Human asymptomatic Ebola infection and strong inflammatory response

Leroy, Eric M.; Baize, Sylvain; Volchkov, Viktor E.; Fisher‐Hoch, Susan P.; Georges‐Courbot, Marie‐Claude; Lansoud-Soukate, J.; Capron, Moníque; Debré, Patrice; McCormick, Joseph B.; Georges, A. J.

doi:10.1016/s0140-6736(00)02405-3

Cited by 377 publications

(310 citation statements)

References 28 publications

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“…EBOV infection has been associated with massive release of inflammatory chemokines and cytokines late in the course of disease (40)(41)(42)(43)(44)(45), either as a cause or effect of pathogenic events. Considering the morphologic similarity of eVLPs to the live virus, serum cytokines were tested at 6 h and 1, 3, 5, 7, 10, 14, and 21 days postvaccination to determine whether eVLPs also induced systemic cytokine release.…”

Section: Resultsmentioning

confidence: 99%

Ebola virus-like particles protect from lethal Ebola virus infection

Warfield

Bosio

Welcher

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

229

258

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The filovirus Ebola causes hemorrhagic fever with 70 -80% human mortality. High case-fatality rates, as well as known aerosol infectivity, make Ebola virus a potential global health threat and possible biological warfare agent. Development of an effective vaccine for use in natural outbreaks, response to biological attack, and protection of laboratory workers is a higher national priority than ever before. Coexpression of the Ebola virus glycoprotein (GP) and matrix protein (

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Section: Resultsmentioning

confidence: 99%

Ebola virus-like particles protect from lethal Ebola virus infection

Warfield

Bosio

Welcher

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

229

258

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“…Thus far, treatment with EBOV-immune sera delays, but does not provide protection against lethal EBOV infection in monkeys (18 -20). Humans that survive filovirus infections have an early proinflammatory response and a persistent rise in anti-EBOV IgG, whereas humans that succumb to infection do not develop detectable virus-specific Ab (21,22). In some instances, high levels of EBOV-specific Ab correlate with protection and in others it does not; therefore, the exact contribution of Ab in protection against EBOV infection is not clear.…”

mentioning

confidence: 99%

Induction of Humoral and CD8+ T Cell Responses Are Required for Protection against Lethal Ebola Virus Infection

Warfield

Olinger

Deal

et al. 2005

The Journal of Immunology

127

142

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Ebola virus (EBOV)-like particles (eVLP), composed of the EBOV glycoprotein and matrix viral protein (VP)40 with a lipid membrane, are a highly efficacious method of immunization against EBOV infection. The exact requirements for immunity against EBOV infection are poorly defined at this time. The goal of this work was to determine the requirements for EBOV immunity following eVLP vaccination. Vaccination of BALB/c or C57BL/6 mice with eVLPs in conjunction with QS-21 adjuvant resulted in mixed IgG subclass responses, a Th1-like memory cytokine response, and protection from lethal EBOV challenge. Further, this vaccination schedule led to the generation of both CD4+ and CD8+ IFN-γ+ T cells recognizing specific peptides within glycoprotein and VP40. The transfer of both serum and splenocytes, but not serum or splenocytes alone, from eVLP-vaccinated mice conferred protection against lethal EBOV infection in these studies. B cells were required for eVLP-mediated immunity to EBOV because B cell-deficient mice vaccinated with eVLPs were not protected from lethal EBOV challenge. We also found that CD8+, but not CD4+, T cells are absolutely required for eVLP-mediated protection against EBOV infection. Further, eVLP-induced protective mechanisms were perforin-independent, but IFN-γ-dependent. Taken together, both EBOV-specific humoral and cytotoxic CD8+ T cell responses are critical to mediate protection against filoviruses following eVLP vaccination.

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“…Firstly, EVD cases can be asymptomatic [7,8]. Secondly, West Africa is one of the poorest regions of the world, their health systems, let alone their surveillance capabilities are severely limited -in a study from the Centers of Disease Control and Prevention (CDC), timeliness of reporting was found to be particularly lacking during the early phases of the EVD outbreak [9].…”

Section: Introductionmentioning

confidence: 99%

A systematic review of early modelling studies of Ebola virus disease in West Africa

et al. 2017

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SUMMARYPhenomenological and mechanistic models are widely used to assist resource planning for pandemics and emerging infections. We conducted a systematic review, to compare methods and outputs of published phenomenological and mechanistic modelling studies pertaining to the 2013-2016 Ebola virus disease (EVD) epidemics in four West African countries -Sierra Leone, Liberia, Guinea and Nigeria. We searched Pubmed, Embase and Scopus databases for relevant English language publications up to December 2015. Of the 874 articles identified, 41 met our inclusion criteria. We evaluated these selected studies based on: the sources of the case data used, and modelling approaches, compartments used, population mixing assumptions, model fitting and calibration approaches, sensitivity analysis used and data bias considerations. We synthesised results of the estimated epidemiological parameters: basic reproductive number (R 0 ), serial interval, latent period, infectious period and case fatality rate, and examined their relationships. The median of the estimated mean R 0 values were between 1·30 and 1·84 in Sierra Leone, Liberia and Guinea. Much higher R 0 value of 9·01 was described for Nigeria. We investigated several issues with uncertainty around EVD modes of transmission, and unknown observation biases from early reported case data. We found that epidemic models offered R 0 mean estimates which are country-specific, but these estimates are not associating with the use of several key disease parameters within the plausible ranges. We find simple models generally yielded similar estimates of R 0 compared with more complex models. Models that accounted for data uncertainty issues have offered a higher case forecast compared with actual case observation. Simple model which offers transparency to public health policy makers could play a critical role for advising rapid policy decisions under an epidemic emergency.

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Human asymptomatic Ebola infection and strong inflammatory response

Cited by 377 publications

References 28 publications

Ebola virus-like particles protect from lethal Ebola virus infection

Ebola virus-like particles protect from lethal Ebola virus infection

Induction of Humoral and CD8+ T Cell Responses Are Required for Protection against Lethal Ebola Virus Infection

A systematic review of early modelling studies of Ebola virus disease in West Africa

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