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Pathogenic analysis of coxsackievirus A10 in rhesus macaques
Suqin Duan1, Fengmei Yang1, Yanyan Li1
1Institute of Medical Biology, Chinese Academy of Medical Sciences & Peking Union Medical College, Yunnan Key Laboratory of Vaccine Research Development on Severe Infectious Disease, Kunming, 650118, China.
Abstract:
Coxsackievirus A10 (CV-A10) is one of the etiological agents associated with hand, foot and mouth disease (HFMD) and also causes a variety of illnesses in humans, including pneumonia, and myocarditis. Different people, particularly young children, may have different immunological responses to infection. Current CV-A10 infection animal models provide only a rudimentary understanding of the pathogenesis and effects of this virus. The characteristics of CV-A10 infection, replication, and shedding in humans remain unknown. In this study, rhesus macaques were infected by CV-A10 via respiratory or digestive route to mimic the HFMD in humans. The clinical symptoms, viral shedding, inflammatory response and pathologic changes were investigated in acute infection (1-11 day post infection) and recovery period (12-180 day post infection). All infected rhesus macaques during acute infection showed obvious viremia and clinical symptoms which were comparable to those observed in humans. Substantial inflammatory pathological damages were observed in multi-organs, including the lung, heart, liver, and kidney. During the acute period, all rhesus macaques displayed clinical signs, viral shedding, normalization of serum cytokines, and increased serum neutralizing antibodies, whereas inflammatory factors caused some animals to develop severe hyperglycemia during the recovery period. In addition, there were no significant differences between respiratory and digestive tract infected animals. Overall, all data presented suggest that the rhesus macaques provide the first non-human primate animal model for investigating CV-A10 pathophysiology and assessing the development of potential human therapies.
Insights
Rhesus macaques infected with Coxsackievirus A10 (CV-A10) exhibit human-like symptoms and multi-organ damage, establishing a valuable non-human primate model. This model aids in understanding CV-A10 pathogenesis and developing therapies for hand, foot, and mouth disease (HFMD).
Area of Science:
- Virology and Immunology
- Infectious Diseases
- Pathogenesis Research
Background:
- Coxsackievirus A10 (CV-A10) is a significant cause of hand, foot, and mouth disease (HFMD), pneumonia, and myocarditis.
- Existing animal models offer limited insight into CV-A10 pathogenesis and human responses.
- Human infection characteristics, replication, and shedding patterns of CV-A10 are largely unknown.
Purpose of the Study:
- To establish and characterize a non-human primate model for CV-A10 infection.
- To investigate the clinical symptoms, viral shedding, and pathological changes in rhesus macaques.
- To evaluate the utility of this model for studying CV-A10 pathophysiology and potential human therapies.
Main Methods:
- Rhesus macaques were infected with CV-A10 via respiratory or digestive routes.
- Clinical symptoms, viral shedding, viremia, and pathological changes were monitored during acute (1-11 days post-infection) and recovery (12-180 days post-infection) phases.
- Inflammatory responses, serum cytokines, neutralizing antibodies, and glucose levels were analyzed.
Main Results:
- Infected macaques displayed viremia and clinical symptoms comparable to human HFMD.
- Significant multi-organ inflammatory damage was observed in the lungs, heart, liver, and kidneys.
- Hyperglycemia occurred during the recovery phase due to inflammatory factors, with no significant route-dependent differences.
Conclusions:
- Rhesus macaques provide the first non-human primate model that accurately mimics CV-A10 pathophysiology in humans.
- This model is suitable for investigating CV-A10 infection dynamics and evaluating therapeutic interventions.
- The study highlights the potential for severe pathological outcomes and metabolic disturbances following CV-A10 infection.
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