Key result
Novel CRISPR-mediated hSCARB2 knock-in mouse model provides a new tool for Enterovirus 71 antiviral development.
Why the study?
The precise mechanism of EV71-induced disease, particularly neuropathogenesis and respiratory disorders, remains not fully understood due to the lack of suitable animal models.
The development of a novel hSCARB2 knock-in mouse model provides a new tool for studying EV71 pathogenesis and developing antiviral drugs and vaccines.
Should not change EV71 clinical practice; extends animal models for antiviral and vaccine research.
Enterovirus 71 (EV71) is associated with severe hand-foot-mouth disease. Recently, outbreaks of EV71 infection with high mortality have been reported in the Asia-Pacific region, posing a great challenge for global public health. To date, the precise mechanism of EV71-induced disease, particularly the neuropathogenesis and respiratory disorders, is still not fully understood because no suitable animal models are available. Human scavenger receptor class B, member 2 (hSCARB2), has been identified as a cellular receptor for EV71. Here, we introduce a novel CRISPR/Cas9-mediated hSCARB2 knock-in (KI) mouse model for the study of EV71 pathogenesis, which is of great significance for the development of antiviral drugs and vaccines.
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Jin et al. (2021) studied Enterovirus 71 (EV71) infection. CRISPR/Cas9-mediated hSCARB2 knock-in (KI) mouse model was evaluated. A novel CRISPR/Cas9-mediated hSCARB2 knock-in mouse model was developed to study Enterovirus 71 pathogenesis, providing a new tool for the development of antiviral drugs and vaccines.
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