First, it would allow for more precise prediction of the infectiousness of infected individuals, including children and pre- or asymptomatic individuals, based on their VL measurements ( 8, 9). A quantitative understanding of the relationship is critical for both nonpharmaceutical and pharmaceutical interventions.
Previously, both VL and log 10 VL have been used as surrogates for infectiousness of influenza ( 5) and SARS-CoV-2 ( 6, 7). Overall, our models provide a quantitative framework for inferring the impact of therapeutics and vaccines that lower VL on the infectiousness of individuals and for evaluating rapid testing strategies. We found that RT-PCR tests perform better than antigen tests assuming equal testing frequency however, more frequent antigen testing may perform equally well with RT-PCR tests at a lower cost but with many more false-negative tests. Using data on VL and the predicted infectiousness, we further incorporated data on antigen and RT-PCR tests and compared their usefulness in detecting infection and preventing transmission. We then develop a model linking viral load (VL) to infectiousness and show a person’s infectiousness increases sublinearly with VL and that the logarithm of the VL in the upper respiratory tract is a better surrogate of infectiousness than the VL itself. Here, we develop viral dynamic models of SARS-CoV-2 infection and fit them to data to estimate key within-host parameters such as the infected cell half-life and the within-host reproductive number. This limits our ability to quantify the impact of interventions on viral transmission. The within-host viral kinetics of SARS-CoV-2 infection and how they relate to a person’s infectiousness are not well understood.
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