Transient Liver Damage and Hemolysis Are Associated With an Inhibition of Ebola Virus Glycoprotein-Specific Antibody Response and Lymphopenia
© The Author(s) 2021. Published by Oxford University Press for the Infectious Diseases Society of America..
Numerous studies have demonstrated the importance of the adaptive immunity for survival following Ebola virus (EBOV) infection. To evaluate the contribution of tissue damage to EBOV-induced immune suppression, acute liver damage or hemolysis, 2 symptoms associated with lethal EBOV infection, were chemically induced in vaccinated mice. Results show that either liver damage or hemolysis was sufficient to inhibit the host humoral response against EBOV glycoprotein and to drastically reduce the level of circulating T cells. This study thus provides a possible mechanism for the limited specific antibody production and lymphopenia in individuals with lethal hemorrhagic fever infections.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2022 |
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Erschienen: |
2022 |
Enthalten in: |
Zur Gesamtaufnahme - volume:225 |
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Enthalten in: |
The Journal of infectious diseases - 225(2022), 10 vom: 16. Mai, Seite 1852-1855 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Fausther-Bovendo, Hugues [VerfasserIn] |
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Links: |
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Themen: |
Antibodies, Viral |
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Anmerkungen: |
Date Completed 19.05.2022 Date Revised 16.09.2023 published: Print Citation Status MEDLINE |
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doi: |
10.1093/infdis/jiab552 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM333289307 |
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520 | |a Numerous studies have demonstrated the importance of the adaptive immunity for survival following Ebola virus (EBOV) infection. To evaluate the contribution of tissue damage to EBOV-induced immune suppression, acute liver damage or hemolysis, 2 symptoms associated with lethal EBOV infection, were chemically induced in vaccinated mice. Results show that either liver damage or hemolysis was sufficient to inhibit the host humoral response against EBOV glycoprotein and to drastically reduce the level of circulating T cells. This study thus provides a possible mechanism for the limited specific antibody production and lymphopenia in individuals with lethal hemorrhagic fever infections | ||
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