RESUMEN
The contributions of asymptomatic infections to herd immunity and community transmission are key to the resurgence and control of COVID-19, but are difficult to estimate using current models that ignore changes in testing capacity. Using a model that incorporates daily testing information fit to the case and serology data from New York City, we show that the proportion of symptomatic cases is low, ranging from 13% to 18%, and that the reproductive number may be larger than often assumed. Asymptomatic infections contribute substantially to herd immunity, and to community transmission together with pre-symptomatic ones. If asymptomatic infections transmit at similar rates than symptomatic ones, the overall reproductive number across all classes is larger than often assumed, with estimates ranging from 3.2 to 4.4. If they transmit poorly, then symptomatic cases have a larger reproductive number ranging from 3.9 to 8.1. Even in this regime, pre-symptomatic and asymptomatic cases together comprise at least 50% of the force of infection at the outbreak peak. We find no regimes in which all infection sub-populations have reproductive numbers lower than 3. These findings elucidate the uncertainty that current case and serology data cannot resolve, despite consideration of different model structures. They also emphasize how temporal data on testing can reduce and better define this uncertainty, as we move forward through longer surveillance and second epidemic waves. Complementary information is required to determine the transmissibility of asymptomatic cases, which we discuss. Regardless, current assumptions about the basic reproductive number of SARS-Cov-2 should be reconsidered. Significance StatementAs health officials face another wave of COVID-19, they require estimates of the proportion of infected cases that develop symptoms, and the extent to which symptomatic and asymptomatic cases contribute to community transmission. Recent asymptomatic testing guidelines are ambiguous. Using an epidemiological model that includes testing capacity, we show that most infections are asymptomatic but contribute substantially to community transmission in the aggregate. Their individual transmissibility remains uncertain. If they transmit as well as symptomatic infections, the epidemic may spread at faster rates than current models often assume. If they do not, then each symptomatic case generates on average a higher number of secondary infections than typically assumed. Regardless, controlling transmission requires community-wide interventions informed by extensive, well-documented asymptomatic testing.