Although COVID-19 has caused severe suffering globally, the efficacy of nonpharmaceutical interventions has been greater than typical models have predicted. Meanwhile, evidence is mounting that the pandemic is characterized by superspreading. Capturing this phenomenon theoretically requires modeling at the scale of individuals. Using a mathematical model, we show that superspreading drastically enhances mitigations which reduce the overall personal contact number and that social clustering increases this effect.

Increasing evidence indicates that superspreading plays a dominant role in COVID-19 transmission. Recent estimates suggest that the dispersion parameter k for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is on the order of 0.1, which corresponds to about 10% of cases being the source of 80% of infections. To investigate how overdispersion might affect the outcome of various mitigation strategies, we developed an agent-based model with a social network that allows transmission through contact in three sectors: “close” (a small, unchanging group of mutual contacts as might be found in a household), “regular” (a larger, unchanging group as might be found in a workplace or school), and “random” (drawn from the entire model population and not repeated regularly). We assigned individual infectivity from a gamma distribution with dispersion parameter k. We found that when k was low (i.e., greater heterogeneity, more superspreading events), reducing random sector contacts had a far greater impact on the epidemic trajectory than did reducing regular contacts; when k was high (i.e., less heterogeneity, no superspreading events), that difference disappeared. These results suggest that overdispersion of COVID-19 transmission gives the virus an Achilles’ heel: Reducing contacts between people who do not regularly meet would substantially reduce the pandemic, while reducing repeated contacts in defined social groups would be less effective. Significance Evidence indicates that superspreading plays a dominant role in COVID-19 transmission, so that a small fraction of infected people causes a large proportion of new COVID-19 cases. We developed an agent-based model that simulates a superspreading disease moving through a society with networks of both repeated contacts and nonrepeated, random contacts. The results indicate that superspreading is the virus’ Achilles’ heel: Reducing random contacts—such as those that occur at sporting events, restaurants, bars, and the like—can control the outbreak at population scales.

We develop the geometric description of submanifolds in Newton-Cartan spacetime. This provides the necessary starting point for a covariant spacetime formulation of Galilean-invariant hydrodynamics on curved surfaces. We argue that this is the natural geometrical framework to study fluid membranes in thermal equilibrium and their dynamics out of equilibrium. A simple model of fluid membranes that only depends on the surface tension is presented and, extracting the resulting stresses, we show that perturbations away from equilibrium yield the standard result for the dispersion of elastic waves. We also find a generalization of the Canham-Helfrich bending energy for lipid vesicles that takes into account the requirements of thermal equilibrium.

Identifying drivers of viral diversity is key to understanding the evolutionary as well as epidemiological dynamics of the COVID-19 pandemic. Using rich viral genomic data sets, we show that periods of steadily rising diversity have been punctuated by sudden, enormous increases followed by similarly abrupt collapses of diversity. We introduce a mechanistic model of saltational evolution with epistasis and demonstrate that these features parsimoniously account for the observed temporal dynamics of inter-genomic diversity. Our results provide support for recent proposals that saltational evolution may be a signature feature of SARS-CoV-2, allowing the pathogen to more readily evolve highly transmissible variants. These findings lend theoretical support to a heightened awareness of biological contexts where increased diversification may occur. They also underline the power of pathogen genomics and other surveillance streams in clarifying the phylodynamics of emerging and endemic infections. In public health terms, our results further underline the importance of equitable distribution of up-to-date vaccines.

Superspreading is known to have played an important role in the transmission dynamics of SARS-CoV-2. In this Comment, the authors discuss how knowledge of the extent and cause of superspreading is important for designing appropriate control measures for emerging infectious diseases. The superspreading that characterized SARS and now COVID-19 can be rapidly quantified; however, its implications for outbreak control were never well understood. Recent studies point to its profound impact on outbreak dynamics and prospects for effective control of a future Disease X. These insights necessitate research into the mechanisms, impact and different modes of superspreading more widely.

The introduction of non-pharmaceutical interventions (NPIs) against COVID-19 disrupted circulation of many respiratory pathogens and eventually caused large, delayed outbreaks, owing to the build up of the susceptible pool during the intervention period. In contrast to other common respiratory pathogens that re-emerged soon after the NPIs were lifted, longer delays (> 3 years) in the outbreaks of Mycoplasma pneumoniae (Mp), a bacterium commonly responsible for respiratory infections and pneumonia, have been reported in Europe and Asia. As Mp cases are continuing to increase in the US, predicting the size of an imminent outbreak is timely for public health agencies and decision makers. Here, we use simple mathematical models to provide robust predictions about a large Mp outbreak ongoing in the US. Our model further illustrates that NPIs and waning immunity are important factors in driving long delays in epidemic resurgence.