Key result
Animal models of EV-D68 infection are essential for characterizing disease pathogenesis and developing targeted vaccines and antiviral therapies.
Why the study?
There are no approved vaccines or treatments for EV-D68, and significant knowledge gaps in pathogenesis constrain the development and evaluation of targeted therapies.
Continued refinement of animal models is essential for understanding EV-D68 pathogenesis and developing countermeasures.
Animal models advance EV-D68 pathogenesis insights; leaves open human predictors of AFM severity and progression.
Human enterovirus D68 (EV-D68) is a globally reemerging respiratory pathogen that is associated with the development of acute flaccid myelitis (AFM) in children. Currently, there are no approved vaccines or treatments for EV-D68 infection, and there is a paucity of data related to the virus and host-specific factors that predict disease severity and progression to the neurologic syndrome. EV-D68 infection of various animal models has served as an important platform for characterization and comparison of disease pathogenesis between historic and contemporary isolates. Still, there are significant gaps in our knowledge of EV-D68 pathogenesis that constrain the development and evaluation of targeted vaccines and antiviral therapies. Continued refinement and characterization of animal models that faithfully reproduce key elements of EV-D68 infection and disease is essential for ensuring public health preparedness for future EV-D68 outbreaks.
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Vermillion et al. (2022) conducted a review in Enterovirus D68 (EV-D68) infection and acute flaccid myelitis (AFM). Animal models was evaluated. Animal models of EV-D68 infection are essential for characterizing disease pathogenesis and developing targeted vaccines and antiviral therapies.
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