tetano
Editor, Senior Moderator
Curr Top Microbiol Immunol. 2020 Jan 23. doi: 10.1007/82_2019_190. [Epub ahead of print] [h=1]ZBP1/DAI-Dependent Cell Death Pathways in Influenza A Virus Immunity and Pathogenesis.[/h]
Thomas PG[SUP]1[/SUP], Shubina M[SUP]2[/SUP], Balachandran S[SUP]3[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Influenza A viruses (IAV) are members of the Orthomyxoviridae family of negative-sense RNA viruses. The greatest diversity of IAV strains is found in aquatic birds, but a subset of strains infects other avian as well as mammalian species, including humans. In aquatic birds, infection is largely restricted to the gastrointestinal tract and spread is through feces, while in humans and other mammals, respiratory epithelial cells are the primary sites supporting productive replication and transmission. IAV triggers the death of most cell types in which it replicates, both in culture and in vivo. When well controlled, such cell death is considered an effective host defense mechanism that eliminates infected cells and limits virus spread. Unchecked or inopportune cell death also results in immunopathology. In this review, we discuss the impact of cell death in restricting virus spread, supporting the adaptive immune response and driving pathogenesis in the mammalian respiratory tract. Recent studies have begun to shed light on the signaling pathways underlying IAV-activated cell death. These pathways, initiated by the pathogen sensor protein ZBP1 (also called DAI and DLM1), cause infected cells to undergo apoptosis, necroptosis, and pyroptosis. We outline mechanisms of ZBP1-mediated cell death signaling following IAV infection.
[h=4]KEYWORDS:[/h] Apoptosis; Caspase-8; Influenza A virus; Necroptosis; Necrosis; RIPK1; RIPK3; ZBP1/DAI
PMID: 31970498 DOI: 10.1007/82_2019_190
Thomas PG[SUP]1[/SUP], Shubina M[SUP]2[/SUP], Balachandran S[SUP]3[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Influenza A viruses (IAV) are members of the Orthomyxoviridae family of negative-sense RNA viruses. The greatest diversity of IAV strains is found in aquatic birds, but a subset of strains infects other avian as well as mammalian species, including humans. In aquatic birds, infection is largely restricted to the gastrointestinal tract and spread is through feces, while in humans and other mammals, respiratory epithelial cells are the primary sites supporting productive replication and transmission. IAV triggers the death of most cell types in which it replicates, both in culture and in vivo. When well controlled, such cell death is considered an effective host defense mechanism that eliminates infected cells and limits virus spread. Unchecked or inopportune cell death also results in immunopathology. In this review, we discuss the impact of cell death in restricting virus spread, supporting the adaptive immune response and driving pathogenesis in the mammalian respiratory tract. Recent studies have begun to shed light on the signaling pathways underlying IAV-activated cell death. These pathways, initiated by the pathogen sensor protein ZBP1 (also called DAI and DLM1), cause infected cells to undergo apoptosis, necroptosis, and pyroptosis. We outline mechanisms of ZBP1-mediated cell death signaling following IAV infection.
[h=4]KEYWORDS:[/h] Apoptosis; Caspase-8; Influenza A virus; Necroptosis; Necrosis; RIPK1; RIPK3; ZBP1/DAI
PMID: 31970498 DOI: 10.1007/82_2019_190