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Virology. 2017 Oct 11;513:29-42. doi: 10.1016/j.virol.2017.10.007. [Epub ahead of print]
Productive replication of avian influenza viruses in chicken endothelial cells is determined by hemagglutinin cleavability and is related to innate immune escape.
Lion A1, Richard M2, Esnault E1, Kut E1, Soubieux D1, Guillory V1, Germond M1, Blondeau C1, Guabiraba R1, Short KR3, Marc D1, Qu?r? P1, Trapp S4.
Author information
Abstract
Endotheliotropism is a hallmark of gallinaceous poultry infections with highly pathogenic avian influenza (HPAI) viruses and a feature that distinguishes HPAI from low pathogenic avian influenza (LPAI) viruses. Here, we used chicken aortic endothelial cells (chAEC) as a novel in vitro infection model to assess the susceptibility, permissiveness, and host response of chicken endothelial cells (EC) to infections with avian influenza (AI) viruses. Our data show that productive replication of AI viruses in chAEC is critically determined by hemagglutinin cleavability, and is thus an exclusive trait of HPAI viruses. However, we provide evidence for a link between limited (i.e. trypsin-dependent) replication of certain LPAI viruses, and the viruses' ability to dampen the antiviral innate immune response in infected chAEC. Strikingly, this cell response pattern was also detected in HPAI virus-infected chAEC, suggesting that viral innate immune escape might be a prerequisite for robust AI virus replication in chicken EC.
Copyright ? 2017 Elsevier Inc. All rights reserved.
KEYWORDS:
Avian influenza; Cell tropism; Chicken; Endothelial cells; Inflammation; Influenza A virus; Innate immunity; Pathogenesis; Poultry; Virus-host interactions
PMID: 29031164 DOI: 10.1016/j.virol.2017.10.007
Productive replication of avian influenza viruses in chicken endothelial cells is determined by hemagglutinin cleavability and is related to innate immune escape.
Lion A1, Richard M2, Esnault E1, Kut E1, Soubieux D1, Guillory V1, Germond M1, Blondeau C1, Guabiraba R1, Short KR3, Marc D1, Qu?r? P1, Trapp S4.
Author information
Abstract
Endotheliotropism is a hallmark of gallinaceous poultry infections with highly pathogenic avian influenza (HPAI) viruses and a feature that distinguishes HPAI from low pathogenic avian influenza (LPAI) viruses. Here, we used chicken aortic endothelial cells (chAEC) as a novel in vitro infection model to assess the susceptibility, permissiveness, and host response of chicken endothelial cells (EC) to infections with avian influenza (AI) viruses. Our data show that productive replication of AI viruses in chAEC is critically determined by hemagglutinin cleavability, and is thus an exclusive trait of HPAI viruses. However, we provide evidence for a link between limited (i.e. trypsin-dependent) replication of certain LPAI viruses, and the viruses' ability to dampen the antiviral innate immune response in infected chAEC. Strikingly, this cell response pattern was also detected in HPAI virus-infected chAEC, suggesting that viral innate immune escape might be a prerequisite for robust AI virus replication in chicken EC.
Copyright ? 2017 Elsevier Inc. All rights reserved.
KEYWORDS:
Avian influenza; Cell tropism; Chicken; Endothelial cells; Inflammation; Influenza A virus; Innate immunity; Pathogenesis; Poultry; Virus-host interactions
PMID: 29031164 DOI: 10.1016/j.virol.2017.10.007