Related Experiment Video
Updated: Nov 8, 2025
Use of Viral Entry Assays and Molecular Docking Analysis for the Identification of Antiviral Candidates against Coxsackievirus A16
Published on: July 15, 2019
A hSCARB2-transgenic mouse model for Coxsackievirus A16 pathogenesis
Yanli Chen1,2, Heng Li1,2, Jinxi Yang1,2
1Institute of Medical Biology, Yunnan Key Laboratory of Vaccine Research and Development On Severe Infectious Diseases, Chinese Academy of Medical Science and Peking Union Medical College, No. 935 Alternating Current Road, Wuhua District, Kunming, 650118, Yunna, China.
Transgenic mice expressing human scavenger receptor B1 (hSCARB2) provide a model for Coxsackievirus A16 (CA16) infection. These mice develop lung and brain pathology, mimicking severe hand, foot, and mouth disease (HFMD) neurological symptoms.
Area of Science:
- Virology
- Immunology
- Pathogenesis
Background:
- Coxsackievirus A16 (CA16) is a neurotropic pathogen linked to severe neurological hand, foot, and mouth disease (HFMD).
- Establishing animal models for CA16 neurological pathology is challenging due to its limited host range.
- Human scavenger receptor class B, member 2 (hSCARB2) is identified as a cellular receptor for CA16.
Purpose of the Study:
- To investigate the pathogenicity of CA16 using a transgenic mouse model expressing hSCARB2.
- To establish a suitable animal model for studying CA16-associated neurological disease.
Main Methods:
- Transgenic mice expressing hSCARB2 were intranasally inoculated with CA16.
- Clinical signs, viral dissemination, pathological changes, and immune responses were monitored at various time points.
Main Results:
- CA16-infected hSCARB2 mice exhibited weight loss and virus replication in the lungs and brain.
- Viral antigens were detected in lung alveolar epithelia and brainstem cells.
- Histopathology revealed interstitial pneumonia and brainstem hemorrhages, with elevated inflammatory cytokines (IL-1β, IL-6, IL-18, IFN-γ) in multiple tissues.
Conclusions:
- hSCARB2-transgenic mice are productively infected by CA16 via the respiratory route.
- These mice demonstrate tropism for lung and brain tissues.
- This model is suitable for investigating the pathogenesis of CA16-associated respiratory and neurological diseases.
