Avian Influenza A (H7N9) viruses isolated from patients with mild and fatal infection differ in pathogenicity and induction of cytokines. (October 2017)

• Record Type: Journal Article
• Authors: Zhou, Junmei; Guo, Xiaolan; Fang, Danyun; Yu, Yufeng; Si, Lulu; Wang, Ying; Zeng, Gucheng; Yan, Huijun; Wu, Jie; Ke, Changwen; Jiang, Lifang
• Is Part Of: Microbial pathogenesis. Volume 111(2017)
• Page Start: 402
• Page End: 409
• Publication Date: 2017-10
• Subjects: Pathogenic microorganisms -- Periodicals; Pathology, Molecular -- Periodicals; Communicable Diseases -- microbiology -- Periodicals; Communicable Diseases -- parasitology -- Periodicals; Micro-organismes pathogènes -- Périodiques; Pathologie moléculaire -- Périodiques; Electronic journals; 616.9041
• DOI: 10.1016/j.micpath.2017.08.022
• Languages: English
• ISSNs: 0882-4010

Abstract

Abstract: Since 2013, a novel Influenza A (H7N9) virus strain has continued to circulate within poultry and causing human disease. Influenza A (H7N9) virus results in two types of infection: mild and severe. The different results of clinical findings may be related with host susceptibility and characteristics of the virus itself. In order to investigate potential pathogenesis of Influenza A (H7N9) virus, we performed pathogenecity and cytokines analysis of two isolates, A/Guangdong/6/2013 H7N9 virus (GD-6) from a patient with a mild infection, and A/Guangdong/7/2013 H7N9 virus (GD-7) from a patient with a fatal infection. We found that GD-7 replicated to higher levels than GD-6 in human peripheral blood mononuclear cells (PBMCs), lung tissues, and mice. Furthermore, GD-7 infection resulted in more severe lung damage in mice lung tissues than GD-6 infection. GD-7 elicited higher levels of interleukin-6 (IL-6) and tumor necrosis factor-α(TNF-α) than GD-6 did. In conclusion, GD-7 was more pathogenic and induced higher levels of proinflammatory cytokines than GD-6 did. Highlights: Influenza A (H7N9) virus results in two types of infection: mild and severe. The different results of clinical findings may be related with host susceptibility and characteristics of the virus itself. In order to investigate potential pathogenesis of Influenza A (H7N9) virus, we performed pathogenecity and cytokines analysis of two isolates, A/Guangdong/6/2013 H7N9 virus (GD-6) from a patient with a mild infection, and A/Guangdong/7/2013 H7N9 virus (GD-7) from a patient with a fatal infection. We found that GD-7 replicated to higher levels than GD-6 in human peripheral blood mononuclear cells (PBMCs), lung tissues, and mice. Furthermore, GD-7 infection resulted in more severe lung damage in mice lung tissues than GD-6 infection. GD-7 elicited higher levels of interleukin-6 (IL-6) and tumor necrosis factor-α(TNF-α) than GD-6 did. In conclusion, GD-7 was more pathogenic and induced higher levels of proinflammatory cytokines than GD-6 did. A critical difference between GD-6 and GD-7 at residue 627 in the PB2 protein with GD-6 having the avian 627E and GD-7 having the mammalian adapted 627K. The effect of this difference to the clinical severity needs further molecular genetical and biological studies.