Explore the vast range of titles available.

The Ebola virus epidemic has topped media and political agendas for months; several countries in west Africa have faced the worst Ebola epidemic in history. At the beginning of the disease outbreak, European Union (EU) policies were notably absent regarding how to respond to the crisis. Although the epidemic is now receding from public view, this crisis has undoubtedly changed the European public perception of Ebola virus disease, which is no longer regarded as a bizarre entity confined in some unknown corner in Africa. Policy makers and researchers in Europe now have an opportunity to consider the lessons learned. In this Personal View, we discuss the EU's response to the Ebola crisis in west Africa. Unfortunately, although ample resources and opportunities for humanitarian and medical action existed, the EU did not use them to promote a rapid and well coordinated response to the Ebola crisis. Lessons learned from this crisis should be used to improve the role of the EU in similar situations in the future, ensuring that European aid can be effectively deployed to set up an improved emergency response system, and supporting the establishment of sustainable health-care services in west Africa.

Addresses the challenge of enabling the development of viable, resilient, and fiscally sustainable health system in Guinea, Liberia, and Sierra Leone. Initiated while Ebola was still raging in all of the three most-affected countries in West Africa, the study identifies the requirements for strengthening the health systems in these countries to go beyond just getting the number of Ebola cases to zero. The overall goal of this study is thus twofold: To assess the capacity of the health systems of the three most-affected countries in terms of their ability to deliver quality health services to their populations, perform core public health functions on a routine basis, and to respond to public health emergencies; and To identify the highest impact strategies to help these countries to strengthen their health systems to be more effective and resilient, drilling down into three key aspects of the health system-- that is, fiscal space for universal health coverage (UHC), development and deployment of an effective health workforce, and continuous disease surveillance.-- Source other than the Library of Congress.

Ebola virus (EBOV) is a highly virulent human pathogen. Recovery of infected patients is associated with efficient EBOV-specific immunoglobulin G (IgG) responses, whereas fatal outcome is associated with defective humoral immunity. As B-cell epitopes on EBOV are poorly defined, we sought to identify specific epitopes in four EBOV proteins (Glycoprotein (GP), Nucleoprotein (NP), and matrix Viral Protein (VP)40 and VP35). For the first time, we tested EBOV IgG+ sera from asymptomatic individuals and symptomatic Gabonese survivors, collected during the early humoral response (seven days after the end of symptoms) and the late memory phase (7-12 years post-infection). We also tested sera from EBOV-seropositive patients who had never had clinical signs of hemorrhagic fever or who lived in non-epidemic areas (asymptomatic subjects). We found that serum from asymptomatic individuals was more strongly reactive to VP40 peptides than to GP, NP or VP35. Interestingly, anti-EBOV IgG from asymptomatic patients targeted three immunodominant regions of VP40 reported to play a crucial role in virus assembly and budding. In contrast, serum from most survivors of the three outbreaks, collected a few days after the end of symptoms, reacted mainly with GP peptides. However, in asymptomatic subjects the longest immunodominant domains were identified in GP, and analysis of the GP crystal structure revealed that these domains covered a larger surface area of the chalice bowl formed by three GP1 subunits. The B-cell epitopes we identified in the EBOV VP35, VP40, NP and GP proteins may represent important tools for understanding the humoral response to this virus and for developing new antibody-based therapeutics or detection methods.

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’.

In this report on the current epidemic, the WHO Ebola Response Team presents data on symptoms, case fatality rate, incubation period, basic reproduction number, and serial interval. Without a greatly increased global response, over 20,000 people may be infected by early November. As of September 14, 2014, a total of 4507 confirmed and probable cases of Ebola virus disease (EVD), as well as 2296 deaths from the virus, had been reported from five countries in West Africa — Guinea, Liberia, Nigeria, Senegal, and Sierra Leone. In terms of reported morbidity and mortality, the current epidemic of EVD is far larger than all previous epidemics combined. The true numbers of cases and deaths are certainly higher. There are numerous reports of symptomatic persons evading diagnosis and treatment, of laboratory diagnoses that have not been included in national databases, and of persons with suspected . . .

In this report, the clinical presentation of some of the first cases of EVD occurring in the West African country of Sierra Leone are described, and factors associated with survival are characterized. The largest and most widespread outbreak of Ebola virus disease (EVD) continues to spread through West Africa, with more than 10,100 cases reported in Guinea, Sierra Leone, Liberia, Senegal, Nigeria, and Mali as of October 25, 2014. 1 The possibility of global spread of the disease was realized recently with the diagnosis of EVD in patients in the United States and Spain. 2 The EVD outbreak appears to have originated near the town of Guéckédou, which is in the forest region of Guinea and close to the borders of Sierra Leone and Liberia. 3 , 4 Sequence analyses indicated that the West African variant . . .

A nanopore DNA sequencer is used for real-time genomic surveillance of the Ebola virus epidemic in the field in Guinea; the authors demonstrate that it is possible to pack a genomic surveillance laboratory in a suitcase and transport it to the field for on-site virus sequencing, generating results within 24 hours of sample collection. Ebola virus genomics surveillance This paper reports the use of nanopore DNA sequencers (known as MinIONs) for real-time genomic surveillance of the Ebola virus epidemic, in the field in Guinea. The authors demonstrate that it is possible to pack a genomic surveillance laboratory in a suitcase and transport it to the field for on-site virus sequencing, generating results within 24 hours of sample collection. The Ebola virus disease epidemic in West Africa is the largest on record, responsible for over 28,599 cases and more than 11,299 deaths 1 . Genome sequencing in viral outbreaks is desirable to characterize the infectious agent and determine its evolutionary rate. Genome sequencing also allows the identification of signatures of host adaptation, identification and monitoring of diagnostic targets, and characterization of responses to vaccines and treatments. The Ebola virus (EBOV) genome substitution rate in the Makona strain has been estimated at between 0.87 × 10 −3 and 1.42 × 10 −3 mutations per site per year. This is equivalent to 16–27 mutations in each genome, meaning that sequences diverge rapidly enough to identify distinct sub-lineages during a prolonged epidemic 2 , 3 , 4 , 5 , 6 , 7 . Genome sequencing provides a high-resolution view of pathogen evolution and is increasingly sought after for outbreak surveillance. Sequence data may be used to guide control measures, but only if the results are generated quickly enough to inform interventions 8 . Genomic surveillance during the epidemic has been sporadic owing to a lack of local sequencing capacity coupled with practical difficulties transporting samples to remote sequencing facilities 9 . To address this problem, here we devise a genomic surveillance system that utilizes a novel nanopore DNA sequencing instrument. In April 2015 this system was transported in standard airline luggage to Guinea and used for real-time genomic surveillance of the ongoing epidemic. We present sequence data and analysis of 142 EBOV samples collected during the period March to October 2015. We were able to generate results less than 24 h after receiving an Ebola-positive sample, with the sequencing process taking as little as 15–60 min. We show that real-time genomic surveillance is possible in resource-limited settings and can be established rapidly to monitor outbreaks.

In its largest outbreak, Ebola virus disease is spreading through Guinea, Liberia, Sierra Leone, and Nigeria. We sequenced 99 Ebola virus genomes from 78 patients in Sierra Leone to ~2000× coverage. We observed a rapid accumulation of interhost and intrahost genetic variation, allowing us to characterize patterns of viral transmission over the initial weeks of the epidemic. This West African variant likely diverged from central African lineages around 2004, crossed from Guinea to Sierra Leone in May 2014, and has exhibited sustained human-to-human transmission subsequently, with no evidence of additional zoonotic sources. Because many of the mutations alter protein sequences and other biologically meaningful targets, they should be monitored for impact on diagnostics, vaccines, and therapies critical to outbreak response.

Ebola viruses are the causative agents of a severe form of viral haemorrhagic fever in man, designated Ebola haemorrhagic fever, and are endemic in regions of central Africa. The exception is the species Reston Ebola virus, which has not been associated with human disease and is found in the Philippines. Ebola virus constitutes an important local public health threat in Africa, with a worldwide effect through imported infections and through the fear of misuse for biological terrorism. Ebola virus is thought to also have a detrimental effect on the great ape population in Africa. Case-fatality rates of the African species in man are as high as 90%, with no prophylaxis or treatment available. Ebola virus infections are characterised by immune suppression and a systemic inflammatory response that causes impairment of the vascular, coagulation, and immune systems, leading to multiorgan failure and shock, and thus, in some ways, resembling septic shock.