A plausible reason for this finding could be a functional redundancy between VPS4A and VPS4B that would compensate for the lack of VPS4A at particular infection stages, as has previously been described for other ESCRT components such as CHMP2 or CHMP4 families in flavivirus infection (Tabata et al., 2016). This evidence concerns the gene VPS4B and Flavivirus Infections.