Mathematics

We investigate a SIRS epidemic model with spatial diffusion and nonlinear incidence rates. We show that for small diffusion rate of the infected class D_I, the infected population tends to be highly localized at certain points inside the domain, forming K spikes. We then study three distinct destabilization mechanisms, as well as a transition from localized spikes to plateau solutions. Two of the instabilities are due to coarsening (spike death) and self-replication (spike birth), and have well-known analogues in other reaction-diffusion systems such as the Schnakenberg model. The third transition is when a single spike becomes unstable and moves to the boundary. This happens when the diffusion of the recovered class, DR becomes sufficiently small. In all cases, the stability thresholds are computed asymptotically and are verified by numerical experiments. We also show that the spike solution can transit into a plateau-type solution when the diffusion rates of recovered and susceptible class are sufficiently small. Implications for disease spread and control through quarantine are discussed.

COVID-19 pandemic has underlined the impact of emergent pathogens as a major threat for human health. The development of quantitative approaches to advance comprehension of the current outbreak is urgently needed to tackle this severe disease. In this work, different mathematical models are proposed to represent SARS-CoV-2 dynamics in infected patients. Considering different starting times of infection, parameters sets that represent infectivity of SARS-CoV-2 are computed and compared with other viral infections that can also cause pandemics. Based on the target cell limited model, SARS-CoV-2 infecting time between susceptible cells is much slower than those reported for Ebola virus infection (about 3 times slower) and influenza infection (60 times slower). The within-host reproductive number for SARS-CoV-2 is consistent to the values of influenza infection (1.7-5.35). The best model to fit the data was including immune cell response, which suggests a slow immune response peaking between 5 to 10 days post onset of symptoms. The model with eclipse phase, time in a latent phase before becoming productively infected cells, was not supported. Interestingly, both, the target cell model and the model with immune responses, predict that SARS-CoV-2 may replicate very slowly in the first days after infection, and it could be below detection levels during the first 4 days post infection. A quantitative comprehension of SARS-CoV-2 dynamics and the estimation of standard parameters of viral infections is the key contribution of this pioneering work. This work can serve for future evaluation of the potential drugs with different methods of action to inhibit SARS-CoV-2.

During an epidemic, the interplay of disease and opinion dynamics can lead to outcomes that are different from those predicted based on disease dynamics alone. Opinions and the behaviors they elicit are complex, so modeling them requires a measure of abstraction and simplification. In this talk, we develop a differential equation model that couples SIR-type disease dynamics with opinion dynamics. We assume a spectrum of opinions that change based on current levels of infection as well as interactions that to some extent amplify the opinions of like-minded individuals. Susceptibility to infection is based on the level of prophylaxis (disease avoidance) that an opinion engenders. In this setting, we observe how the severity of an epidemic is influenced by the distribution of opinions at disease introduction, the relative rates of opinion and disease dynamics, and the amount of opinion amplification. Some insight is gained by considering how the effective reproduction number is influenced by the combination of opinion and disease dynamics.

We present a simulation study of the spread of an epidemic like COVID-19 with temporary immunity on finite spatial and non-spatial network models. In particular, we assume that an epidemic spreads stochastically on a scale-free network and that each infected individual in the network gains a temporary immunity after its infectious period is over. After the temporary immunity period is over, the individual becomes susceptible to the virus again. When the underlying contact network is embedded in Euclidean geometry, we model three different intervention strategies that aim to control the spread of the epidemic: social distancing, restrictions on travel, and restrictions on maximal number of social contacts per node. Our first finding is that on a finite network, a long enough average immunity period leads to extinction of the pandemic after the first peak, analogous to the concept of ``herd immunity''. For each model, there is a critical average immunity duration $L_c$ above which this happens. Our second finding is that all three interventions manage to flatten the first peak (the travel restrictions most efficiently), as well as decrease the critical immunity duration $L_c$, but elongate the epidemic. However, when the average immunity duration $L$ is shorter than $L_c$, the price for the flattened first peak is often a high second peak: for limiting the maximal number of contacts, the second peak can be as high as 1/3 of the first peak, and twice as high as it would be without intervention. Thirdly, interventions introduce oscillations into the system and the time to reach equilibrium is, for almost all scenarios, much longer. We conclude that network-based epidemic models can show a variety of behaviors that are not captured by the continuous compartmental models.

Community spread of coronavirus disease 2019 (COVID-19) continues to be high in many areas, likely due, in part, to insufficient testing and contact tracing. As regional test kit shortages are likely to continue with increased transmission, it is important that available testing capacity be used effectively. To date, testing for COVID-19 has largely been restricted to persons reporting symptoms, with no additional criteria being systematically employed to select who is tested. In situations when testing capacity is limited, we propose the use of a clinical prediction rule to allow for prioritized testing of people who are most likely to test positive for COVID-19. Using data from the University of Utah Health system, we developed a robust, deployable clinical prediction rule which incorporates data on demographics and clinical characteristics to predict which patients are most likely to test positive. We then incorporated prioritized testing into a stochastic SEIR model for COVID-19 to measure changes in disease burden compared to a model with indiscriminate testing. Our best performing clinical prediction rule achieved an AUC of 0.7. When incorporated into the SEIR model, prioritized testing resulted in a delay in the timing of the infection peak, a meaningful reduction in both the total number of infected individuals and the peak height of the infection curve, and thus a reduction in the excess demand on local hospital resources. These effects were strongest for lower values of Rt and higher proportions of infected individuals seeking testing.