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Updated: Jun 26, 2025

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
Pathogenicity and transcriptomic profiling reveals immunology molecular hallmarks after CA10 virus infection
Wanjun Peng1, Jing Wu1, Binbin Zhao1
1NHC Key Laboratory of Human Disease Comparative Medicine, Beijing Key Laboratory for Animal Models of Emerging and Remerging Infectious Diseases, Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences and Comparative Medicine Center, Peking Union Medical College, Beijing, China.
Coxsackievirus A 10 (CA10) infection in mice causes paralysis and weight loss, with significant immune gene changes in affected tissues. This study enhances understanding of hand, foot, and mouth disease (HFMD) pathology.
Area of Science:
- Virology
- Immunology
- Pathology
Background:
- Hand, foot, and mouth disease (HFMD) is a common viral illness.
- Enteroviruses, including coxsackievirus A 10 (CA10), are causative agents.
- CA10 prevalence has increased recently.
Purpose of the Study:
- To investigate the pathogenicity of CA10.
- To identify host gene responses to CA10 infection.
- To compare CA10 with other HFMD-associated enteroviruses.
Main Methods:
- Established CA10 infection model in ICR mice.
- Utilized RNA sequencing to screen differentially expressed genes (DEGs).
- Compared CA10 with Coxsackievirus A 16 (CA16) and Enterovirus 71 (EV71) infections.
Main Results:
- CA10 infection led to hind limb paralysis and weight loss in mice.
- Viral replication and inflammation were observed in skeletal muscle.
- DEGs in blood, muscle, thymus, and spleen showed heterogeneity; muscle DEGs were enriched in immune pathways.
- CA10 infection may inhibit T helper cell differentiation and growth compared to CA16 and EV71.
- Common DEGs across all three viruses were linked to immune responses, including Toll-like receptor and NOD-like pathways.
Conclusions:
- Identified key genes involved in the host response to CA10 infection.
- Provided insights into the molecular mechanisms of CA10-induced HFMD pathology.
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