With poliovirus nearly eradicated, focus has shifted to enteroviruses like EV-D68, which can cause acute flaccid myelitis (AFM). This study utilizes CRISPR screening to uncover that MFSD6 is a vital host factor necessary for EV-D68 to infect respiratory and neural cells. The study shows that knocking out MFSD6 prevents viral entry, enhancing understanding of the mechanisms driving EV-D68's neuropathogenesis and highlighting potential avenues for therapeutic intervention in viral infections linked to AFM.
In our study, we identified the multipass membrane transporter MFSD6 as a critical entry factor for EV-D68, showing that its knockout effectively blocks viral infection in cultured cells.
The alarming rise of EV-D68 suggests crucial implications for public health as it is closely linked to acute flaccid myelitis, complicating the ongoing management of viral infections.
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