DermKnowledgeBASE: Ebola Virus Infection

Ebola Virus Infection

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The text is the summary of recent articles on Ebola Virus Infection at 75 thresold from National Library of Medicine (NLM). This information is subject to NCBI's Disclaimer and Copyright notice.


Monoclonal antibody (mAb)-based therapies hold promise as treatment options for Ebola virus infections [1]. Using histology in combination with immunohistochemistry and in situ hybridization in a retrospective review of a guinea pig confirmation-of-virulence study, we demonstrate for the first time Ebola virus infection in hepatic Oval Cells, the endocardium and stroma of the atrioventricular valves and chordae tendinae, satellite Cells of peripheral ganglia, neurofibroblasts and Schwann Cells of peripheral nerves and ganglia, smooth Muscle Cells of the uterine myometrium and vaginal wall, acini of the parotid salivary glands, thyroid follicular cells, adrenal medullary Cells, pancreatic islet Cells, endometrial glandular and surface epithelium, and the epithelium of the vagina, Penis and, prepuce [2]. Histopathological and immunopathological analyses of Ebola virus have revealed that histopathological changes in skin tissue are associated with various degrees of endothelial cell swelling and Necrosis [3]. The discovery of microRNAs (miRNAs) in Ebola virus implies that Immune escape, endothelial cell rupture, and tissue dissolution during Ebola virus infection are a result of the effects of Ebola virus miRNAs [4]. These RNA sequences tended to bind to the same thrombospondin protein, THSD4, emphasizing the potential importance of the synergistic binding of miRNAs from Ebola virus, Propionibacterium acnes, and humans to the target [5].

The severity of the cytokine storm is consistently linked with fatal disease outcome [6]. Previous findings have demonstrated that specific T-cell subsets are key contributors to the onset of a cytokine storm [7]. In this study, we investigated the role of Tim-1, a T-cell-receptor-independent trigger of T-cell activation [8]. We first demonstrated that Tim-1-knockout (KO) mice survive lethal Ebola virus challenge [9]. We then used a series of in vitro assays to demonstrate that Ebola virus directly binds primary T Cells in a Tim-1-phosphatidylserine-dependent manner [10].

Previously, by repurposing virtual screening of 6438 drugs from DrugBank, ibuprofen was selected as a possible inhibitor of the Ebola virus infection [11]. In this study, we examined whether Ebola virus proteins affect BST2-mediated induction of NF-κB [12]. We found that the Ebola virus matrix protein, VP40, and envelope glycoprotein, GP, each cooperate with BST2 to induce NF-κB activity, with maximal activity when all three proteins are expressed [13]. Activation of NF-κB by the Ebola virus proteins either alone or together with BST2 requires the canonical NF-κB signaling pathway [14]. BST2 with a glycosylphosphatidylinositol (GPI) anchor signal deletion, which is not expressed at the plasma membrane and is unable to entrap virions, activated NF-κB in concert with the Ebola virus proteins at least as effectively as wild-type BST2 [15].

We asked how proinflammatory signaling by the host protein BST2/tetherin, which is mediated by the transcription factor NF-κB, responds to Ebola virus proteins [16]. Ebola virus GP1,2, the Ebola virus matrix protein VP40, and BST2 are at least additive with respect to the induction of NF-κB activity [17]. Several HIS mouse models have recently been used to study Ebola virus (EBOV) infection and disease [18]. This result suggests that IgM-secreting hybridomas are predominantly generated by DNA vaccination [19]. The patient died in the village and post-mortem testing confirmed Ebola Virus infection [20].

These macrocyclic peptides showed remarkably high affinity to recombinant Zaire Ebola virus VP24 (eVP24), with a dissociation constant in the single digit nanomolar range, and could also successfully disrupt the eVP24-KPNA interaction [21]. The commercial cyclic peptides which we used in this study were obtained from the selected chemical companies [22]. Conjugation of the commercial cyclic peptides to HIV-1 Tat peptide was done in order to accumulate it inside the endosome [23]. MH has a critical role in addressing medicine-related issues, such as human cloning legislation and the treatment of Ebola virus infection [24]. To date, none of demographic and clinical features, except younger age, have been consistently shown to affect mortality outcome in Children infected with Ebola virus [25].

What is Known: • The 2014-2015 West Africa Ebola epidemic is the largest and most widespread outbreak of Ebola virus disease (EVD) in history, with more than 11,000 deaths in Guinea, Liberia, and Sierra Leone [26]. What is New: • Demographic and clinical characteristics of the nationwide cohort of pediatric patients with laboratory-confirmed EVD in Guinea are reported [27]. To assess the degree of asymptomatic infection occurring during an Ebola virus disease (EVD) outbreak, we carried out a serological survey in the Djera district of the Equateur province of the Democratic Republic of the Congo affected by an Ebola outbreak in 2014 [28]. Careful consideration of immunogenicity post vaccination is essential but has been somewhat stifled because of the wide array of immunological assays and outputs that have been used in the numerous clinical trials [29]. The pathogenesis of Ebola virus (EBOV) disease (EVD) is poorly characterized [30].

Testing for Ebola virus was done by real-time PCR and for malaria by a rapid diagnostic test [31]. Furthermore, depletion of CD8 and CD4 T Cells resulted in loss of early control of virus replication, viremia and fatal Ebola virus disease (EVD) [32]. Identifying the causes of these Persistent illnesses is paramount to develop appropriate therapeutic protocols [33]. Major concern is pilgrimage seasons with possible transmission to Middle East populations [34]. Efficacy was difficult to evaluate because of numerous unknowns (especially evolution of neutralizing antibodies), prior to the cessation of active transmission [35].

References: 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 ,

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