Modeling of the Long-Term Epidemic Dynamics of COVID-19 in the United States.

Coronavirus 2019 (COVID-19) is causing a severe pandemic that has resulted in millions of confirmed cases and deaths around the world. In the absence of effective drugs for treatment, non-pharmaceutical interventions are the most effective approaches to control the disease. Although some countries have the pandemic under control, all countries around the world, including the United States (US), are still in the process of controlling COVID-19, which calls for an effective epidemic model to describe the transmission dynamics of COVID-19. Meeting this need, we have extensively investigated the transmission dynamics of COVID-19 from 22 January 2020 to 14 February 2021 for the 50 states of the United States, which revealed the general principles underlying the spread of the virus in terms of intervention measures and demographic properties. We further proposed a time-dependent epidemic model, named T-SIR, to model the long-term transmission dynamics of COVID-19 in the US. It was shown in this paper that our T-SIR model could effectively model the epidemic dynamics of COVID-19 for all 50 states, which provided insights into the transmission dynamics of COVID-19 in the US. The present study will be valuable to help understand the epidemic dynamics of COVID-19 and thus help governments determine and implement effective intervention measures or vaccine prioritization to control the pandemic.

Molecular Mechanism of Evolution and Human Infection with SARS-CoV-2.

The outbreak of a novel coronavirus, which was later formally named the severe acute respiratory coronavirus 2 (SARS-CoV-2), has caused a worldwide public health crisis. Previous studies showed that SARS-CoV-2 is highly homologous to SARS-CoV and infects humans through the binding of the spike protein to ACE2. Here, we have systematically studied the molecular mechanisms of human infection with SARS-CoV-2 and SARS-CoV by protein-protein docking and MD simulations. It was found that SARS-CoV-2 binds ACE2 with a higher affinity than SARS-CoV, which may partly explain that SARS-CoV-2 is much more infectious than SARS-CoV. In addition, the spike protein of SARS-CoV-2 has a significantly lower free energy than that of SARS-CoV, suggesting that SARS-CoV-2 is more stable and may survive a higher temperature than SARS-CoV. This provides insights into the evolution of SARS-CoV-2 because SARS-like coronaviruses have originated in bats. Our computation also suggested that the RBD-ACE2 binding for SARS-CoV-2 is much more temperature-sensitive than that for SARS-CoV. Thus, it is expected that SARS-CoV-2 would decrease its infection ability much faster than SARS-CoV when the temperature rises. These findings would be beneficial for the disease prevention and drug/vaccine development of SARS-CoV-2.