Previously, Clososki et al [13] have shown that viral load after 48h in vitro Vero CCL81-SARS-CoV2 culture in the presence of TDF leads to a ~15-fold decrease compared to control culture (i.e. with no antiviral). We aimed to estimate the reduction in viral replication that could be attributed to TDF. Viral load, measured as Cycle threshold (Ct) values obtained from quantitative PCR, were available from monolayers treated with TDF at 3,10,30 and 90 μM (each in triplicate) and monolayers without TDF. We defined the TDF per-cell viral yield inhibition [20] as the average reduction of infected cells arising from one infected cell in the previous cycle, and was computed as the viral replication under 3-10 μM of TDF--assumed to approximate the expected therapeutic range--, relative to the replication in the absence of the antiviral. However, this computation is not straightforward as the exact length of the SARS-CoV-2 viral cycle is not known and might substantially vary [21]. Thus, we aimed to estimate a credible range of the TDF inhibition under the assumption that on average, a complete viral cycle remains between 12h and 36h [20] . First we computed the experimental Viral-load Relative ratio (VR) as the ratio between the 2-ΔΔCt values obtained from each of the TDF-SARS-CoV2 cultures at either 3 or 10 μM divided by the average 2-ΔΔCt of the control cultures (i.e., without antiviral, n=3). Alternatively, the estimation of VR can be roughly computed by assuming that every increase of 3.3 units in the Ct value corresponds with a 10-fold decrease in the viral load [22].