tetano
Editor, Senior Moderator
Virulence
. 2021 Dec;12(1):1629-1646.
doi: 10.1080/21505594.2021.1939608.
Too young to die? How aging affects cellular innate immune responses to influenza virus and disease severity
Christopher M Harpur[SUP] 1 2 [/SUP], Mélanie A Le Page[SUP] 1 2 [/SUP], Michelle D Tate[SUP] 1 2 [/SUP]
Affiliations
Abstract
Influenza is a respiratory viral infection that causes significant morbidity and mortality worldwide. The innate immune cell response elicited during influenza A virus (IAV) infection forms the critical first line of defense, which typically is impaired as we age. As such, elderly individuals more commonly succumb to influenza-associated complications, which is reflected in most aged animal models of IAV infection. Here, we review the important roles of several major innate immune cell populations in influenza pathogenesis, some of which being deleterious to the host, and the current knowledge of how age-associated numerical, phenotypic and functional cell changes impact disease development. Further investigation into age-related modulation of innate immune cell responses, using appropriate animal models, will help reveal how immunity to IAV may be compromised by aging and inform the development of novel therapies, tailored for use in this vulnerable group.
Keywords: aging; host-pathogen interactions; influenza; pathogenesis.
. 2021 Dec;12(1):1629-1646.
doi: 10.1080/21505594.2021.1939608.
Too young to die? How aging affects cellular innate immune responses to influenza virus and disease severity
Christopher M Harpur[SUP] 1 2 [/SUP], Mélanie A Le Page[SUP] 1 2 [/SUP], Michelle D Tate[SUP] 1 2 [/SUP]
Affiliations
- PMID: 34152253
- DOI: 10.1080/21505594.2021.1939608
Abstract
Influenza is a respiratory viral infection that causes significant morbidity and mortality worldwide. The innate immune cell response elicited during influenza A virus (IAV) infection forms the critical first line of defense, which typically is impaired as we age. As such, elderly individuals more commonly succumb to influenza-associated complications, which is reflected in most aged animal models of IAV infection. Here, we review the important roles of several major innate immune cell populations in influenza pathogenesis, some of which being deleterious to the host, and the current knowledge of how age-associated numerical, phenotypic and functional cell changes impact disease development. Further investigation into age-related modulation of innate immune cell responses, using appropriate animal models, will help reveal how immunity to IAV may be compromised by aging and inform the development of novel therapies, tailored for use in this vulnerable group.
Keywords: aging; host-pathogen interactions; influenza; pathogenesis.