Key result
Actin treadmilling inhibition resulted in the loss of rotavirus apical preferential release, suggesting a major role for actin in polarized rotavirus release.
Actin treadmilling plays a major role in the polarized apical release of rotavirus from infected enterocytes.
Actin modulation merits exploration as a rotavirus control strategy; leaves open in vivo efficacy and human translation.
Rotaviruses are characterized by polarized release from the apical side of infected enterocytes, and the rotavirus VP4 spike protein specifically binds to the actin network at the apical pole of differentiated enterocytic cells. To determine the functional consequences of this VP4-actin interaction, fluorescence recovery after photobleaching experiments were carried out to measure the diffusional mobility of VP4 associated with the microfilaments. Results show that VP4 binds to barbed ends of microfilaments by using actin treadmilling. Actin treadmilling inhibition results in the loss of rotavirus apical preferential release, suggesting a major role for actin in polarized rotavirus release.
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Gardet et al. (2007) studied Rotavirus infection. Actin treadmilling inhibition was evaluated on Diffusional mobility of VP4 and polarized rotavirus release. Actin treadmilling inhibition resulted in the loss of rotavirus apical preferential release, suggesting a major role for actin in polarized rotavirus release.
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