Key result
The actin inhibitor jasplakinolide blocked the nonlytic cell egress of rotavirus and prevented the intracellular localization and cell surface targeting of the spike protein VP4 in MA104 cells.
Population
Nonpolarized MA104 cells infected with rotavirus
Design
Preclinical
Authors
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May inform host-directed antiviral strategies; leaves open in vivo efficacy and clinical translation.
Rotavirus exits nonpolarized cells by a nonlytic, actin-dependent mechanism, and the spike protein VP4 is incorporated into mature infectious virus at the cell surface.
Trejo-Cerro et al. (2017) studied Rotavirus infection. Jasplakinolide was evaluated on Cell egress of rotavirus and intracellular localization of VP4. The actin inhibitor jasplakinolide blocked the nonlytic cell egress of rotavirus and prevented the intracellular localization and cell surface targeting of the spike protein VP4 in MA104 cells.
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