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Updated: May 1, 2026

Arbovirus Infections As Screening Tools for the Identification of Viral Immunomodulators and Host Antiviral Factors
Published on: September 13, 2018
Differential interferon pathway gene expression patterns in Rhabdomyosarcoma cells during Enterovirus 71 or
Wei Zhang1, Lei Zhang2, Zhiyong Wu2
1Center for Molecular Virology, CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, PR China; University of the Chinese Academy of Sciences, Beijing, 100101, PR China.
Abstract:
Exposure of cells to type I interferon (IFN) induces an antiviral state that prevents viral infection, but viruses can utilize multiple tactics to antagonize the host immune system. Enterovirus 71 (EV71) and Coxsackievirus A16 (CVA16) are two major pathogens that cause hand, foot, and mouth disease (HFMD), which is prevalent among children. We found that both EV71 and CA16 have different reactions to type I IFN pretreatment and induction patterns of type I IFN on Rhabdomyosarcoma (RD) cells. Further, a human-α and β IFN PCR array was employed to analyze the expressions of 84 genes related to the type I IFN pathway. We found significant up-regulation of multiple genes in the presence of type I IFN and differential regulation patterns during EV71 or CA16 infection in RD cells. For instance, EV71 infection repressed the JAK-STAT signaling pathway and interferon-stimulated gene (ISG) expression, whereas CA16 infection normally triggers the JAK-STAT pathway, leading to the expression of ISGs. Taken together, this study provides a comprehensive view of the differential impacts of EV71 and CA16 infection on 84 genes in the IFN pathway, shedding light on the different resistances of these viruses to type I IFN treatment and cytotoxic effects in RD cells.
Insights
Enterovirus 71 and Coxsackievirus A16 exhibit distinct responses to type I interferon (IFN) signaling. Understanding these differences in hand, foot, and mouth disease (HFMD) pathogenesis is crucial for developing effective antiviral strategies.
Area of Science:
- Virology
- Immunology
- Molecular Biology
Background:
- Type I interferon (IFN) establishes an antiviral state, but viruses employ countermeasures.
- Enterovirus 71 (EV71) and Coxsackievirus A16 (CVA16) are key pathogens causing hand, foot, and mouth disease (HFMD).
Purpose of the Study:
- To investigate the differential impact of EV71 and CVA16 infections on the type I IFN pathway in Rhabdomyosarcoma (RD) cells.
- To elucidate the distinct host immune evasion strategies employed by EV71 and CVA16.
Main Methods:
- Exposure of RD cells to type I IFN and subsequent infection with EV71 or CVA16.
- Analysis of type I IFN pretreatment and induction patterns.
- Utilizing a human-α and β IFN PCR array to assess the expression of 84 type I IFN-related genes.
Main Results:
- EV71 and CVA16 displayed differential responses to type I IFN pretreatment and induction.
- EV71 infection repressed the JAK-STAT signaling pathway and interferon-stimulated gene (ISG) expression.
- CVA16 infection activated the JAK-STAT pathway and promoted ISG expression.
Conclusions:
- EV71 and CVA16 exhibit distinct modulation of the type I IFN pathway during infection.
- These differences in IFN pathway regulation contribute to the viruses' varied resistance to type I IFN treatment and cytotoxic effects.
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