Statins impair rotavirus replication. (a) Caco2 cells were infected with rotavirus SA11 strain (MOI 0.7) and subsequently treated with different concentrations of atorvastatin (n = 7), lovastatin (n = 7), or simvastatin (n = 5) for 48 hours, then the intra- (left) and extracellular (right) rotavirus RNA levels were measured by qRT-PCR, and (b) rotavirus VP4 protein were measured with 50 µM atorvastatin, lovastatin, and simvastatin treatment for 48 hours respectively by western blot. In MA104 cells, (c) treated as described in a, the intra- (left) and extracellular (right) rotavirus RNA levels with the three statins treatments respectively (n = 5), and (d) the expressions of the rotavirus VP4 protein, treated as described in b. In HSI organoids, (e) treated as described in a, the inner rotavirus RNA level with the treatments of the three statins respectively (n = 3), and (f) the expression of rotavirus VP4 protein, treated as described in b. (g) The titers of infectious rotavirus particles were measured by TCID50 assays with 50 µM three statins treatments respectively in MA104 cells (n = 6). (h) The 96-hour time course experiments of atorvastatin (left), lovastatin (middle), and simvastatin (right) treatments respectively (n = 3) on the intracellular rotavirus RNA replication. All data presented as mean ± SEM, *p < .05, **p < .01, ***p < .001