Multitype branching process with non-homogeneous Poisson and contagious Poisson immigration

In a multitype branching process, it is assumed that immigrants arrive according to a non-homogeneous Poisson or a contagious Poisson process (both processes are formulated as a non-homogeneous birth process with an appropriate choice of transition intensities). We show that the normalized numbers of objects of the various types alive at time t for supercritical, critical, and subcritical cases jointly converge in distribution under those two different arrival processes. Furthermore, we provide some transient expectation results when there are only two types of particles.

Effects of Fogging and Mosquito Repellent on the Probability of Disease Extinction for Dengue Fever

A Continuous-Time Markov Chain model is constructed based on the a deterministic model of dengue fever transmission including mosquito fogging and the use of repellent. The basic reproduction number (R0) for the corresponding deterministic model is obtained. This number indicates the possible occurrence of an endemic at the early stages of the infection period. A multitype branching process is used to approximate the Markov chain. The construction of offspring probability generating functions related to the infected states is used to calculate the probability of disease extinction and the probability of an outbreak (P0). Sensitivity analysis is shown for variation of control parameters and for indices of the basic reproduction number. These results allow for a better understanding of the relation of the basic reproduction number with other indicators of disease transmission.

Unified model of short- and long-term HIV viral rebound for clinical trial planning

Antiretroviral therapy (ART) effectively controls HIV infection, suppressing HIV viral loads. Typically suspension of therapy is rapidly followed by rebound of viral loads to high, pre-therapy levels. Indeed, a recent study showed that approximately 90% of treatment interruption study participants show viral rebound within at most a few months of therapy suspension, but the remaining 10%, showed viral rebound some months, or years, after ART suspension. Some may even never rebound. We investigate and compare branching process models aimed at gaining insight into these viral dynamics. Specifically, we provide a theory that explains both short- and long-term viral rebounds, and post-treatment control, via a multitype branching process with time-inhomogeneous rates, validated with data from Li et al. (Li et al. 2016 AIDS 30 , 343–353. ( doi:10.1097/QAD.0000000000000953 )). We discuss the associated biological interpretation and implications of our best-fit model. To test the effectiveness of an experimental intervention in delaying or preventing rebound, the standard practice is to suspend therapy and monitor the study participants for rebound. We close with a discussion of an important application of our modelling in the design of such clinical trials.

Demographic Dynamics in Multitype Populations with Migrations

This research work deals with mathematical modeling in complex biological systems in which several types of individuals coexist in various populations. Migratory phenomena among the populations are allowed. We propose a class of mathematical models to describe the demographic dynamics of these type of complex systems. The probability model is defined through a sequence of random matrices in which rows and columns represent the various populations and the several types of individuals, respectively. We prove that this stochastic sequence can be studied under the general setting provided by the multitype branching process theory. Probabilistic properties and limiting results are then established. As application, we present an illustrative example about the population dynamics of biological systems formed by long-lived raptor colonies.

Not all fun and games: Potential incidence of SARS-CoV-2 infections during the Tokyo 2020 Olympic Games

<abstract> <p>The Tokyo 2020 Olympic and Paralympic Games represent the most diverse international mass gathering event held since the start of the coronavirus disease 2019 (COVID-19) pandemic. Postponed to summer 2021, the rescheduled Games were set to be held amidst what would become the highest-ever levels of COVID-19 transmission in the host city of Tokyo. At the same time, the Delta variant of concern was gaining traction as the dominant viral strain and Japan had yet to exceed fifteen percent of its population fully vaccinated against COVID-19. To quantify the potential number of secondary cases that might arise during the Olympic Games, we performed a scenario analysis using a multitype branching process model. We considered the different contributions to transmission of Games accredited individuals, the general Tokyo population, and domestic spectators. In doing so, we demonstrate how transmission might evolve in these different groups over time, cautioning against any loosening of infection prevention protocols and supporting the decision to ban all spectators. If prevention measures were well observed, we estimated that the number of new cases among Games accredited individuals would approach zero by the end of the Games. However, if transmission was not controlled our model indicated hundreds of Games accredited individuals would become infected and daily incidence in Tokyo would reach upwards of 4,000 cases. Had domestic spectators been allowed (at 50% venue capacity), we estimated that over 250 spectators might have arrived infected to Tokyo venues, potentially generating more than 300 additional secondary infections while in Tokyo/at the Games. We also found the number of cases with infection directly attributable to hypothetical exposure during the Games was highly sensitive to the local epidemic dynamics. Therefore, reducing and maintaining transmission levels below epidemic levels using public health measures would be necessary to prevent cross-group transmission.</p> </abstract>

Stochastic investigation of HIV infection and the emergence of drug resistance

<abstract><p>Drug-resistant HIV-1 has caused a growing concern in clinic and public health. Although combination antiretroviral therapy can contribute massively to the suppression of viral loads in patients with HIV-1, it cannot lead to viral eradication. Continuing viral replication during sub-optimal therapy (due to poor adherence or other reasons) may lead to the accumulation of drug resistance mutations, resulting in an increased risk of disease progression. Many studies also suggest that events occurring during the early stage of HIV-1 infection (i.e., the first few hours to days following HIV exposure) may determine whether the infection can be successfully established. However, the numbers of infected cells and viruses during the early stage are extremely low and stochasticity may play a critical role in dictating the fate of infection. In this paper, we use stochastic models to investigate viral infection and the emergence of drug resistance of HIV-1. The stochastic model is formulated by a continuous-time Markov chain (CTMC), which is derived based on an ordinary differential equation model proposed by Kitayimbwa et al. that includes both forward and backward mutations. An analytic estimate of the probability of the clearance of HIV infection of the CTMC model near the infection-free equilibrium is obtained by a multitype branching process approximation. The analytical predictions are validated by numerical simulations. Unlike the deterministic dynamics where the basic reproduction number $ \mathcal{R}_0 $ serves as a sharp threshold parameter (i.e., the disease dies out if $ \mathcal{R}_0 &lt; 1 $ and persists if $ \mathcal{R}_0 &gt; 1 $), the stochastic models indicate that there is always a positive probability for HIV infection to be eradicated in patients. In the presence of antiretroviral therapy, our results show that the chance of clearance of the infection tends to increase although drug resistance is likely to emerge.</p></abstract>

Lineage reconstruction from clonal correlations

A central task in developmental biology is to learn the sequence of fate decisions that leads to each mature cell type in a tissue or organism. Recently, clonal labeling of cells using DNA barcodes has emerged as a powerful approach for identifying cells that share a common ancestry of fate decisions. Here we explore the idea that stochasticity of cell fate choice during tissue development could be harnessed to read out lineage relationships after a single step of clonal barcoding. By considering a generalized multitype branching process, we determine the conditions under which the final distribution of barcodes over observed cell types encodes their bona fide lineage relationships. We then propose a method for inferring the order of fate decisions. Our theory predicts a set of symmetries of barcode covariance that serves as a consistency check for the validity of the method. We show that broken symmetries may be used to detect multiple paths of differentiation to the same cell types. We provide computational tools for general use. When applied to barcoding data in hematopoiesis, these tools reconstruct the classical hematopoietic hierarchy and detect couplings between monocytes and dendritic cells and between erythrocytes and basophils that suggest multiple pathways of differentiation for these lineages.

An Algorithmic Approach to Modelling the Co-Evolution of Parasites and Their Hosts

This paper is a reformulation of the paper, Mode 1958 Evolution 12:158 - 165, which was written in terms of a deterministic paradigm, using di erential equations In this paper, however, the working paradigm will be stochastic, and from the mathematical point of view, it will be a stochastic process that may be viewed as a branching process within a branching process. In particular, it will be assumed that the population of host plants will evolve as a multitype branching process, and the pathogen, which grows on the leaves of the host in every generation of the host, will also be assumed to evolve as a multitype branching processes during each generation of the host. The contents of this paper, were motivated by problems in Agriculture in which Plant Pathologists and Plant Breeders work together to control the damage inflicted by a pathogen on a growing crop of a cultivar such as flax, wheat. and many other cultivars. The focus of attention in this paper is the development of algorithms that will guide the development of software to run Monte Carol simulation experiments taking into account mutations in the host and pathogen. The writing of software to implement the algorithms developed in this paper would require a major e ort, and is, therefore, beyond the scope of this paper