搜索结果：Ebola-infected

Coalescent models are used to study the transmission dynamics of rapidly evolving pathogens from molecular sequence data obtained from infected individuals. However coalescent parameters, such as effective population size, offer limited interpretability for transmission dynamics. In this work, we derive a coalescent model for exposed-infected population dynamics that allows us to infer the number of infected individuals and the effective reproduction number over time from the sample genealogy. The model can be interpreted as a two-deme model in which coalescence is restricted to individuals from different demes (exposed and infected). We propose a new data-augmentation framework with Phase-type distribution for Bayesian inference of epidemiological parameters. We study the performance of our approach on simulations and apply it to re-analyze the 2014 Ebola outbreak in Liberia.

Ebola virus disease is a severe hemorrhagic fever with rapid transmission through infected fluids and surfaces. We develop a fractional-order model using Caputo derivatives to capture memory effects in disease dynamics. An eight-compartment structure distinguishes symptomatic, asymptomatic, and post-mortem transmission pathways. We prove global well-posedness, derive the basic reproduction number $\mathcal{R}_0$, and establish stability theorems. Sensitivity analysis shows $\mathcal{R}_0$ is most sensitive to transmission rate, incubation period, and deceased infectivity. Treatment-safe burial synergy achieves 86.5\% morbidity-mortality control, with safe burial being most effective. Our disease-informed neural network achieves near-perfect predictive accuracy ($R^2$: 0.991-0.999, 99.1-99.9\% accuracy), closely matching real epidemic behavior.

We develop and analyze an SIRSD epidemic model, which extends the classical SIR framework by incorporating waning immunity and disease-induced mortality. A rigorous well-posedness analysis ensures the existence, uniqueness, positivity, and boundedness of solutions, guaranteeing the model's epidemiological feasibility. To facilitate theoretical investigations and data-driven modeling, we reformulated the system in normalized variables. To capture and predict complex nonlinear epidemic dynamics, we use the Koopman operator framework with extended dynamic mode decomposition (EDMD) and an epidemiologically informed dictionary of observables. We compare two Koopman approximations: one based on a minimal epidemiological dictionary and another enriched with nonlinear and cross terms. We generate synthetic data using a nonstandard finite difference (NSFD) scheme for four representative epidemics: SARS-CoV-2, seasonal influenza, Ebola, and measles. Numerical experiments demonstrate that the Koopman-based approach effectively identifies dominant epidemic modes and accurately predicts key outbreak characteristics, including peak infection dynamics.

Towards the end of an infectious disease outbreak, when a period has elapsed without new case notifications, a key question for public health policy makers is whether the outbreak can be declared over. This requires the benefits of a declaration (e.g., relaxation of outbreak control measures) to be balanced against the risk of a resurgence in cases. To support this decision making, mathematical methods have been developed to quantify the end-of-outbreak probability. Here, we propose a new approach to this problem that accounts for a range of features of real-world outbreaks, specifically: (i) incomplete case ascertainment; (ii) reporting delays; (iii) individual heterogeneity in transmissibility; and (iv) whether cases were imported or infected locally. We showcase our approach using two case studies: Covid-19 in New Zealand in 2020, and Ebola virus disease in the Democratic Republic of the Congo in 2018. In these examples, we found that the date when the estimated probability of no future infections reached 95% was relatively consistent across a range of modelling assumptions. This suggests that our modelling framework can generate robust quantitative estimates that can be used by

This study introduces the Supervised Magnitude-Altitude Scoring (SMAS) methodology, a machine learning-based approach, for analyzing gene expression data obtained from nonhuman primates (NHPs) infected with Ebola virus (EBOV). We utilize a comprehensive dataset of NanoString gene expression profiles from Ebola-infected NHPs, deploying the SMAS system for nuanced host-pathogen interaction analysis. SMAS effectively combines gene selection based on statistical significance and expression changes, employing linear classifiers such as logistic regression to accurately differentiate between RT-qPCR positive and negative NHP samples. A key finding of our research is the identification of IFI6 and IFI27 as critical biomarkers, demonstrating exceptional predictive performance with 100% accuracy and Area Under the Curve (AUC) metrics in classifying various stages of Ebola infection. Alongside IFI6 and IFI27, genes, including MX1, OAS1, and ISG15, were significantly upregulated, highlighting their essential roles in the immune response to EBOV. Our results underscore the efficacy of the SMAS method in revealing complex genetic interactions and response mechanisms during EBOV infection. This

We extend the classical Susceptible-Infected-Recovered (SIR) model to a network-based framework where the degree distribution of nodes follows a Poisson distribution. This extension incorporates an additional parameter representing the mean node degree, allowing for the inclusion of heterogeneity in contact patterns. Using this enhanced model, we analyze epidemic data from the 2018-20 Ebola outbreak in the Democratic Republic of the Congo, employing a survival approach combined with the Hamiltonian Monte Carlo method. Our results suggest that network-based models can more effectively capture the heterogeneity of epidemic dynamics compared to traditional compartmental models, without introducing unduly overcomplicated compartmental framework.

To fight against infectious diseases (e.g., SARS, COVID-19, Ebola, etc.), government agencies, technology companies and health institutes have launched various contact tracing approaches to identify and notify the people exposed to infection sources. However, existing tracing approaches can lead to severe privacy and security concerns, thereby preventing their secure and widespread use among communities. To tackle these problems, this paper proposes CoAvoid, a decentralized, privacy-preserved contact tracing system that features good dependability and usability. CoAvoid leverages the Google/Apple Exposure Notification (GAEN) API to achieve decent device compatibility and operating efficiency. It utilizes GPS along with Bluetooth Low Energy (BLE) to dependably verify user information. In addition, to enhance privacy protection, CoAvoid applies fuzzification and obfuscation measures to shelter sensitive data, making both servers and users agnostic to information of both low and high-risk populations. The evaluation demonstrates good efficacy and security of CoAvoid. Compared with four state-of-art contact tracing applications, CoAvoid can reduce upload data by at least 90% and simult

Objectives. This review gathers information on the potential role of antihistamines as anti-infective agents and identifies gaps in research that have impaired its applicability in human health. Methods. The literature search encompassed MEDLINE, PubMed and Google Scholar from 1990 to 2022. Results. The literature search identified 12 antihistamines with activity against different pathogens. Eight molecules were second-generation antihistamines with intrinsically lower tendency to cross the blood brain barrier thereby with reduced side effects. Only five antihistamines had in vivo evaluations in rodents while one study utilized a wax moth model to determine astemizole anti-Cryptococcus sp. activity combined with fluconazole. In vitro studies showed that clemastine was active against Plasmodium, Leishmania, and Trypanosoma, while terfenadine suppressed Candida spp. and Staphylococcus aureus growth. In vitro assays found that SARS-coV-2 was inhibited by doxepin, azelastine, desloratadine, and clemastine. Different antihistamines inhibited Ebola virus (diphenhydramine, chlorcyclizine), Hepatitis C virus (chlorcyclizine), and Influenza virus (carbinoxamine, chlorpheniramine). Generally

2014 Ebola outbreaks can offer lessons for the COVOID-19 and the ongoing variant surveillance and the use of multi method approach to detect public health preparedness. We are increasingly seeing a delay and disconnect of the transmission of locally situated information to the hierarchical system for making the overall preparedness and response more proactive than reactive for dealing with emergencies such as 2014 Ebola. For our COVID-19, it is timely to consider whether digital surveillance networks and support systems can be used to bring the formal and community based ad hoc networks required for facilitating the transmission of both strong (i.e., infections, confirmed cases, deaths in hospital or clinic settings) and weak alters from the community. This will allow timely detection of symptoms of isolated suspected cases for making the overall surveillance and intervention strategy far more effective. The use of digital surveillance networks can further contribute to the development of global awareness of complex emergencies such as Ebola for constructing information infrastructure required to develop, monitor and analysis of community based global emergency surveillance in deve

Stochastic epidemic models provide an interpretable probabilistic description of the spread of a disease through a population. Yet, fitting these models to partially observed data is a notoriously difficult task due to intractability of the likelihood for many classical models. To remedy this issue, this article introduces a novel data-augmented MCMC algorithm for exact Bayesian inference under the stochastic SIR model, given only discretely observed counts of infection. In a Metropolis-Hastings step, the latent data are jointly proposed from a surrogate process carefully designed to closely resemble the SIR model, from which we can efficiently generate epidemics consistent with the observed data. This yields a method that explores the high-dimensional latent space efficiently, and scales to outbreaks with hundreds of thousands of individuals. We show that the Markov chain underlying the algorithm is uniformly ergodic, and validate its performance via thorough simulation experiments and a case study on the 2013-2015 outbreak of Ebola Haemorrhagic Fever in Western Africa.

Epidemics like Covid-19 and Ebola have impacted people's lives significantly. The impact of mobility of people across the countries or states in the spread of epidemics has been significant. The spread of disease due to factors local to the population under consideration is termed the endogenous spread. The spread due to external factors like migration, mobility, etc. is called the exogenous spread. In this paper, we introduce the Exo-SIR model, an extension of the popular SIR model and a few variants of the model. The novelty in our model is that it captures both the exogenous and endogenous spread of the virus. First, we present an analytical study. Second, we simulate the Exo-SIR model with and without assuming contact network for the population. Third, we implement the Exo-SIR model on real datasets regarding Covid-19 and Ebola. We found that endogenous infection is influenced by exogenous infection. Furthermore, we found that the Exo-SIR model predicts the peak time better than the SIR model. Hence, the Exo-SIR model would be helpful for governments to plan policy interventions at the time of a pandemic.

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