Chronological and Spatial Analysis of the 1996 Ebola Reston Virus Outbreak in a Monkey Breeding Facility in the Philippines.

Miranda, Mary Elizabeth; Yoshikawa, Yasuhiro; Manalo, Daria L.; Calaor, Alan B.; Miranda, Noel Lee J.; Cho, Fumiaki; Ikegami, Tetsuro; Ksiazek, Thomas G.

doi:10.1538/expanim.51.173

Cited by 23 publications

(15 citation statements)

References 6 publications

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“…Aerosol transmission among humans has not been reported. However, evidence of intercage transmission of RESTV was observed in the 1989–1990 epizootic cases of RESTV in the Hazleton facility in Reston, Virginia, and demonstration of high concentrations of ebolavirus in nasal secretions and alveoli in experimental infection implicated the potency of aerosol transmission of ebolavirus (Baskerville et al, 1978, 1985; Bowen et al, 1978; Jahrling et al, 1990, 1996; Dalgard et al, 1992; Jaax et al, 1995; Miranda et al, 1999, 2002). Furthermore, the rhesus macaques experimentally challenged with aerosolized EBOV developed the same disease as macaques infected parenterally (Johnson et al, 1995).…”

Section: Non-human Primate Modelsmentioning

confidence: 99%

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Animal models for Ebola and Marburg virus infections

Nakayama¹,

Saijo²

2013

Front. Microbiol.

141

148

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Ebola and Marburg hemorrhagic fevers (EHF and MHF) are caused by the Filoviridae family, Ebolavirus and Marburgvirus (ebolavirus and marburgvirus), respectively. These severe diseases have high mortality rates in humans. Although EHF and MHF are endemic to sub-Saharan Africa. A novel filovirus, Lloviu virus, which is genetically distinct from ebolavirus and marburgvirus, was recently discovered in Spain where filoviral hemorrhagic fever had never been reported. The virulence of this virus has not been determined. Ebolavirus and marburgvirus are classified as biosafety level-4 (BSL-4) pathogens and Category A agents, for which the US government requires preparedness in case of bioterrorism. Therefore, preventive measures against these viral hemorrhagic fevers should be prepared, not only in disease-endemic regions, but also in disease-free countries. Diagnostics, vaccines, and therapeutics need to be developed, and therefore the establishment of animal models for EHF and MHF is invaluable. Several animal models have been developed for EHF and MHF using non-human primates (NHPs) and rodents, which are crucial to understand pathophysiology and to develop diagnostics, vaccines, and therapeutics. Rhesus and cynomolgus macaques are representative models of filovirus infection as they exhibit remarkably similar symptoms to those observed in humans. However, the NHP models have practical and ethical problems that limit their experimental use. Furthermore, there are no inbred and genetically manipulated strains of NHP. Rodent models such as mouse, guinea pig, and hamster, have also been developed. However, these rodent models require adaptation of the virus to produce lethal disease and do not mirror all symptoms of human filovirus infection. This review article provides an outline of the clinical features of EHF and MHF in animals, including humans, and discusses how the animal models have been developed to study pathophysiology, vaccines, and therapeutics.

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Section: Non-human Primate Modelsmentioning

confidence: 99%

“…In an outbreak of RESTV in the Hazleton facility in Reston, Virginia, aerosol transmission between NHPs may have occurred (Jahrling et al, 1990; Dalgard et al, 1992; Miranda et al, 1999, 2002). To address the assumed aerosol transmission of filovirus, a vaccine that induces a strong immune response in the respiratory tract was developed.…”

Section: Vaccinesmentioning

confidence: 99%

Animal models for Ebola and Marburg virus infections

Nakayama¹,

Saijo²

2013

Front. Microbiol.

141

148

View full text Add to dashboard Cite

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“…Three ebolaviruses [Ebola virus (EBOV), Bundibugyo (BDBV), and Sudan virus (SUDV)], and two marburgviruses [Marburg virus (MARV) and Ravn virus (RAVV)] are associated with highly lethal outbreaks of filovirus disease in humans and non-human primates, and are endemic in equatorial regions of the African continent (recently reviewed in (Feldmann and Geisbert, 2011; Hartman et al, 2010; MacNeil et al, 2011; Paessler and Walker, 2013; Pourrut et al, 2005). One ebolavirus, Reston virus (RESTV), is thought to be avirulent in humans (Morikawa et al, 2007), but has been associated with multiple incidents of filovirus disease in monkeys exported from the Philippines to the US or Europe for research (Miranda et al, 2002; Rollin et al, 1999). More recently, RESTV was shown to circulate in domesticated pigs in the Philippines (Barrette et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Cell entry by a novel European filovirus requires host endosomal cysteine proteases and Niemann–Pick C1

Ndungo

Jangra

et al. 2014

Virology

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Lloviu virus (LLOV), a phylogenetically divergent filovirus, is the proposed etiologic agent of die-offs of Schreiber’s long-fingered bats (Miniopterus schreibersii) in western Europe. Studies of LLOV remain limited because the infectious agent has not yet been isolated. Here, we generated a recombinant vesicular stomatitis virus expressing the LLOV spike glycoprotein (GP) and used it to show that LLOV GP resembles other filovirus GP proteins in structure and function. LLOV GP must be cleaved by endosomal cysteine proteases during entry, but is much more protease-sensitive than EBOV GP. The EBOV/MARV receptor, Niemann Pick C1 (NPC1), is also required for LLOV entry, and its second luminal domain is recognized with high affinity by a cleaved form of LLOV GP, suggesting that receptor binding would not impose a barrier to LLOV infection of humans and non-human primates. The use of NPC1 as an intracellular entry receptor may be a universal property of filoviruses.

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“…1,2 Even the geographic distributions of filoviruses have presented challenges, with mysteries including the geographic origin of Ebola Reston virus. 3 The known geographic distribution of outbreaks of Ebola virus-caused hemorrhagic fever in recent years has appeared to be more consistent geographically and ecologically than that of outbreaks caused by Marburg virus. Ebola viruses (Ebola Ivory Coast, Ebola Zaire, and Ebola Sudan viruses) are known principally from evergreen tropical forest regions in central Africa, and have shown few unexpected occurrences in terms of geography and ecology.…”

Section: Introductionmentioning

confidence: 99%

Geographic Potential for Outbreaks of Marburg Hemorrhagic Fever

Peterson¹,

Lash²,

Carroll³

et al. 2006

The American Journal of Tropical Medicine and Hygiene

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Abstract. Marburg virus represents one of the least well-known of the hemorrhagic fever-causing viruses worldwide; in particular, its geographic potential in Africa remains quite mysterious. Ecologic niche modeling was used to explore the geographic and ecologic potential of Marburg virus in Africa. Model results permitted a reinterpretation of the geographic point of infection in the initiation of the 1975 cases in Zimbabwe, and also anticipated the potential for cases in Angola, where a large outbreak recently (2004)(2005) occurred. The geographic potential for additional outbreaks is outlined, including in several countries in which the virus is not known. Overall, results demonstrate that ecologic niche modeling can be a powerful tool in understanding geographic distributions of species and other biologic phenomena such as zoonotic disease transmission from natural reservoir populations.

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Chronological and Spatial Analysis of the 1996 Ebola Reston Virus Outbreak in a Monkey Breeding Facility in the Philippines.

Cited by 23 publications

References 6 publications

Animal models for Ebola and Marburg virus infections

Animal models for Ebola and Marburg virus infections

Cell entry by a novel European filovirus requires host endosomal cysteine proteases and Niemann–Pick C1

Geographic Potential for Outbreaks of Marburg Hemorrhagic Fever

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