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Influenza A Virus Studies in a Mouse Model of Infection
Published on: September 7, 2017
High Pathogenicity of Influenza A (H10N8) Virus in Mice
Haiying Chen1, Lihong Huang1, Hui Li1
1Department of Infectious Diseases, Nanchang Center for Disease Control and Prevention, Nanchang, China; College of Veterinary Medicine, South China Agricultural University, Guangzhou, China.
Abstract:
Three human cases of H10N8 virus infections were initially reported in China in late 2013 and early 2014, two of which were fatal. This was the first time the H10N8 subtype has been detected in humans, and the pathogenicity of this virus remains under characterized. We first assessed its pathogenicity by infecting BALB/c mice with two H10N8 isolates, A/Jiangxi-Donghu/346-1/2013 and A/Chicken/Jiangxi/102/2013. The human isolate (H346-1) demonstrated stronger capability of replication and induced higher cytokine response in vivo than the chicken isolate (C102). In addition, H346-1 was fatal to mice, while all mice (N = 14) in C102-infected group survived during the infection course without weight loss. We hypothesized that the 627K mutation in the PB2 gene (PB2-K627) in H346-1 was associated with high pathogenicity in mice. Taken together, this study based on mouse model provides some insight into understanding the pathogenicity of the emerging viruses in mammals.
Insights
The H10N8 virus, detected in humans, showed varied pathogenicity in mice. A human isolate with PB2-K627 mutation proved fatal, unlike the chicken isolate, highlighting viral adaptation in mammals.
Area of Science:
- Virology
- Infectious Diseases
- Mammalian Pathogenesis
Background:
- The H10N8 influenza A virus subtype was first identified in human cases in China (2013-2014), with a high fatality rate.
- The pathogenicity and mammalian adaptation of this novel human-infecting avian influenza virus remain largely uncharacterized.
Purpose of the Study:
- To assess and compare the pathogenicity of two H10N8 virus isolates in a mouse model.
- To investigate the potential role of specific genetic mutations in H10N8 virus virulence.
Main Methods:
- Infection of BALB/c mice with two H10N8 virus isolates: a human isolate (A/Jiangxi-Donghu/346-1/2013) and a chicken isolate (A/Chicken/Jiangxi/102/2013).
- Evaluation of viral replication, cytokine response, weight changes, and survival rates in infected mice.
- Analysis of the PB2 gene for the presence of the 627K mutation.
Main Results:
- The human H10N8 isolate (H346-1) exhibited significantly higher replication and induced a stronger cytokine response in mice compared to the chicken isolate (C102).
- H346-1 infection was lethal in mice, whereas all C102-infected mice survived without significant weight loss.
- The human isolate possessed the 627K mutation in its PB2 gene (PB2-K627).
Conclusions:
- The H10N8 virus demonstrates differential pathogenicity in mammals, with the human isolate showing increased virulence.
- The PB2-K627 mutation is a potential factor contributing to the enhanced pathogenicity of H10N8 in the mouse model.
- This study provides initial insights into the mammalian adaptation and virulence of emerging H10N8 avian influenza viruses.
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