Master of Science / Department of Electrical and Computer Engineering / Faryad Darabi Sahneh / Recent experience of Ebola outbreak of 2014 highlighted the importance of immediate response to impede Ebola transmission at its very early stage. To this aim, efficient and effective allocation of limited resources is crucial. Among standard interventions is the practice of following up with physical contacts of individuals diagnosed with Ebola virus disease -- known as contact tracing. In an effort to objectively understand the effect of possible contact tracing protocols, we explicitly develop a model of Ebola transmission incorporating contact tracing. Our modeling framework has several features to suit early–stage Ebola transmission: 1) the network model is patient–centric because when number of infected cases are small only the myopic networks of infected individuals matter and the rest of possible social contacts are irrelevant, 2) the Ebola disease model is individual–based and stochastic because at the early stages of spread, random fluctuations are significant and must be captured appropriately, 3) the contact tracing model is parameterizable to analyze the impact of critical aspects of contact tracing protocols. Notably, we propose an activity driven network approach to contact tracing, and develop a Monte-Carlo method to compute the basic reproductive number of the disease spread in different scenarios. Exhaustive simulation experiments suggest that while contact tracing is important in stopping the Ebola spread, it does not need to be done too urgently. This result is due to rather long incubation period of Ebola disease infection. However, immediate hospitalization of infected cases is crucial and requires the most attention and resource allocation. Moreover, to investigate the impact of mitigation strategies in the 2014 Ebola outbreak, we consider reported data in Guinea, one the three West Africa countries that had experienced the Ebola virus disease outbreak. We formulate a multivariate sequential Monte Carlo filter that utilizes mechanistic models for Ebola virus propagation to simultaneously estimate the disease progression states and the model parameters according to reported incidence data streams. This method has the advantage of performing the inference online as the new data becomes available and estimating the evolution of the basic reproductive ratio R₀(t) throughout the Ebola outbreak. Our analysis identifies a peak in the basic reproductive ratio close to the time of Ebola cases reports in Europe and the USA.

VOVES, Petr. Úloha Světové zdravotnické organizace v případu epidemie viru eboly na území západní Afriky v roce 2014. Praha, 2017. 95 s. Diplomová práce (Mgr.) Univerzita Karlova, Fakulta sociálních věd, Institut politologických studií. Katedra mezinárodních vztahů. Vedoucí diplomové práce PhDr. Irah Kučerová, Ph.D. Abstract The M.A. thesis deals with the World Health Organization's response to the outbreak of the ebola virus disease in Guinea, Liberia and Sierra Leone in 2014. The spread of the disease is mapped from its very beginning at the end of December 2013 until the creation of UNMEER in September 2014, which was the first international medical mission ever created by UN Security Council. The purpose of this thesis is to evaluate the particular problems, which limit WHO's role in a timely and effective response to the public health threats of international concern (PHEIC) under the reformed International Health Regulations (IHR). The response of WHO representatives to the spread of the disease is evaluated taking into account the available material and competence capacities of the organization as well as its previous practice in this field. The specific misconduct of WHO representatives is explained in the context of longstanding WHO's problems, which are mainly linked to the vertical fragmentation...

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<p dir="ltr">The recent global pandemic, COVID-19, has revealed to all the importance of understanding the complex relationship between viruses and hosts. Before COVID-19, I started my study of viral protein-host lipid interactions in the hemorrhagic fevers Ebola and Marburg viruses. These viruses contain a matrix protein that interacts with the plasma membrane to facilitate the formation of both authentic viruses and virus-like particles. My goal was to understand the limitations of their specific host lipid interactions. However, when the COVID-19 pandemic began, so to be our swift response in the development of a biosafety level 2 compatible model. This model can be used for studying severe acute respiratory distress syndrome 2 (SARS-CoV-2) assembly, egress, and entry. This model enabled exponentially greater access to more facilities to study the intricacies of SARS-CoV-2 assembly. With more access to studying the virus in a safe model, our goal is to push the understanding of viral assembly faster. I then began to take apart the individual pieces of the model and started to look at understanding the roles that they play independently. The membrane protein is the most abundant structural protein and I studied the specific lipid interactions of the soluble fraction of the protein. Physicians observed nucleocapsid protein mutations in the clinic with the increasing number of SARS-CoV-2 variants that are on the rise. The microscopy data collected can give us more insight into perhaps how the nucleocapsid protein induces the formation of filopodia structures at the plasma membrane. The envelope protein proved to be a challenge, but I determined a specific envelope and ceramide interaction in cells. The envelope protein was also causing the formation of microvesicles for an undefined function. I was able to determine the subcellular localization of the protein to the mitochondria. The localization to the mitochondria appears to induce depolarization of the mitochondria membrane action potential and induces the increase in mitochondria dysfunction signal, cytochrome c. Although the mitochondria were dysfunctional, there was no increase in apoptosis signal in the presence of the protein alone.</p>