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T cell-dependence of Lassa fever pathogenesis

Lassa virus (LASV), the causative agent of Lassa fever (LF), is endemic in West Africa, accounting for substantial morbidity and mortality. In spite of ongoing research efforts, LF pathogenesis and mechanisms of LASV immune control remain poorly understood. While normal laboratory mice are resistant...

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Published in:PLoS pathogens 2010-03, Vol.6 (3), p.e1000836-e1000836
Main Authors: Flatz, Lukas, Rieger, Toni, Merkler, Doron, Bergthaler, Andreas, Regen, Tommy, Schedensack, Mariann, Bestmann, Lukas, Verschoor, Admar, Kreutzfeldt, Mario, Brück, Wolfgang, Hanisch, Uwe-Karsten, Günther, Stephan, Pinschewer, Daniel D
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Rieger, Toni
Merkler, Doron
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Regen, Tommy
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Brück, Wolfgang
Hanisch, Uwe-Karsten
Günther, Stephan
Pinschewer, Daniel D
description Lassa virus (LASV), the causative agent of Lassa fever (LF), is endemic in West Africa, accounting for substantial morbidity and mortality. In spite of ongoing research efforts, LF pathogenesis and mechanisms of LASV immune control remain poorly understood. While normal laboratory mice are resistant to LASV, we report that mice expressing humanized instead of murine MHC class I (MHC-I) failed to control LASV infection and develop severe LF. Infection of MHC-I knockout mice confirmed a key role for MHC-I-restricted T cell responses in controlling LASV. Intriguingly we found that T cell depletion in LASV-infected HHD mice prevented disease, irrespective of high-level viremia. Widespread activation of monocyte/macrophage lineage cells, manifest through inducible NO synthase expression, and elevated IL-12p40 serum levels indicated a systemic inflammatory condition. The absence of extensive monocyte/macrophage activation in T cell-depleted mice suggested that T cell responses contribute to deleterious innate inflammatory reactions and LF pathogenesis. Our observations in mice indicate a dual role for T cells, not only protecting from LASV, but also enhancing LF pathogenesis. The possibility of T cell-driven enhancement and immunopathogenesis should be given consideration in future LF vaccine development.
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subjects Animals
Arenavirus - immunology
beta 2-Microglobulin - genetics
beta 2-Microglobulin - immunology
Causes of
Cytokines
Dependence
Development and progression
Fever
Genetic aspects
Health aspects
Immune response
Immunology
Immunology/Immune Response
Immunology/Immunity to Infections
Immunology/Innate Immunity
Infections
Infectious Diseases/Viral Infections
Interleukin-12 Subunit p40 - immunology
Interleukin-12 Subunit p40 - metabolism
Lassa fever
Lassa Fever - immunology
Lassa Fever - prevention & control
Lassa virus - immunology
Lymphocytes
Macrophages - immunology
Macrophages - metabolism
Macrophages - virology
Major Histocompatibility Complex - genetics
Major Histocompatibility Complex - immunology
Mice
Mice, Inbred C57BL
Mice, Mutant Strains
Monocytes - immunology
Monocytes - metabolism
Monocytes - virology
Morbidity
Mortality
Nitric oxide
Pathogenesis
T cells
T-Lymphocytes - immunology
T-Lymphocytes - virology
Vaccines
Viral Vaccines - immunology
title T cell-dependence of Lassa fever pathogenesis
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