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Functional Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand Production by Avian Influenza Virus–Infected Macrophages

Identifieur interne : 004073 ( Main/Exploration ); précédent : 004072; suivant : 004074

Functional Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand Production by Avian Influenza Virus–Infected Macrophages

Auteurs : Jianfang Zhou ; Helen K. W. Law ; Chung Yan Cheung [République populaire de Chine] ; Iris H. Y. Ng [République populaire de Chine] ; J. S. Malik Peiris [République populaire de Chine] ; Yu Lung Lau

Source :

RBID : ISTEX:6ADFA73BD5AB2AE9E6248B3C9C89DFD6566DB7BA

Abstract

Severe human disease associated with influenza A H5N1 virus was first detected in Hong Kong in 1997. Its recent reemergence in Asia and high associated mortality highlight the need to understand its pathogenesis. We investigated the roles of death receptor ligands (DRLs) in H5N1 infection. Significant up-regulation of tumor necrosis factor (TNF)–related apoptosis-inducing ligand (TRAIL) and TNF-α, but not Fas ligand (FasL) mRNA, was detected in human monocyte–derived macrophages (MDMs) infected with avian influenza viruses A/Hong Kong/483/97 (H5N1/97) or its precursor, A/Quail/Hong Kong/G1/97. H5N1/97-infected MDMs exhibited the strongest induction of apoptosis in Jurkat T cells, and it could be reduced by TRAIL–receptor 2 blocking antibody. Furthermore, influenza virus infection enhanced the sensitivity of Jurkat T cells to apoptosis induced by TNF-α, TRAIL, and FasL. Our data suggested that functional TRAIL produced by influenza virus–infected MDMs was related to their cytotoxicity and that the enhanced sensitization to DRL-induced apoptosis detected in avian influenza may contribute to disease pathogenesis

Url:
DOI: 10.1086/500954


Affiliations:


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