Ebola haemorrhagic fever: experimental infection of monkeys

Bowen, E. T. W.; Platt, G.S.; Simpson, David; McArdell, L.B.; Raymond, Reid

doi:10.1016/0035-9203(78)90058-5

Cited by 97 publications

(59 citation statements)

References 7 publications

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“…4 The isolation of the aetiologic agent of Ebola haemorrhagic fever was reported for the first time during 1977. 5 According to the US Centers for Disease Control and Prevention, 4 since 1976 there have been 34 known outbreaks of Ebola. Before the latest outbreak, the deadliest episode was the first recorded outbreak in 1976 which killed 280 people in Central Africa.…”

Section: Introductionmentioning

confidence: 99%

bibliometric analysis of research on Ebola in Science Citation Index Expanded

Pouris¹,

Ho²

2017

S. Afr. J. Sci.

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An unprecedented outbreak of the Ebola virus in 2014 claimed more than 1000 lives in West Africa and the World Health Organization declared a global public health emergency. This outbreak will undoubtedly promote additional research related to the Ebola virus and will create debate related to experimental drugs. This article identified the quantum of research in the field since 1991; the scientific disciplines that contributed to the field; the countries, organisations and authors that supported such research and the most cited articles. An increasing trend in annual production during 1991–2013 was observed. Journal of Virology, Journal of Infectious Diseases, and Virology were the three most productive journals in the field. Similarly, the field of virology dominated the 73 categories in which the Ebola research was classified. A total of 63 countries contributed to Ebola-related research, led by the USA. The most productive institutions were the United States Army Medical Research Institute of Infectious Diseases, the Centers for Disease Control and Prevention, and the National Institute of Allergy and Infectious Diseases. African countries were more likely to be involved in international collaboration than independent research. The most influential article exhibited a notable citation pattern and presented global trends in emerging infectious diseases.

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Section: Introductionmentioning

confidence: 99%

bibliometric analysis of research on Ebola in Science Citation Index Expanded

Pouris¹,

Ho²

2017

S. Afr. J. Sci.

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“…EBOV replicates to high titers in the liver (12)(13)(14), and fatal infection is associated with alterations in circulating enzyme levels indicative of liver damage (15)(16)(17). Microscopic analysis of infected livers shows histopathologic lesions, including hepatocyte damage and death (14,18,19).…”

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confidence: 99%

Mechanisms and Consequences of Ebolavirus-Induced Lymphocyte Apoptosis

Bradfute

Swanson

Smith

et al. 2009

The Journal of Immunology

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Ebolavirus (EBOV) is a member of the filovirus family and causes severe hemorrhagic fever, resulting in death in up to 90% of infected humans. EBOV infection induces massive bystander lymphocyte apoptosis; however, neither the cellular apoptotic pathway(s) nor the systemic implications of lymphocyte apoptosis in EBOV infection are known. In this study, we show data suggesting that EBOV-induced lymphocyte apoptosis in vivo occurs via both the death receptor (extrinsic) and mitochondrial (intrinsic) pathways, as both Fas-associated death domain dominant negative transgenic mice and mice overexpressing bcl-2 were resistant to EBOV-induced lymphocyte apoptosis. Surprisingly, inhibiting lymphocyte apoptosis during EBOV infection did not result in improved animal survival. Furthermore, we show for the first time that hepatocyte apoptosis likely occurs in EBOV infection, and that mice lacking the proapoptotic genes Bim and Bid had reduced hepatocyte apoptosis and liver enzyme levels postinfection. Collectively, these data suggest that EBOV induces multiple proapoptotic stimuli and that blocking lymphocyte apoptosis is not sufficient to improve survival in EBOV infection. These data suggest that hepatocyte apoptosis may play a role in the pathogenesis of EBOV infection, whereas lymphocyte apoptosis appears to be nonessential for EBOV disease progression.

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“…Several nonhuman primate species have been used to model EBOV (Zaire) HF including African green monkeys (Chlorocebus aethiops, formerly Cercopithecus aethiops), 4,5,14 cynomolgus macaques (Macaca fascicularis), 5,7,[15][16][17] rhesus macaques (Macaca mulatta), 4 -7,18 -20 and hamadryad baboons (Papio hamadryas). [21][22][23][24][25][26] Similar pathological features of EBOV infection have been documented among these species; however, African green monkeys do not present with a macular cutaneous rash, which is a characteristic feature of disease in macaques and baboons.…”

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confidence: 99%

“…4 -6,15,18 -21 Importantly, this rash is also a prominent feature of human disease. 4,14 We focused much of our recent work on cynomolgus macaques, the species most frequently used for filoviral vaccine studies. 7,17 Our cynomolgus monkey model uses a challenge dose and route that reflects a likely laboratory exposure and has been uniformly lethal with animals dying 6 to 7 days after exposure.…”

mentioning

confidence: 99%

Pathogenesis of Ebola Hemorrhagic Fever in Cynomolgus Macaques

Geisbert

Hensley

Larsen

et al. 2003

The American Journal of Pathology

535

327

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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 sus-

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Ebola haemorrhagic fever: experimental infection of monkeys

Cited by 97 publications

References 7 publications

bibliometric analysis of research on Ebola in Science Citation Index Expanded

bibliometric analysis of research on Ebola in Science Citation Index Expanded

Mechanisms and Consequences of Ebolavirus-Induced Lymphocyte Apoptosis

Pathogenesis of Ebola Hemorrhagic Fever in Cynomolgus Macaques

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