Several recent studies used results of SARS-CoV-2 RT-qPCR, Ct (threshold cycle), as proxies of viral load1. Unfortunately, an important aspect of this virus’ biology is neglected: Coronaviruses being (+)ssRNA viruses the form of RNA they use for replication is identical to the form used for transcription. It is therefore not obvious which process, replication or transcription, is quantified by RT-qPCR. To make matters more complicated, Coronaviruses produce several kinds of mRNA, genomic (= full size) and subgenomic (carrying only some genes), hence modulating their gene expression1. As shown by Finkel et al. the different mRNAs of SARS-CoV-2 occur at different densities in cell cultures. Because of their location on the viral genome the different targets of RT-qPCR are differentially affected, some being carried by more types of mRNA than others. Further, gene expression being affected by environmental and genetic factors, the quantity of RNA revealed by RT-qPCR may consequently vary due to differences in replication rates, in expression rates, or in both. It is thus unclear how good a proxy of viral load Ct values are, or what differences in Ct values may reflect.Even though the process underlying them is poorly characterized, and despite additional known biases in sample quality and RT-PCR protocols, quantitative analyses of Ct may nevertheless be highly informative e.g. in allowing to detect patterns in ‘levels of RNA’ in patients with different properties (gender, age, severe vs. mild disease, stage of infection) or in allowing to relate these patterns to epidemic properties in populations. For example, given that a priori replication levels should be the same for all genes of these monopartite viruses, differences in Ct among markers lying in different viral genes for should reflect different expression profiles. Such observations could thus help reveal interesting, and potentially epidemiologically significant, variations e.g. among SARS-CoV-2 variants.