Marburg and Ebola Virus Infections
James H. S. Gear in CRC Handbook of Viral and Rickettsial Hemorrhagic Fevers, 2019
The most recent episode of MVD was a curious case seen in a young white man who became ill with falciparum malaria 7 days after his arrival in South Africa from his home in Fort Victoria, Zimbabwe. His clinical and laboratory features were consistent with malaria, which was confirmed and successfully treated. The patient’s condition was also compatible with a viral hemorrhagic fever. However, in view of the confirmation of malaria and his response to treatment, it is doubtful if this line of thought would have been pursued had it not been for the fact that the patient’s home in Zimbabwe was a locality visited by the Australian index case of the second MVD outbreak 7 years before. Acute and convalescent sera tested by the Centers for Disease Control (CDC) in the U.S. showed specific Marburg virus seroconversion from negative to positive, though the virus was not isolated.
Viruses
Loretta A. Cormier, Pauline E. Jolly in The Primate Zoonoses, 2017
In the laboratory setting, humans have been infected with Marburg virus through exposure to grivet monkeys (Chlorocebus aethiops). In 1967, and outbreak occurred in laboratory workers who had contact with grivets imported from Uganda (Martini 1973). Thirty-one people were infected, primarily through caring for infected monkeys, but secondary infections also occurred. One was through medical staff caring for a sick patient (human), another through an accidental needle stick, and another through sexual contact with a laboratory worker. No case has been identified of transmission of Marburg from wild primates to humans outside of the laboratory setting (Pigott et al. 2015).
Other Double-Stranded DNA Viruses
Paul Pumpens, Peter Pushko, Philippe Le Mercier in Virus-Like Particles, 2022
Schweneker et al. (2017) constructed a MVA coexpressing VP40 and GP of Ebola virus (EBOV) Mayinga and the nucleoprotein of Taï Forest virus (TAFV) to launch noninfectious EBOV VLPs (Chapter 31). Lázaro-Frías et al. (2018) used the same approach to generate an MVA-based vaccine against Zaire Ebolavirus (EBOV) and Sudan Ebolavirus (SUDV). Malherbe et al. (2020) constructed the MVA-driven vaccine expressing Marburg virus (MARV) VLPs (Chapter 31) from the MARV envelope glycoprotein GP and the matrix protein VP40. The electron microscopy confirmed self-assembly and budding of the MARV VLPs from infected cells.
Clinical Manifestations and Pathogenesis of Uveitis in Ebola Virus Disease Survivors
Published in Ocular Immunology and Inflammation, 2018
Steven Yeh, Jessica G. Shantha, Brent Hayek, Ian Crozier, Justine R. Smith
Marburg virus disease (MVD), another viral hemorrhagic fever also caused by a filovirus, bears clinical features similar to EVD, including a high case fatality rate and association with uveitis.12 Specifically, in 1975, following a MVD outbreak in Johannesburg, a nurse who provided care for two MVD patients developed high fever, hepatitis, disseminated intravascular coagulation, and conjunctival injection and was subsequently confirmed to have MVD.13 Three months after recovery, the nurse developed eye pain and blurred vision and presented with acute hypertensive iritis with white keratic precipitates. When the anterior uveitis failed to improve despite intensive treatment with topical corticosteroid, an anterior chamber paracentesis was performed. Vero cell culture with the aqueous fluid resulted in typical Marburg virus inclusion bodies within the cell cytoplasm. A second aqueous humor sample, collected 2 weeks later, did not yield Marburg virus in cell culture. The patient’s clinical course was punctuated by recurrences approximately 2 and 6 months later, which were treated successfully.13
Treatment-focused Ebola trials, supportive care and future of filovirus care
Published in Expert Review of Anti-infective Therapy, 2018
Maryam Keshtkar-Jahromi, Karen A.O Martins, Anthony P. Cardile, Ronald B. Reisler, George W Christopher, Sina Bavari
Marburgvirus and Ebolavirus genus belong to filovirus family. Genus Ebolavirus includes five species (Zaire ebolavirus (EBOV), Sudan ebolavirus, Reston ebolavirus, and Bundibugyo ebolavirus). Genus Marburgvirus includes Marburg Marburgvirus species with Marburg virus (MARV) and Ravn virus strains in this species [1]. It is nearly impossible to consider filovirus therapeutics and vaccines without referencing the unprecedented 2014–2016 outbreak in West Africa. In many ways, the outbreak significantly advanced interinstitutional collaborations and redefined the roles and responsibilities of international institutions like the World Health Organization (WHO) and Medecins Sans Frontieres, as well as the USA institutes like the Centers for Disease Control and Prevention, the National Institutes of Health, the Department of Health and Human Services, and the Department of Defense (DoD). Unfortunately, out of the well-intentioned response came little in the way of regulated clinical research or clinical trials. Clinical trials – particularly clinical trials in a region only minimally exposed to current clinical trial standards and regulations – take time and investment to establish. The organizations that made inroads into that process during the outbreak should be lauded for their clear thinking and attempts to gather meaningful data from a tragic human situation. However, 3 years later, we still have no approved therapeutic for the treatment of filovirus infection.
Small animal models of filovirus disease: recent advances and future directions
Published in Expert Opinion on Drug Discovery, 2018
Robert W. Cross, Karla A. Fenton, Thomas W. Geisbert
There are two primary genera: Marburgvirus and Ebolavirus. Discovered in 1967, Marburgvirus contains that has two genetically distinct members, Lake Victoria Marburg virus (MARV) and Ravn virus (RAVV). There is an estimated 20% sequence divergence between MARV and RAVV. Outbreaks of marburgviruses have primarily occurred in Central and Southern Africa and have ranged in size from 1 to 252 cases with ~ 20–90% case fatality rates (CFR) [1,11–13]. Little is known in regard to the differences in pathogenicity of the known MARV and RAVV variants in humans thus inferences from epidemiological data are often made such that the Angola variant of MARV is likely the most virulent variant from the number of cases and high CFR (252 cases and 227 fatalities-90% CFR) of the originating outbreak. Additionally, the observed higher disease severity and shortened mean time to death (MTD) in NHP and rodent models has been reported for the Angola variant when compared with other MARV variants [14,15]