| Literature DB >> 32433769 |
Satoshi Fukuyama1, Kiyoko Iwatsuki-Horimoto1, Maki Kiso1, Noriko Nakajima2, Robert W Gregg3, Hiroaki Katsura1, Yuriko Tomita1, Tadashi Maemura1,4,5, Tiago Jose da Silva Lopes1,4, Tokiko Watanabe1, Jason E Shoemaker1,3,6, Hideki Hasegawa7, Seiya Yamayoshi1, Yoshihiro Kawaoka1,5.
Abstract
The avian influenza A(H7N9) virus has caused high mortality rates in humans, especially in the elderly; however, little is known about the mechanistic basis for this. In the current study, we used nonhuman 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 age 20-26 years) caused more severe symptoms than infection of young animals (defined as age 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, 1 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.Entities:
Keywords: Aging; dysregulated immunity; immune senescence; influenza; nonhuman primate
Year: 2020 PMID： 32433769 PMCID： PMC7459135 DOI： 10.1093/infdis/jiaa267
Source DB: PubMed Journal: J Infect Dis ISSN： 0022-1899 Impact factor: 5.226