Our simple within-host modeling approach might not capture important disease mechanisms, such as immune-driven pathogenesis [44]. Further, viral replication can occur in different tissues heterogeneously and at different clinical stages [45], which would lead to more complex dynamics than those represented by our model. Nevertheless, even in the presence of partial immune response, our model shows that the overall antiviral efficacy will ultimately depend on when and where it is available relative to the within-host SARS-CoV-2 distribution.