Perspectives on West Africa Ebola Virus Disease Outbreak, 2013-2016.
Ontology highlight
ABSTRACT:
SUBMITTER: Spengler JR
PROVIDER: S-EPMC4880067 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:The 2013-2016 West Africa Ebola virus disease epidemic was notable for its scope, scale, and complexity. This briefing presents a series of distinguishing epidemiological features that set this outbreak apart. Compared to one concurrent and 23 previous outbreaks of the disease over 40 years, this was the only occurrence of Ebola virus disease involving multiple nations and qualifying as a pandemic. Across multiple measures of magnitude, the 2013-2016 outbreak was accurately described using superlatives: largest and deadliest in terms of numbers of cases and fatalities; longest in duration; and most widely dispersed geographically, with outbreak-associated cases occurring in 10 nations. In contrast, the case-fatality rate was much lower for the 2013-2016 outbreak compared to the other 24 outbreaks. A population of particular interest for ongoing monitoring and public health surveillance is comprised of more than 17,000 "survivors," Ebola patients who successfully recovered from their illness. The daunting challenges posed by this outbreak were met by an intensive international public health response. The near-exponential rate of increase of incident Ebola cases during mid-2014 was successfully slowed, reversed, and finally halted through the application of multiple disease containment and intervention strategies.
| S-EPMC5314891 | biostudies-literature
Project description:The 2013-2016 West Africa Ebola virus disease pandemic was the largest, longest, deadliest, and most geographically expansive outbreak in the 40-year interval since Ebola was first identified. Fear-related behaviors played an important role in shaping the outbreak. Fear-related behaviors are defined as "individual or collective behaviors and actions initiated in response to fear reactions that are triggered by a perceived threat or actual exposure to a potentially traumatizing event. FRBs modify the future risk of harm." This review examines how fear-related behaviors were implicated in (1) accelerating the spread of Ebola, (2) impeding the utilization of life-saving Ebola treatment, (3) curtailing the availability of medical services for treatable conditions, (4) increasing the risks for new-onset psychological distress and psychiatric disorders, and (5) amplifying the downstream cascades of social problems. Fear-related behaviors are identified for each of these outcomes. Particularly notable are behaviors such as treating Ebola patients in home or private clinic settings, the "laying of hands" on Ebola-infected individuals to perform faith-based healing, observing hands-on funeral and burial customs, foregoing available life-saving treatment, and stigmatizing Ebola survivors and health professionals. Future directions include modeling the onset, operation, and perpetuation of fear-related behaviors and devising strategies to redirect behavioral responses to mass threats in a manner that reduces risks and promotes resilience.
| S-EPMC5241909 | biostudies-literature
Project description:The unprecedented magnitude of the 2013-2016 Makona Ebola virus (M-EBOV) epidemic likely resulted from multiple epidemiologic factors that set it apart from previous outbreaks. Nonetheless, genetic adaptations that distinguish M-EBOV from previous isolates may also have contributed to the scale of the epidemic. Of particular interest is a M-EBOV glycoprotein (GP) variant, GP-A82V, that was first detected at the inflection point of the 2013-2016 outbreak - when the number of cases increased exponentially - and which completely supplanted the earlier M-EBOV sequence. We found that, as compared with the earlier strain, GP-A82V increased the ability of M-EBOV to fuse with and infect cells of primate origin, including human blood dendritic cells, without altering innate immune signaling in target cells. Residue 82 is located at the NPC1-binding site on M-EBOV GP and the increased infectivity of GP-A82V was restricted to cells from species in which the NPC1 orthologue bears primate-defining residues at the critical interface. We utilized HIV-derived lentiviral vectors pseudotyped with founder and A82V containing M-EBOV GPs to explore the potential that this modification alters how human monocyte-derived dendritic cells (MDDCs) respond to EBOV GP stimulation.
2017-08-31 | GSE84865 | GEO
Project description:The 2014-2016 Ebola virus (EBOV) disease outbreak affected over 29000 people and left behind the biggest cohort (over 17000 individuals) of Ebola survivors in history. Although the persistence of EBOV in body fluids of survivors was reported before the recent outbreak, new evidence revealed that the virus can be detected up to 18 months in the semen, which represents the biggest risk of Ebola resurgence in affected communities. In this study, we review the knowledge on the Ebola flare-ups that occurred after the peak of the 2014-2016 Ebola epidemic in West Africa.
| S-EPMC6249578 | biostudies-other
Project description:The 2013-2016 Ebola outbreak in West Africa is the largest on record with 28 616 confirmed, probable and suspected cases and 11 310 deaths officially recorded by 10 June 2016, the true burden probably considerably higher. The case fatality ratio (CFR: proportion of cases that are fatal) is a key indicator of disease severity useful for gauging the appropriate public health response and for evaluating treatment benefits, if estimated accurately. We analysed individual-level clinical outcome data from Guinea, Liberia and Sierra Leone officially reported to the World Health Organization. The overall mean CFR was 62.9% (95% CI: 61.9% to 64.0%) among confirmed cases with recorded clinical outcomes. Age was the most important modifier of survival probabilities, but country, stage of the epidemic and whether patients were hospitalized also played roles. We developed a statistical analysis to detect outliers in CFR between districts of residence and treatment centres (TCs), adjusting for known factors influencing survival and identified eight districts and three TCs with a CFR significantly different from the average. From the current dataset, we cannot determine whether the observed variation in CFR seen by district or treatment centre reflects real differences in survival, related to the quality of care or other factors or was caused by differences in reporting practices or case ascertainment.This article is part of the themed issue 'The 2013-2016 West African Ebola epidemic: data, decision-making and disease control'.
| S-EPMC5394646 | biostudies-literature
Project description:Under a traditional paradigm, only those with the expected background knowledge consume academic literature. The lay press, as well as government and non-government agencies, play a complementary role of extracting findings of high interest or importance and translating them for general viewing. The need for accurate reporting and public advising is paramount when attempting to tackle epidemic outbreaks through behavior change. Yet, public trust in media outlets is at a historic low. The Crisis and Emergency Risk Communication (CERC) model for media reporting on public health emergencies was established in 2005 and has subsequently been used to analyze media reporting on outbreaks of influenza and measles as well as smoking habits and medication compliance. However, no media analysis had yet been performed on the 2013-2016 Ebola Virus Disease (EVD) outbreak. This study compared the EVD information relayed by lay press sources with general review articles in the academic literature through a mixed-methods analysis. These findings suggest that comprehensive review articles could not serve as a source to clarify and contextualize the uncertainties around the EVD outbreak, perhaps due to adherence to technical accuracy at the expense of clarity within the context of outbreak conditions. This finding does not imply inferiority of the academic literature, nor does it draw direct causation between confusion in review articles and public misunderstanding. Given the erosion of the barriers siloing academia, combined with the demands of today's fast-paced media environment, contemporary researchers should realize that no study is outside the public forum and to therefore consider shifting the paradigm to take personal responsibility in the process of accurately translating their scientific words into public policy actions to best serve as a source of clarity.
| S-EPMC5480889 | biostudies-literature
Project description:BackgroundFor the 2013-2016 Ebola epidemic in West Africa, the largest Ebola virus disease (EVD) epidemic to date, we aim to analyse the patient mix in detail to characterise key sources of spatiotemporal heterogeneity in the case fatality ratios (CFR).MethodsWe applied a non-parametric Boosted Regression Trees (BRT) imputation approach for patients with missing survival outcomes and adjusted for model imperfection. Semivariogram analysis and kriging were used to investigate spatiotemporal heterogeneities.ResultsCFR estimates varied significantly between districts and over time over the course of the epidemic. BRT modelling accounted for most of the spatiotemporal variation and interactions in CFR, but moderate spatial autocorrelation remained for distances up to approximately 90?km. Combining district-level CFR estimates and kriged district-level residuals provided the best linear unbiased predicted map of CFR accounting for the both explained and unexplained spatial variation. Temporal autocorrelation was not observed in the district-level residuals from the BRT estimates.ConclusionsThis study provides new insight into the epidemiology of the 2013-2016 West African Ebola epidemic with a view of informing future public health contingency planning, resource allocation and impact assessment. The analytical framework developed in this analysis, coupled with key domain knowledge, could be deployed in real time to support the response to ongoing and future outbreaks.
| S-EPMC7191269 | biostudies-literature
Project description:The Ebola virus disease (EVD) epidemic in West Africa in 2013-2015 spread heterogeneously across the three hardest-hit countries Guinea, Liberia and Sierra Leone and the estimation of national transmission of EVD provides little information about local dynamics. To investigate district-level transmissibility of EVD, we applied a statistical modelling approach to estimate the basic reproduction number (R0) for each affected district and each country using weekly incident case numbers. We estimated growth rates during the early exponential phase of the outbreak using exponential regression of the case counts on the first eight weeks since onset. To take into account the heterogeneity between and within countries, we fitted a mixed effects model and calculated R0 based on the predicted individual growth rates and the reported serial interval distribution. At district level, R0 ranged from 0.36 (Dubréka) to 1.72 (Beyla) in Guinea, from 0.53 (Maryland) to 3.37 (Margibi) in Liberia and from 1.14 (Koinadugu) to 2.73 (Western Rural) in Sierra Leone. At national level, we estimated an R0 of 0.97 (95% CI 0.77-1.18) for Guinea, 1.26 (95% CI 0.98-1.55) for Liberia and 1.66 (95% CI 1.32-2.00) for Sierra Leone. Socio-demographic variables related to urbanisation such as high population density and high wealth index were found positively associated with R0 suggesting that the consequences of fast urban growth in West Africa may have contributed to the increased spread of EVD.
| S-EPMC4951043 | biostudies-literature
Project description:Ebola virus causes a severe haemorrhagic fever in humans with high case fatality and significant epidemic potential. The 2013-2016 outbreak in West Africa was unprecedented in scale, being larger than all previous outbreaks combined, with 28 646 reported cases and 11 323 reported deaths. It was also unique in its geographical distribution and multicountry spread. It is vital that the lessons learned from the world's largest Ebola outbreak are not lost. This article aims to provide a detailed description of the evolution of the outbreak. We contextualize this outbreak in relation to previous Ebola outbreaks and outline the theories regarding its origins and emergence. The outbreak is described by country, in chronological order, including epidemiological parameters and implementation of outbreak containment strategies. We then summarize the factors that led to rapid and extensive propagation, as well as highlight the key successes, failures and lessons learned from this outbreak and the response.This article is part of the themed issue 'The 2013-2016 West African Ebola epidemic: data, decision-making and disease control'.
| S-EPMC5394636 | biostudies-other
Project description:The recent Ebola epidemic exemplified the importance of understanding and controlling emerging infections. Despite the importance of T cells in clearing virus during acute infection, little is known about Ebola-specific CD8+ T cell responses. We investigated immune responses of individuals infected with Ebola virus (EBOV) during the 2013-2016 West Africa epidemic in Sierra Leone, where the majority of the >28,000 EBOV disease (EVD) cases occurred. We examined T cell memory responses to seven of the eight Ebola proteins (GP, sGP, NP, VP24, VP30, VP35, and VP40) and associated HLA expression in survivors. Of the 30 subjects included in our analysis, CD8+ T cells from 26 survivors responded to at least one EBOV antigen. A minority, 10 of 26 responders (38%), made CD8+ T cell responses to the viral GP or sGP. In contrast, 25 of the 26 responders (96%) made response to viral NP, 77% to VP24 (20 of 26), 69% to VP40 (18 of 26), 42% (11 of 26) to VP35, with no response to VP30. Individuals making CD8+ T cells to EBOV VP24, VP35, and VP40 also made CD8+ T cells to NP, but rarely to GP. We identified 34 CD8+ T cell epitopes for Ebola. Our data indicate the immunodominance of the EBOV NP-specific T cell response and suggest that its inclusion in a vaccine along with the EBOV GP would best mimic survivor responses and help boost cell-mediated immunity during vaccination.
| S-EPMC6094108 | biostudies-literature