Pathophysiology of Shock and Hemorrhage in a Fulminating Viral Infection (Ebola)

Fisher‐Hoch, Susan P.; Platt, G.S.; Neild, Guy H.; Southee, T.; Baskerville, A.; Raymond, Reid; Lloyd, Graham; Simpson, David

doi:10.1093/infdis/152.5.887

Cited by 175 publications

(92 citation statements)

References 20 publications

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“…Results from many studies have shown biochemical and histological evidence of disseminated intravascular coagulation in both experimentally infected NHPs and humans 19,20,22,23,40,[44][45][46][49][50][51]53,54,70,[73][74][75][76][77][78][79] . The mechanisms that cause these coagulation disorders are not fully understood, but the expression or release of tissue factor from filovirus-infected monocytes and macro phages seems to play a role 54,55 .…”

Section: Box 1 | Animal Modelsmentioning

confidence: 99%

Post-exposure treatments for Ebola and Marburg virus infections

Cross

Mire

Feldmann

et al. 2018

Nat Rev Drug Discov

111

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| The filoviruses -Ebola virus and Marburg virus -cause lethal haemorrhagic fever in humans and non-human primates (NHPs). Filoviruses present a global health threat both as naturally acquired diseases and as potential agents of bioterrorism. In the recent 2013-2016 outbreak of Ebola virus, the most promising therapies for post-exposure use with demonstrated efficacy in the gold-standard NHP models of filovirus disease were unable to show statistically significant protection in patients infected with Ebola virus. This Review briefly discusses these failures and what has been learned from these experiences, and summarizes the current status of post-exposure medical countermeasures in development, including antibodies, small interfering RNA and small molecules. We outline how our current knowledge could be applied to the identification of novel interventions and ways to use interventions more effectively. R E V I E W SNATURE REVIEWS | DRUG DISCOVERY VOLUME 17 | JUNE 2018 | 413 © 2 0 1 8 M a c m i l l a n P u b l i s h e r s L i m i t e d , p a r t o f S p r i n g e r N a t u r e . A l l r i g h t s r e s e r v e d . AstheniaMuscular weakness. MyalgiaMuscular pain. ArthralgiaJoint pain. LeukopeniaA condition of having a low number of circulating leukocytes, including neutrophils, eosinophils, basophils, lymphocytes and monocytes. LymphocytopeniaA condition of having a low number of circulating leukocytes, including natural killer cells, T cells and B cells. ThrombocytopeniaA condition of having a low number of circulating thrombocytes, also known as platelets.and Ebolavirus. The Marburgvirus genus contains a single species, Marburg marburgvirus, which contains two members, Marburg virus (MARV) and Ravn virus (RAVV). The Ebolavirus genus consists of five distinct species: Bundibugyo ebolavirus (BDBV), Reston ebolavirus (RESTV), Sudan ebolavirus (SUDV), Tai Forest ebolavirus (TAFV; previously termed 'Côte d'Ivoire ebolavirus' but more commonly known as 'Ivory Coast ebolavirus') and Zaire ebolavirus (EBOV). MARV, RAVV, BDBV, SUDV and EBOV are important human pathogens, with case fatality rates often up to 90% for MARV, RAVV and EBOV, and around 55% for SUDV 8,10 . On the basis of two small outbreaks in 2007 and 2012, BDBV seems to be the least pathogenic, with a case fatality rate of about 40-48% 11,12 . In 1994, TAFV was associated with a number of deaths in chimpanzees and a single symptomatic but non-lethal human infection in the Republic of Côte d'Ivoire 13,14 . RESTV is lethal for macaques but is not thought to cause disease in humans 15 . An outbreak of RESTV was reported in pigs in the Philippines in 2008; however, it remains uncertain whether the disease observed in the pigs was caused by RESTV or other agents reported to have co-infected the animals 16 . Clinical manifestationsClinical and laboratory signs of disease caused by filovirus infection are nonspecific and usually associated with an incubation period of 2-21 days (mean 4-10 days) 8,17 . Illness begins with an abrupt onset of fever, astheni...

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Section: Box 1 | Animal Modelsmentioning

confidence: 99%

Post-exposure treatments for Ebola and Marburg virus infections

Cross

Mire

Feldmann

et al. 2018

Nat Rev Drug Discov

111

View full text Add to dashboard Cite

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“…The ribonucleoprotein (RNP) complex that mediates transcription and replication of the viral genome comprises 4 of these proteins: nucleoprotein (NP), VP35, VP30, and the RNA-dependent RNA polymerase (L). The 3 other proteins-glycoprotein (GP), VP40, and VP24-are membrane-associated proteins [5].…”

Section: E Zaire Ebolavirus (Ebov)mentioning

confidence: 99%

Analysis of Ebolavirus with Decision Tree and Apriori algorithm

Go¹,

Lee²,

Yoon³

2014

IJMLC

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Abstract-EbolaVirus, which has high facilities up to 90%, is introduced into the human population through close contact with the blood, secretions, organs or other bodily fluids of infected animals. It is mostly occurred in Central and West Africa, near tropical rainforests and their host are bats. In this paper, we analyzed the DNA sequences of 5 Ebolavirus : Bundibugyo Ebolavirus, Reston Ebolavirus, Sudan Ebolavirus, TaiForest Ebolavirus, and Zaire Ebolavirus and investigated the difference between them based on the genus they are involved in. Furthermore, we look for the frequency of the amino acid and find the similarities between the Ebolaviruses.Index Terms-Ebolavirus, bundibugyo ebolavirus, reston ebolavirus, sudan ebolavirus, taiforest ebolavirus, zaire ebolavirus, decision tree, apriori algorithm.

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“…Pretreating rhesus monkeys with antioxidants, such as vitamin E, failed to confer any beneficial or protective effect to ZEBOV-infected rhesus monkeys (Ref. 64). …”

Section: Regulation Of the Pro-inflammatory Responsementioning

confidence: 99%

Ebola virus: new insights into disease aetiopathology and possible therapeutic interventions

Geisbert

Hensley

2004

Expert Rev. Mol. Med.

112

106

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Ebola virus (EBOV) gained public notoriety in the last decade largely as a consequence of the highly publicised isolation of a new EBOV species in a suburb of Washington, DC, in 1989, together with the dramatic clinical presentation of EBOV infection and high case-fatality rate in Africa (near 90% in some outbreaks), and the unusual and striking morphology of the virus. Furthermore, there are no vaccines or effective therapies currently available. Progress in understanding the origins of the pathophysiological changes that make EBOV infections of humans so devastating has been slow, primarily because these viruses require special containment for safe research. However, an increasing understanding of the mechanisms of EBOV pathogenesis, facilitated by the development of new tools to elucidate critical regulatory elements in the viral life cycle, is providing new targets that can be exploited for therapeutic interventions. Notably, identifying factors triggering the haemorrhagic complications that characterise EBOV infections led to the development of a strategy to modulate coagulopathy; this therapeutic modality successfully mitigated the effects of EBOV haemorrhagic fever in nonhuman primates. This review summarises our current understanding of EBOV pathogenesis and discusses various approaches to therapeutic intervention based on our current understanding of how EBOV produces a lethal infection.

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Pathophysiology of Shock and Hemorrhage in a Fulminating Viral Infection (Ebola)

Cited by 175 publications

References 20 publications

Post-exposure treatments for Ebola and Marburg virus infections

Post-exposure treatments for Ebola and Marburg virus infections

Analysis of Ebolavirus with Decision Tree and Apriori algorithm

Ebola virus: new insights into disease aetiopathology and possible therapeutic interventions

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