Key result
EV-A71 infection in humanized mice activated human T cell responses and increased proinflammatory cytokine production, mimicking histological symptoms of human disease.
A humanized mouse model of EV-A71 infection successfully recapitulates human immune responses and pathological changes, providing a platform for evaluating future therapeutics.
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Humanized EV-A71 model recapitulates immune pathology; leaves open translation to clinical therapies pending human validation.
Despite causing self-limited hand-food-and-mouth disease in younger children, EV-A71 is consistently associated with severe forms of neurological complications and pulmonary edema. Nevertheless, only limited vaccines and drugs have been developed over the years, which is possibly due to a lack of models that can more accurately recapitulate human specificity, since human is the only natural host for wild-type EV-A71 infection. Our humanized mouse model not only mimics histological symptoms in patients but also allows us to investigate the function of the human immune system during infection. It was found that human T cell responses were activated, accompanied by an increase in the production of proinflammatory cytokines in EV-A71-infected humanized mice, which might contribute to the exacerbation of disease pathogenesis. Collectively, this model allows us to delineate the modulation of human immune responses during EV-A71 infection and may provide a platform to evaluate anti-EV-A71 drug candidates in the future.
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Ke et al. (2018) studied Enterovirus A71 (EV-A71) infection. EV-A71 infection was evaluated on Human immune responses and pathological changes. EV-A71 infection in humanized mice activated human T cell responses and increased proinflammatory cytokine production, mimicking histological symptoms of human disease.
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