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Use of Viral Entry Assays and Molecular Docking Analysis for the Identification of Antiviral Candidates against Coxsackievirus A16
Published on: July 15, 2019
Coxsackievirus A16 in a 1-Day-Old Mouse Model of Central Nervous System Infection Shows Lower Neurovirulence than
1Department of Pathology, University of Malaya, Kuala Lumpur, Malaysia.
Insights
Coxsackievirus A16 (CV-A16) and enterovirus A71 (EV-A71) cause hand, foot, and mouth disease. CV-A16 shows lower neurovirulence and distinct neuropathology compared to EV-A71 in a neonatal mouse model.
Area of Science:
- Virology
- Neurology
- Pathology
Background:
- Coxsackievirus A16 (CV-A16) and enterovirus A71 (EV-A71) are leading causes of hand, foot, and mouth disease in children.
- While both viruses can cause severe neurological complications, the specific differences in their central nervous system (CNS) infections are not well understood.
Purpose of the Study:
- To comparatively analyze the neuropathology and neurovirulence of CV-A16 and EV-A71 using a neonatal mouse model.
- To elucidate the distinct mechanisms of CNS invasion and replication for these two enteroviruses.
Main Methods:
- Development and validation of novel serotype-specific probes for in situ hybridization to detect viral RNA.
- Infection of 1-day-old mice with clinically isolated CV-A16 and EV-A71 strains.
- Comparative analysis of viral antigen and RNA distribution, neuropathological changes, and lethal dose 50 (LD50).
Main Results:
- CV-A16 RNA and antigens were detected in brainstem and spinal cord neurons, confirming neurovirulence but at lower densities than EV-A71.
- CV-A16 exhibited a higher LD50, indicating lower overall neurovirulence compared to EV-A71.
- Evidence suggests potential neuroinvasion via retrograde axonal transport in peripheral motor nerves, with viral RNA/antigens found in the anterior horn white matter.
Conclusions:
- CV-A16 demonstrates distinct neuropathological features and lower neurovirulence than EV-A71 in the studied neonatal mouse model.
- The findings highlight differences in the CNS infection dynamics of these two common enteroviruses.
- Retrograde axonal transport may represent a significant route for neuroinvasion by these viruses.
Abstract:
Coxsackievirus A16 (CV-A16) and enterovirus A71 (EV-A71) are the major causes of hand, foot and mouth disease in young children. Although less so with CV-A16, both viruses are associated with serious neurological syndromes, but the differences between their central nervous system infections remain unclear. We conducted a comparative infection study using clinically-isolated CV-A16 and EV-A71 strains in a 1-day-old mouse model to better understand the neuropathology and neurovirulence of the viruses. New serotype-specific probes for in situ hybridization were developed and validated to detect CV-A16 and EV-A71 RNA in infected tissues. Demonstration of CV-A16 virus antigens/RNA, mainly in the brainstem and spinal cord neurons, confirmed neurovirulence, but showed lower densities than in EV-A71 infected animals. A higher lethal dose50 for CV-A16 suggested that CV-A16 is less neurovirulent. Focal virus antigens/RNA in the anterior horn white matter and adjacent efferent motor nerves suggested that neuroinvasion is possibly via retrograde axonal transport in peripheral motor nerves.
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