tetano
Editor, Senior Moderator
Cell Microbiol. 2020 Jan 28. doi: 10.1111/cmi.13170. [Epub ahead of print] [h=1]Influenza A virus interactions with macrophages: lessons from epithelial cells.[/h]
Meischel T[SUP]1[/SUP], Villalon-Letelier F[SUP]1[/SUP], Saunders PM[SUP]1[/SUP], Reading PC[SUP]1,[/SUP][SUP]2[/SUP], Londrigan SL[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Influenza viruses are an important cause of respiratory infection worldwide. In humans, infection with seasonal influenza A virus (IAV) is generally restricted to the respiratory tract where productive infection of airway epithelial cells promotes viral amplification, dissemination and disease. Alveolar macrophages (MΦ) are also among the first cells to detect and respond to IAV, where they play a pivotal role in mounting effective innate immune responses. In contrast to epithelial cells, IAV infection of MΦ is a "dead end" for most seasonal strains, where replication is abortive and newly-synthesised virions are not released. While the key replicative stages leading to productive IAV infection in epithelial cells are defined, there is limited knowledge about the abortive IAV life-cycle in MΦ. In this review we will explore host factors and viral elements that support the early stages (entry) through to the late stages (viral egress) of IAV replication in epithelial cells. Similarities, differences and unknowns for each key stage of the IAV replicative cycle in MΦ will then be highlighted. Herein, we provide mechanistic insights into MΦ-specific control of seasonal IAV replication through abortive infection, which may in turn, contribute to effective host defence. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
[h=4]KEYWORDS:[/h] infection; influenza virus; macrophages; viral replication; virus
PMID: 31990121 DOI: 10.1111/cmi.13170
Meischel T[SUP]1[/SUP], Villalon-Letelier F[SUP]1[/SUP], Saunders PM[SUP]1[/SUP], Reading PC[SUP]1,[/SUP][SUP]2[/SUP], Londrigan SL[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Influenza viruses are an important cause of respiratory infection worldwide. In humans, infection with seasonal influenza A virus (IAV) is generally restricted to the respiratory tract where productive infection of airway epithelial cells promotes viral amplification, dissemination and disease. Alveolar macrophages (MΦ) are also among the first cells to detect and respond to IAV, where they play a pivotal role in mounting effective innate immune responses. In contrast to epithelial cells, IAV infection of MΦ is a "dead end" for most seasonal strains, where replication is abortive and newly-synthesised virions are not released. While the key replicative stages leading to productive IAV infection in epithelial cells are defined, there is limited knowledge about the abortive IAV life-cycle in MΦ. In this review we will explore host factors and viral elements that support the early stages (entry) through to the late stages (viral egress) of IAV replication in epithelial cells. Similarities, differences and unknowns for each key stage of the IAV replicative cycle in MΦ will then be highlighted. Herein, we provide mechanistic insights into MΦ-specific control of seasonal IAV replication through abortive infection, which may in turn, contribute to effective host defence. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
[h=4]KEYWORDS:[/h] infection; influenza virus; macrophages; viral replication; virus
PMID: 31990121 DOI: 10.1111/cmi.13170