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.

Our results indicate that EVD molecular signatures overlap with those of sepsis, imply that pancreatic enzymes contribute to tissue damage in fatal EVD, and suggest that Ebola virus infection may induce aberrant Neutrophils whose activity could explain hallmarks of fatal EVD [1]. In this Review, we discuss how the experience and data generated from that outbreak have helped to advance the understanding of the use of these countermeasures for post-exposure prophylaxis against Ebola virus infection [2]. In future outbreaks, post-exposure prophylaxis could play an important part in reducing community transmission of Ebola virus by providing more immediate protection than does immunisation as well as providing additional protection for health-care workers who are inadvertently exposed over the course of their work [3]. A machine learning model trained on anti-Ebola virus (EBOV) screening data previously identified tilorone as a potent in vitro EBOV inhibitor, making it a candidate for the treatment of Ebola virus disease (EVD) [4]. DNA vaccination is an attractive method for inducing protective immunity to a variety of pathogens, but the low immunogenicity seen in larger animals and humans has hindered its usage [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].

From April 24-29, 2015, interview teams approached every household in the seven villages and collected information on demographics, knowledge of EVD, attitudes about quarantine to prevent the spread of EVD, and their quarantine experiences and practices [21]. Knowledge, attitudes, and practices among members of households actively monitored or quarantined to prevent transmission of Ebola Virus Disease - Margibi County, Liberia: February-March 2015 [22]. 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 [23]. The commercial cyclic peptides which we used in this study were obtained from the selected chemical companies [24]. Conjugation of the commercial cyclic peptides to HIV-1 Tat peptide was done in order to accumulate it inside the endosome [25].

MH has a critical role in addressing medicine-related issues, such as human cloning legislation and the treatment of Ebola virus infection [26]. 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 [27]. 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 [28]. What is New: • Demographic and clinical characteristics of the nationwide cohort of pediatric patients with laboratory-confirmed EVD in Guinea are reported [29]. 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 [30].

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 [31]. The pathogenesis of Ebola virus (EBOV) disease (EVD) is poorly characterized [32]. Testing for Ebola virus was done by real-time PCR and for malaria by a rapid diagnostic test [33]. Furthermore, depletion of CD8 and CD4 T Cells resulted in loss of early control of virus replication, viremia and fatal Ebola virus disease (EVD) [34]. Identifying the causes of these Persistent illnesses is paramount to develop appropriate therapeutic protocols [35].

Major concern is pilgrimage seasons with possible transmission to Middle East populations [36]. Efficacy was difficult to evaluate because of numerous unknowns (especially evolution of neutralizing antibodies), prior to the cessation of active transmission [37]. Infection transmission was thus inexplicable through the acknowledged transmission routes [38]. We formulated two hypotheses: inapparent exposures to blood/bodily fluids or transmission due to asymptomatic/mildly symptomatic carriers [39]. We recruited healthy adults aged 18-50 years who were HIV negative, had no history of Ebola virus infection, and had no previous immunisation with other Ebola vaccine candidates [40].

To investigate this issue, we analyzed US-focused news stories about Ebola virus disease during July 1-November 30, 2014 [41]. ECT members assessed and approved testing for Ebola virus infection at MDH [42]. We demonstrate that lysine residue 326 in VP40 is involved in SUMOylation, and by analyzing a mutant in this residue we show that SUMO conjugation regulates the stability of VP40 and the incorporation of SUMO into the VLPs [43]. Clinical studies have shown that Oral administration of CBD, compared to placebo, significantly reduces anxiety, has antinociceptive and anticonvulsant actions, and may be therapeutic for insomnia [44].

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 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 ,

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About Me

I have varied research interests ranging from eHealth, Health Information Exchange, Clinical Trials and Research, Contact Dermatitis, Bioinformatics, and Cosmetic Dermatology. I have work experience in Canada as an eHealth analyst, and in Dubai and India as a Specialist Dermatologist.


Bell Raj Eapen
Hamilton, ON