destroyed by the strong cytotoxic lymphocyte response.Shawon GuptaMonika BraunNicole D TischlerMalin StoltzKarin B SundströmNiklas K BjörkströmHans-Gustaf LjunggrenJonas KlingströmPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 9, Iss 3, p e1003272 (2013)
institution DOAJ
collection DOAJ
language EN
topic Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
spellingShingle Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
Shawon Gupta
Monika Braun
Nicole D Tischler
Malin Stoltz
Karin B Sundström
Niklas K Björkström
Hans-Gustaf Ljunggren
Jonas Klingström
Hantavirus-infection confers resistance to cytotoxic lymphocyte-mediated apoptosis.
description Hantaviruses cause hemorrhagic fever with renal syndrome (HFRS) and hantavirus cardio-pulmonary syndrome (HCPS; also called hantavirus pulmonary syndrome (HPS)), both human diseases with high case-fatality rates. Endothelial cells are the main targets for hantaviruses. An intriguing observation in patients with HFRS and HCPS is that on one hand the virus infection leads to strong activation of CD8 T cells and NK cells, on the other hand no obvious destruction of infected endothelial cells is observed. Here, we provide an explanation for this dichotomy by showing that hantavirus-infected endothelial cells are protected from cytotoxic lymphocyte-mediated induction of apoptosis. When dissecting potential mechanisms behind this phenomenon, we discovered that the hantavirus nucleocapsid protein inhibits the enzymatic activity of both granzyme B and caspase 3. This provides a tentative explanation for the hantavirus-mediated block of cytotoxic granule-mediated apoptosis-induction, and hence the protection of infected cells from cytotoxic lymphocytes. These findings may explain why infected endothelial cells in hantavirus-infected patients are not destroyed by the strong cytotoxic lymphocyte response.
format article
author Shawon Gupta
Monika Braun
Nicole D Tischler
Malin Stoltz
Karin B Sundström
Niklas K Björkström
Hans-Gustaf Ljunggren
Jonas Klingström
author_facet Shawon Gupta
Monika Braun
Nicole D Tischler
Malin Stoltz
Karin B Sundström
Niklas K Björkström
Hans-Gustaf Ljunggren
Jonas Klingström
author_sort Shawon Gupta
title Hantavirus-infection confers resistance to cytotoxic lymphocyte-mediated apoptosis.
title_short Hantavirus-infection confers resistance to cytotoxic lymphocyte-mediated apoptosis.
title_full Hantavirus-infection confers resistance to cytotoxic lymphocyte-mediated apoptosis.
title_fullStr Hantavirus-infection confers resistance to cytotoxic lymphocyte-mediated apoptosis.
title_full_unstemmed Hantavirus-infection confers resistance to cytotoxic lymphocyte-mediated apoptosis.
title_sort hantavirus-infection confers resistance to cytotoxic lymphocyte-mediated apoptosis.
publisher Public Library of Science (PLoS)
publishDate 2013
url https://doaj.org/article/1b22078f2aa1413caf87523ca18aa9f1
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AT monikabraun hantavirusinfectionconfersresistancetocytotoxiclymphocytemediatedapoptosis
AT nicoledtischler hantavirusinfectionconfersresistancetocytotoxiclymphocytemediatedapoptosis
AT malinstoltz hantavirusinfectionconfersresistancetocytotoxiclymphocytemediatedapoptosis
AT karinbsundstrom hantavirusinfectionconfersresistancetocytotoxiclymphocytemediatedapoptosis
AT niklaskbjorkstrom hantavirusinfectionconfersresistancetocytotoxiclymphocytemediatedapoptosis
AT hansgustafljunggren hantavirusinfectionconfersresistancetocytotoxiclymphocytemediatedapoptosis
AT jonasklingstrom hantavirusinfectionconfersresistancetocytotoxiclymphocytemediatedapoptosis
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