Introduction: Evidence for minimally symptomatic Ebola virus (EBOV) infection is limited. During the 2013-16 outbreak in West Africa, it was not considered epidemiologically relevant to published models or projections of intervention effects. In order to improve our understanding of the transmission dynamics of EBOV in humans, we investigated the occurrence of minimally symptomatic EBOV infection in quarantined contacts of reported Ebola virus disease cases in a recognized 'hotspot.'
Methodology/principal Findings: We conducted a cross-sectional serosurvey in Sukudu, Kono District, Sierra Leone, from October 2015 to January 2016. A blood sample was collected from 187 study participants, 132 negative controls (individuals with a low likelihood of previous exposure to Ebola virus), and 30 positive controls (Ebola virus disease survivors). IgG responses to Ebola glycoprotein and nucleoprotein were measured using Alpha Diagnostic International ELISA kits with plasma diluted at 1:200. Optical density was read at 450 nm (subtracting OD at 630nm to normalize well background) on a ChroMate 4300 microplate reader. A cutoff of 4.7 U/mL for the anti-GP ELISA yielded 96.7% sensitivity and 97.7% specificity in distinguishing positive and negative controls. We identified 14 seropositive individuals not known to have had Ebola virus disease. Two of the 14 seropositive individuals reported only fever during quarantine while the remaining 12 denied any signs or symptoms during quarantine.
Conclusions/significance: By using ELISA to measure Zaire Ebola virus antibody concentrations, we identified a significant number of individuals with previously undetected EBOV infection in a 'hotspot' village in Sierra Leone, approximately one year after the village outbreak. The findings provide further evidence that Ebola, like many other viral infections, presents with a spectrum of clinical manifestations, including minimally symptomatic infection. These data also suggest that a significant portion of Ebola transmission events may have gone undetected during the outbreak. Further studies are needed to understand the potential risk of transmission and clinical sequelae in individuals with previously undetected EBOV infection.
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http://dx.doi.org/10.1371/journal.pntd.0005087 | DOI Listing |
J Clin Epidemiol
December 2024
Department of Internal Medicine, American University of Beirut, Beirut, Lebanon; Department of Health Research Methods, Evidence, and Impact, McMaster University, Hamilton, ON, Canada.
Objective: To describe the processes of reconciling overlapping guidance and prioritizing practice questions for a World Health Organization (WHO) guideline on Infection Prevention and Control (IPC) for Ebola and Marburg disease.
Methods: This work involved the reconciliation of guidance, the generation of potential practice questions and the prioritization of those questions. Contributors included the WHO secretariat, the WHO steering group, the guideline methodologists, and the guideline development group (GDG).
Epidemiologia (Basel)
December 2024
Division of Infectious Diseases, Medical Service, South Texas Veterans Healthcare System, 7400 Merton Minter Blvd, San Antonio, TX 78229, USA.
Poland suffered an epidemic of louse-borne typhus from 1916-1923, with 400,000 cases and more than 130,000 deaths. The causative factors were depressed economic conditions and a refugee crisis that engulfed Poland after World War I. The recognition of the epidemic in 1919 stimulated the creation of the League of Red Cross Societies (LRCS).
View Article and Find Full Text PDFEmerg Microbes Infect
December 2024
Institute of Virology, Philipps-Universität Marburg, 35043 Marburg, Germany.
Ebola virus (EBOV) transcription is essentially regulated via dynamic dephosphorylation of its viral transcription activator VP30 by the host phosphatase PP2A. The nucleoprotein NP has emerged as a third key player in the regulation of this process by recruiting both the regulatory subunit B56 of PP2A and its substrate VP30 to initiate VP30 dephosphorylation and hence viral transcription. Both binding sites are located in close proximity to each other in NP's C-terminal disordered region.
View Article and Find Full Text PDFJ Infect Dis
December 2024
Biostatistics Research Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Background: The robustness and persistence of vaccine antigen-induced antibodies are often used as proxy indicators of vaccine efficacy, but immune responses to vaccine vectors are typically less well-defined. Our study considered the kinetics of immunoglobulin (IgG) responses against the vector (vesicular stomatitis Indiana virus [VSIV]) nucleoprotein (N) and the inserted antigen (Ebola virus [EBOV]) glycoprotein (GP1,2) components of the rVSVΔG-ZEBOV-GP (rVSV-ZEBOV) vaccine and evaluated their use as biomarkers to confirm self-reported vaccination status.
Methods: From the Partnership for Research on Ebola Virus in Liberia (PREVAIL) I clinical trial (NCT02344407), we randomly selected 212 participants who received rVSV-ZEBOV (n=107) or placebo (n=105).
Antiviral Res
December 2024
Guangdong Provincial Key Laboratory of New Drug Screening & NMPA Key Laboratory for Research and Evaluation of Drug Metabolism & Guangdong-Hong Kong-Macao Joint Laboratory for New Drug Screening, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou, Guangdong, China; Key Laboratory of Infectious Diseases Research in South China, Ministry of Education, Southern Medical University, Guangzhou, Guangdong, China. Electronic address:
The Ebola virus, a filovirus, has been responsible for significant human fatalities since its discovery. Despite extensive research, effective small-molecule drugs remain elusive due to its complex pathogenesis. Inhibition of RNA synthesis is a promising therapeutic target, and the VP30 protein plays a critical role in this process.
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