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Register a new userStability analysis of a novel Delay Differential Equation of HIV Infection of CD4$^+$ T-cells
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In this paper, we investigate a novel 3-compartment model of HIV infection of CD4$^+$ T-cells with a mass action term by including t
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HIV-1 can disseminate between susceptible cells by two mechanisms: cell-free infection following fluid-phase diffusion of virions and by highly-efficient direct cell-to-cell transmission at immune cell contacts. The contribution of this hybrid spreading mechanism, which is also a characteristic of some important computer worm outbreaks, to HIV-1 progression in vivo remains unknown. Here we present a new mathematical model that explicitly incorporates the ability of HIV-1 to use hybrid spreading mechanisms and evaluate the consequences for HIV-1 pathogenenesis. The model captures the major phases of the HIV-1 infection course of a cohort of treatment naive patients and also accurately predicts the results of the Short Pulse Anti-Retroviral Therapy at Seroconversion (SPARTAC) trial. Using this model we find that hybrid spreading is critical to seed and establish infection, and that cell-to-cell spread and increased CD4+ T cell activation are important for HIV-1 progression. Notably, the model predicts that cell-to-cell spread becomes increasingly effective as infection progresses and thus may present a considerable treatment barrier. Deriving predictions of various treatments influence on HIV-1 progression highlights the importance of earlier intervention and suggests that treatments effectively targeting cell-to-cell HIV-1 spread can delay progression to AIDS. This study suggests that hybrid spreading is a fundamental feature of HIV infection, and provides the mathematical framework incorporating this feature with which to evaluate future therapeutic strategies.
In order to analyze the effectiveness of three successive nationwide lockdown enforced in India, we present a data-driven analysis of four key parameters, reducing the transmission rate, restraining the growth rate, flattening the epidemic curve and improving the health care system. These were quantified by the consideration of four different metrics, namely, reproduction rate, growth rate, doubling time and death to recovery ratio. The incidence data of the COVID-19 (during the period of 2nd March 2020 to 31st May 2020) outbreak in India was analyzed for the best fit to the epidemic curve, making use of the exponential growth, the maximum likelihood estimation, sequential Bayesian method and estimation of time-dependent reproduction. The best fit (based on the data considered) was for the time-dependent approach. Accordingly, this approach was used to assess the impact on the effective reproduction rate. The period of pre-lockdown to the end of lockdown 3, saw a $45%$ reduction in the rate of effective reproduction rate. During the same period the growth rate reduced from $393%$ during the pre-lockdown to $33%$ after lockdown 3, accompanied by the average doubling time increasing form $4$-$6$ days to $12$-$14$ days. Finally, the death-to-recovery ratio dropped from $0.28$ (pre-lockdown) to $0.08$ after lockdown 3. In conclusion, all the four metrics considered to assess the effectiveness of the lockdown, exhibited significant favourable changes, from the pre-lockdown period to the end of lockdown 3. Analysis of the data in the post-lockdown period with these metrics will provide greater clarity with regards to the extent of the success of the lockdown.
In times of outbreaks, an essential requirement for better monitoring is the evaluation of the number of undiagnosed infected individuals. An accurate estimate of this fraction is crucial for the assessment of the situation and the establishment of protective measures. In most current studies using epidemics models, the total number of infected is either approximated by the number of diagnosed individuals or is dependent on the model parameters and assumptions, which are often debated. We here study the relationship between the fraction of diagnosed infected out of all infected, and the fraction of infected with known contaminator out of all diagnosed infected. We show that those two are approximately the same in exponential models and across most models currently used in the study of epidemics, independently of the model parameters. As an application, we compute an estimate of the effective number of infected by the SARS-CoV-2 virus in various countries.
A classic measure of ecological stability describes the tendency of a community to return to equilibrium after small perturbation. While many advances show how the network structure of these communities severely constrains such tendencies, few if any of these advances address one of the most fundamental properties of network structure: heterogeneity among nodes with different numbers of links. Here we systematically explore this property of degree heterogeneity and find that its effects on stability systematically vary with different types of interspecific interactions. Degree heterogeneity is always destabilizing in ecological networks with both competitive and mutualistic interactions while its effects on networks of predator-prey interactions such as food webs depend on prey contiguity, i.e., the extent to which the species consume an unbroken sequence of prey in community niche space. Increasing degree heterogeneity stabilizes food webs except those with the most contiguity. These findings help explain previously unexplained observations that food webs are highly but not completely contiguous and, more broadly, deepens our understanding of the stability of complex ecological networks with important implications for other types of dynamical systems.
We have learned to live with many potentially deadly viruses for which there is no vaccine, no immunity, and no cure. We do not live in constant fear of these viruses, instead, we have learned how to outsmart them and reduce the harm they cause. A new mathematical model that combines the spread of diseases that do not confer immunity together with the evolution of human behaviors indicates that we may be able to fight new diseases with the same type of strategy we use to fight viruses like HIV.
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