tetano
Editor, Senior Moderator
J Infect Dis
. 2020 May 20;jiaa267.
doi: 10.1093/infdis/jiaa267. Online ahead of print.
Pathogenesis of Influenza A(H7N9) Virus in Aged Non-Human Primates
Satoshi Fukuyama[SUP] 1 [/SUP], Kiyoko Iwatsuki-Horimoto[SUP] 1 [/SUP], Maki Kiso[SUP] 1 [/SUP], Noriko Nakajima[SUP] 2 [/SUP], Robert W Gregg[SUP] 3 [/SUP], Hiroaki Katsura[SUP] 1 [/SUP], Yuriko Tomita[SUP] 1 [/SUP], Tadashi Maemura[SUP] 1 4 5 [/SUP], Tiago Jose da Silva Lopes[SUP] 1 4 [/SUP], Tokiko Watanabe[SUP] 1 [/SUP], Jason E Shoemaker[SUP] 1 3 6 [/SUP], Hideki Hasegawa[SUP] 7 [/SUP], Seiya Yamayoshi[SUP] 1 [/SUP], Yoshihiro Kawaoka[SUP] 1 5 [/SUP]
Affiliations
Abstract
The avian influenza A(H7N9) virus has caused high mortality in humans, especially in the elderly; however, little is known about the mechanistic basis for this. In this study, we employed non-human primates to evaluate the effect of aging on the pathogenicity of A(H7N9) virus. We observed that A(H7N9) virus infection of aged animals (defined as 20-26 years) caused more severe symptoms than infection of young animals (defined as 2-3 years). In aged animals, lung inflammation was weak and virus infection was sustained. Although cytokine and chemokine expression in the lungs of most aged animals was lower than that in the lungs of young animals, one aged animal showed severe symptoms and dysregulated proinflammatory cytokine and chemokine production. These results suggest that attenuated or dysregulated immune responses in aged animals are responsible for the severe symptoms observed among elderly patients infected with A(H7N9) virus.
Keywords: Aging; dysregulated immunity; immune senescence; influenza; non-human primate.
. 2020 May 20;jiaa267.
doi: 10.1093/infdis/jiaa267. Online ahead of print.
Pathogenesis of Influenza A(H7N9) Virus in Aged Non-Human Primates
Satoshi Fukuyama[SUP] 1 [/SUP], Kiyoko Iwatsuki-Horimoto[SUP] 1 [/SUP], Maki Kiso[SUP] 1 [/SUP], Noriko Nakajima[SUP] 2 [/SUP], Robert W Gregg[SUP] 3 [/SUP], Hiroaki Katsura[SUP] 1 [/SUP], Yuriko Tomita[SUP] 1 [/SUP], Tadashi Maemura[SUP] 1 4 5 [/SUP], Tiago Jose da Silva Lopes[SUP] 1 4 [/SUP], Tokiko Watanabe[SUP] 1 [/SUP], Jason E Shoemaker[SUP] 1 3 6 [/SUP], Hideki Hasegawa[SUP] 7 [/SUP], Seiya Yamayoshi[SUP] 1 [/SUP], Yoshihiro Kawaoka[SUP] 1 5 [/SUP]
Affiliations
- PMID: 32433769
- DOI: 10.1093/infdis/jiaa267
Abstract
The avian influenza A(H7N9) virus has caused high mortality in humans, especially in the elderly; however, little is known about the mechanistic basis for this. In this study, we employed non-human primates to evaluate the effect of aging on the pathogenicity of A(H7N9) virus. We observed that A(H7N9) virus infection of aged animals (defined as 20-26 years) caused more severe symptoms than infection of young animals (defined as 2-3 years). In aged animals, lung inflammation was weak and virus infection was sustained. Although cytokine and chemokine expression in the lungs of most aged animals was lower than that in the lungs of young animals, one aged animal showed severe symptoms and dysregulated proinflammatory cytokine and chemokine production. These results suggest that attenuated or dysregulated immune responses in aged animals are responsible for the severe symptoms observed among elderly patients infected with A(H7N9) virus.
Keywords: Aging; dysregulated immunity; immune senescence; influenza; non-human primate.