Subscribe to the gold package and get unlimited access to Shamra Academy
Register a new userEarly pathogen replacement in a model of Influenza and Respiratory Syncytial Virus with partial vaccination. A computational study
72
0
0.0
(
0
)
Ask ChatGPT about the research
No Arabic abstract
In this paper, we carry out a computational study using the spectral decomposition of the fluctuations of a two-pathogen epidemic model around its deterministic attractor, i.e., steady state or limit cycle, to examine the role of partial vaccination and between-host pathogen interaction on early pathogen replacement during seasonal epidemics of influenza and respiratory syncytial virus.
rate research
Read More
Under the hypothesis that both influenza and respiratory syncytial virus (RSV) are the two leading causes of acute respiratory infections (ARI), in this paper we have used a standard two-pathogen epidemic model as a regressor to explain, on a yearly basis, high season ARI data in terms of the contact rates and initial conditions of the mathematical model. The rationale is that ARI high season is a transient regime of a noisy system, e.g., the system is driven away from equilibrium every year by fluctuations in variables such as humidity, temperature, viral mutations and human behavior. Using the value of the replacement number as a phenotypic trait associated to fitness, we provide evidence that influenza and RSV coexists throughout the ARI high season through superinfection.
The evolutionary dynamics of human Influenza A virus presents a challenging theoretical problem. An extremely high mutation rate allows the virus to escape, at each epidemic season, the host immune protection elicited by previous infections. At the same time, at each given epidemic season a single quasi-species, that is a set of closely related strains, is observed. A non-trivial relation between the genetic (i.e., at the sequence level) and the antigenic (i.e., related to the host immune response) distances can shed light into this puzzle. In this paper we introduce a model in which, in accordance with experimental observations, a simple interaction rule based on spatial correlations among point mutations dynamically defines an immunity space in the space of sequences. We investigate the static and dynamic structure of this space and we discuss how it affects the dynamics of the virus-host interaction. Interestingly we observe a staggered time structure in the virus evolution as in the real Influenza evolutionary dynamics.
Interactions among multiple infectious agents are increasingly recognized as a fundamental issue in the understanding of key questions in public health, regarding pathogen emergence, maintenance, and evolution. The full description of host-multipathogen systems is however challenged by the multiplicity of factors affecting the interaction dynamics and the resulting competition that may occur at different scales, from the within-host scale to the spatial structure and mobility of the host population. Here we study the dynamics of two competing pathogens in a structured host population and assess the impact of the mobility pattern of hosts on the pathogen competition. We model the spatial structure of the host population in terms of a metapopulation network and focus on two strains imported locally in the system and having the same transmission potential but different infectious periods. We find different scenarios leading to competitive success of either one of the strain or to the codominance of both strains in the system. The dominance of the strain characterized by the shorter or longer infectious period depends exclusively on the structure of the population and on the the mobility of hosts across patches. The proposed modeling framework allows the integration of other relevant epidemiological, environmental and demographic factors opening the path to further mathematical and computational studies of the dynamics of multipathogen systems.
Influenza viruses enter a cell via endocytosis after binding to the surface. During the endosomal journey, acidification triggers a conformational change of the virus spike protein hemagglutinin (HA) that results in escape of the viral genome from the endosome to the cytoplasm. A quantitative understanding of the processes involved in HA mediated fusion with the endosome is still missing. We develop here a stochastic model to estimate the change of conformation of HAs inside the endosome nanodomain. Using a Markov-jump process to model the arrival of protons to HA binding sites, we compute the kinetics of their accumulation and the mean first time for HAs to be activated. This analysis reveals that HA proton binding sites possess a high chemical barrier, ensuring a stability of the spike protein at sub-acidic pH. Finally, we predict that activating more than 3 adjacent HAs is necessary to prevent a premature fusion.
This paper describes a mathematical model for the spread of a virus through an isolated population of a given size. The model uses three, color-coded components, called molecules (red for infected and still contagious; green for infected, but no longer contagious; and blue for uninfected). In retrospect, the model turns out to be a digital analogue for the well-known SIR model of Kermac and McKendrick (1927). In our RGB model, the number of accumulated infections goes through three phases, beginning at a very low level, then changing to a transition ramp of rapid growth, and ending in a plateau of final values. Consequently, the differential change or growth rate begins at 0, rises to a peak corresponding to the maximum slope of the transition ramp, and then falls back to 0. The properties of these time variations, including the slope, duration, and height of the transition ramp, and the width and height of the infection rate, depend on a single parameter - the time that a red molecule is contagious divided by the average time between collisions of the molecules. Various temporal milestones, including the starting time of the transition ramp, the time that the accumulating number of infections obtains its maximum slope, and the location of the peak of the infection rate depend on the size of the population in addition to the contagious lifetime ratio. Explicit formulas for these quantities are derived and summarized. Finally, Appendix E has been added to describe the effect of vaccinations.
Log in to be able to interact and post comments
comments
Fetching comments
Sign in to be able to follow your search criteria
