Ebola virus disease: A narrative review

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Abstract

<p xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" class="first" dir="auto" id="d2119575e99">Ebola virus disease (EVD), which is also referred to as Ebola hemorrhagic fever, is a highly contagious and frequently lethal sickness caused by the Ebola virus. In 1976, the disease emerged in two simultaneous outbreaks in Sudan and the Democratic Republic of Congo. Subsequently, it has caused intermittent outbreaks in several African nations. The virus is primarily spread via direct contact with the bodily fluids of an infected individual or animal. EVD is distinguished by symptoms such as fever, fatigue, muscle pain, headache, and hemorrhage. The outbreak of EVD in West Africa in 2014-2016 emphasized the need for effective control and prevention measures. Despite advancements and the identification of new treatments for EVD, the primary approach to treatment continues to be centered around providing supportive care. Early detection and supportive care can enhance the likelihood of survival. This includes intravenous fluids, electrolyte replacement, and treatment of secondary infections. Experimental therapies, for instance, monoclonal antibodies and antiviral drugs, have shown promising results in animal studies and some clinical trials. Some African countries have implemented the use of vaccines developed for EVD, but their effectiveness and long-term safety are still being studied. This article provides an overview of the history, transmission, symptoms, diagnosis, treatment, epidemiology, and Ebola coinfection, as well as highlights the ongoing research efforts to develop effective treatments and vaccines to combat this deadly virus. </p>

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Finlay W. McNab, Katrin Mayer-Barber, Alan Sher … (2015)

Type I interferons (IFNs) have diverse effects on innate and adaptive immune cells during infection with viruses, bacteria, parasites and fungi, directly and/or indirectly through the induction of other mediators. Type I IFNs are important for host defence against viruses. However, recently, they have been shown to cause immunopathology in some acute viral infections, such as influenza virus infection. Conversely, they can lead to immunosuppression during chronic viral infections, such as lymphocytic choriomeningitis virus infection. During bacterial infections, low levels of type I IFNs may be required at an early stage, to initiate cell-mediated immune responses. High concentrations of type I IFNs may block B cell responses or lead to the production of immunosuppressive molecules, and such concentrations also reduce the responsiveness of macrophages to activation by IFNγ, as has been shown for infections with Listeria monocytogenes and Mycobacterium tuberculosis. Recent studies in experimental models of tuberculosis have demonstrated that prostaglandin E2 and interleukin-1 inhibit type I IFN expression and its downstream effects, demonstrating that a cross-regulatory network of cytokines operates during infectious diseases to provide protection with minimum damage to the host.

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Sabue Mulangu, Lori Dodd, Richard Davey … (2019)

Although several experimental therapeutics for Ebola virus disease (EVD) have been developed, the safety and efficacy of the most promising therapies need to be assessed in the context of a randomized, controlled trial.

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Pathogenesis of Ebola hemorrhagic fever in cynomolgus macaques: evidence that dendritic cells are early and sustained targets of infection.

Thomas W. Geisbert, Lisa Hensley, Tom Larsen … (2003)

Ebola virus (EBOV) infection causes a severe and fatal hemorrhagic disease that in many ways appears to be similar in humans and nonhuman primates; however, little is known about the development of EBOV hemorrhagic fever. In the present study, 21 cynomolgus monkeys were experimentally infected with EBOV and examined sequentially over a 6-day period to investigate the pathological events of EBOV infection that lead to death. Importantly, dendritic cells in lymphoid tissues were identified as early and sustained targets of EBOV, implicating their important role in the immunosuppression characteristic of EBOV infections. Bystander lymphocyte apoptosis, previously described in end-stage tissues, occurred early in the disease-course in intravascular and extravascular locations. Of note, apoptosis and loss of NK cells was a prominent finding, suggesting the importance of innate immunity in determining the fate of the host. Analysis of peripheral blood mononuclear cell gene expression showed temporal increases in tumor necrosis factor-related apoptosis-inducing ligand and Fas transcripts, revealing a possible mechanism for the observed bystander apoptosis, while up-regulation of NAIP and cIAP2 mRNA suggest that EBOV has evolved additional mechanisms to resist host defenses by inducing protective transcripts in cells that it infects. The sequence of pathogenetic events identified in this study should provide new targets for rational prophylactic and chemotherapeutic interventions.