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Register a new userHeterogeneity and Superspreading Effect on Herd Immunity
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We model and calculate the fraction of infected population necessary to reach herd immunity, taking into account the heterogeneity in infectiousness and susceptibility, as well as the correlation between those two parameters. We show that these cause the effective reproduction number to decrease more rapidly, and consequently have a drastic effect on the estimate of the necessary percentage of the population that has to contract the disease for herd immunity to be reached. We quantify the difference between the size of the infected population when the effective reproduction number decreases below 1 vs. the ultimate fraction of population that had contracted the disease. This sheds light on an important distinction between herd immunity and the end of the disease and highlights the importance of limiting the spread of the disease even if we plan to naturally reach herd immunity. We analyze the effect of various lock-down scenarios on the resulting final fraction of infected population. We discuss implications to COVID-19 and other pandemics and compare our theoretical results to population-based simulations. We consider the dependence of the disease spread on the architecture of the infectiousness graph and analyze different graph architectures and the limitations of the graph models.
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Epidemics generally spread through a succession of waves that reflect factors on multiple timescales. On short timescales, super-spreading events lead to burstiness and overdispersion, while long-term persistent heterogeneity in susceptibility is expected to lead to a reduction in the infection peak and the herd immunity threshold (HIT). Here, we develop a general approach to encompass both timescales, including time variations in individual social activity, and demonstrate how to incorporate them phenomenologically into a wide class of epidemiological models through parameterization. We derive a non-linear dependence of the effective reproduction number Re on the susceptible population fraction S. We show that a state of transient collective immunity (TCI) emerges well below the HIT during early, high-paced stages of the epidemic. However, this is a fragile state that wanes over time due to changing levels of social activity, and so the infection peak is not an indication of herd immunity: subsequent waves can and will emerge due to behavioral changes in the population, driven (e.g.) by seasonal factors. Transient and long-term levels of heterogeneity are estimated by using empirical data from the COVID-19 epidemic as well as from real-life face-to-face contact networks. These results suggest that the hardest-hit areas, such as NYC, have achieved TCI following the first wave of the epidemic, but likely remain below the long-term HIT. Thus, in contrast to some previous claims, these regions can still experience subsequent waves.
The contact structure of a population plays an important role in transmission of infection. Many ``structured models capture aspects of the contact structure through an underlying network or a mixing matrix. An important observation in such models, is that once a fraction $1-1/mathcal{R}_0$ has been infected, the residual susceptible population can no longer sustain an epidemic. A recent observation of some structured models is that this threshold can be crossed with a smaller fraction of infected individuals, because the disease acts like a targeted vaccine, preferentially immunizing higher-risk individuals who play a greater role in transmission. Therefore, a limited ``first wave may leave behind a residual population that cannot support a second wave once interventions are lifted. In this paper, we systematically analyse a number of mean-field models for networks and other structured populations to address issues relevant to the Covid-19 pandemic. In particular, we consider herd-immunity under several scenarios. We confirm that, in networks with high degree heterogeneity, the first wave confers herd-immunity with significantly fewer infections than equivalent models with lower degree heterogeneity. However, if modelling the intervention as a change in the contact network, then this effect might become more subtle. Indeed, modifying the structure can shield highly connected nodes from becoming infected during the first wave and make the second wave more substantial. We confirm this finding by using an age-structured compartmental model parameterised with real data and comparing lockdown periods implemented either as a global scaling of the mixing matrix or age-specific structural changes. We find that results regarding herd immunity levels are strongly dependent on the model, the duration of lockdown and how lockdown is implemented.
We revisit well-established concepts of epidemiology, the Ising-model, and percolation theory. Also, we employ a spin $S$ = 1/2 Ising-like model and a (logistic) Fermi-Dirac-like function to describe the spread of Covid-19. Our analysis reinforces well-established literature results, namely: emph{i}) that the epidemic curves can be described by a Gaussian-type function; emph{ii}) that the temporal evolution of the accumulative number of infections and fatalities follow a logistic function, which has some resemblance with a distorted Fermi-Dirac-like function; emph{iii}) the key role played by the quarantine to block the spread of Covid-19 in terms of an emph{interacting} parameter, which emulates the contact between infected and non-infected people. Furthermore, in the frame of elementary percolation theory, we show that: emph{i}) the percolation probability can be associated with the probability of a person being infected with Covid-19; emph{ii}) the concepts of blocked and non-blocked connections can be associated, respectively, with a person respecting or not the social distancing, impacting thus in the probability of an infected person to infect other people. Increasing the number of infected people leads to an increase in the number of net connections, giving rise thus to a higher probability of new infections (percolation). We demonstrate the importance of social distancing in preventing the spread of Covid-19 in a pedagogical way. Given the impossibility of making a precise forecast of the disease spread, we highlight the importance of taking into account additional factors, such as climate changes and urbanization, in the mathematical description of epidemics. Yet, we make a connection between the standard mathematical models employed in epidemics and well-established concepts in condensed matter Physics, such as the Fermi gas and the Landau Fermi-liquid picture.
The competitive exclusion principle asserts that coexisting species must occupy distinct ecological niches (i.e. the number of surviving species can not exceed the number of resources). An open question is to understand if and how different resource dynamics affect this bound. Here, we analyze a generalized consumer resource model with externally supplied resources and show that -- in contrast to self-renewing resources -- species can occupy only half of all available environmental niches. This motivates us to construct a new schema for classifying ecosystems based on species packing properties.
The basic reproductive number -- $R_0$ -- is one of the most common and most commonly misapplied numbers in public health. Although often used to compare outbreaks and forecast pandemic risk, this single number belies the complexity that two different pathogens can exhibit, even when they have the same $R_0$. Here, we show how to predict outbreak size using estimates of the distribution of secondary infections, leveraging both its average $R_0$ and the underlying heterogeneity. To do so, we reformulate and extend a classic result from random network theory that relies on contact tracing data to simultaneously determine the first moment ($R_0$) and the higher moments (representing the heterogeneity) in the distribution of secondary infections. Further, we show the different ways in which this framework can be implemented in the data-scarce reality of emerging pathogens. Lastly, we demonstrate that without data on the heterogeneity in secondary infections for emerging infectious diseases like COVID-19, the uncertainty in outbreak size ranges dramatically. Taken together, our work highlights the critical need for contact tracing during emerging infectious disease outbreaks and the need to look beyond $R_0$ when predicting epidemic size.
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