Journal articles: 'Marburg virus disease'

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Mahmud, S. M. Neaz, Mahbubur Rahman, Antora Kar, Nasreen Jahan, and Arif Khan. "Designing of an Epitope- Based Universal Peptide Vaccine against Highly Conserved Regions in RNA Dependent RNA Polymerase Protein of Human Marburg Virus: A Computational Assay." Anti-Infective Agents 18, no. 3 (September 11, 2020): 294–305. http://dx.doi.org/10.2174/2211352517666190717143949.

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Introduction: Marburg viruses are a group of negative-stranded RNA virus. It was first identified in 1967 during a small outbreak. During that outbreak, the fatality rate increased highly and so many people died by the Marburg virus. Later seven strains of Marburg virus were identified from those infected humans. This virus causes Marburg Virus Disease (MVD) in human referred to as Marburg hemorrhagic fever. Marburg virus is endemic only to Africa; however, there have been outbreaks in Europe and the U.S.A. in recent times. Objective: However, the Marburg virus has a high fatality rate, so a preventive measure should be taken to prevent infection. As there is no effective therapeutic agent available against these viruses, effective vaccine design touching all strains would be a great step for human health. Methods: In our recent study, we used in silico analysis for designing a novel epitope-based vaccine against all strains of Marburg virus. As it consists of several structural proteins and multiple sequence alignment (MSA) of Glycoproteins, RNA-directed RNA polymerases, Nucleoproteins, Vp24 proteins, Vp30, Vp35, and Vp40 proteins showed all strains of Marburg virus were conserved in RNA-directed RNA polymerase proteins. Using that protein’s conserved region, T-cell and B-cell epitopes were determined. Results: Among the predicted epitope, only TIGNRAPYI was found to be highly immunogenic with 100% conservancy among all strain of human Marburg virus. The analysis also showed both types I and II major histocompatibility complex molecules interact with this epitope and found to be nonallergenic too. Conclusion: In vivo study of the proposed peptide is suggested for novel universal vaccine production that might be an effective way to prevent human Marburg virus disease.

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Chakraborty, Sandip, Deepak Chandran, Ranjan K. Mohapatra, Mahmoud Alagawany, Mohd Iqbal Yatoo, Md Aminul Islam, Anil K. Sharma, and Kuldeep Dhama. "Marburg Virus Disease – A Mini-Review." Journal of Experimental Biology and Agricultural Sciences 10, no. 4 (August 30, 2022): 689–96. http://dx.doi.org/10.18006/2022.10(4).689.696.

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Marburg virus disease (MVD) is a highly fatal disease caused by the Marburg virus (MARV) which belongs to the family Filoviridae. The disease has been recently reported from Ghana, an African country, and nearly 15 outbreaks of MVD have been reported in the past five decades. Various species of bats viz., Rousettus aegyptiacus, Hipposideros caffer, and certain Chiroptera act as the natural source of infection. Pathophysiology of the disease reveals severe antiviral suppression due to changes in gene expression and interferon-stimulated gene (ISG) production in the hepatic cells. With the progression of the disease, there may be the development of pain in the abdomen, nausea, vomition, pharyngitis, and diarrhea along with the onset of hemorrhagic manifestations which may lead to the death of a patient. The advent of molecular detection techniques and kits viz., reverse transcription polymerase chain reaction (RT-PCR) kit has greatly aided in the diagnosis of MVD. Identification of the virus in the specimen with great accuracy can be done by whole viral genome sequencing. The use of a combination of MR-186-YTE (monoclonal antibody) and an antiviral drug named remdesivir in the NHP model is greatly effective for eliminating MARV. The protective effect of a Vesicular stomatitis virus (VSV) (recombinant) - based vaccine expressing the glycoprotein of MARV has been revealed through animal model studies, other vaccines are also being developed. Proper health education, personal hygiene and precautions by health care workers while handling patients, good laboratory facilities and service along with the establishment of enhanced surveillance systems are the need of the hour to tackle this highly fatal disease. This article presents an overview of different aspects and salient features of MARV / MVD, and prevention and control strategies to be adopted.

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Amman, Brian R., Amy J. Schuh, César G. Albariño, and Jonathan S. Towner. "Marburg Virus Persistence on Fruit as a Plausible Route of Bat to Primate Filovirus Transmission." Viruses 13, no. 12 (November 30, 2021): 2394. http://dx.doi.org/10.3390/v13122394.

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Marburg virus (MARV), the causative agent of Marburg virus disease, emerges sporadically in sub-Saharan Africa and is often fatal in humas. The natural reservoir for this zoonotic virus is the frugivorous Egyptian rousette bat (Rousettus aegyptiacus) that when infected, sheds virus in the highest amounts in oral secretions and urine. Being fruit bats, these animals forage nightly for ripened fruit throughout the year, including those types often preferred by humans. During feeding, they continually discard partially eaten fruit on the ground that could then be consumed by other Marburg virus susceptible animals or humans. In this study, using qRT-PCR and virus isolation, we tested fruit discarded by Egyptian rousette bats experimentally infected with a natural bat isolate of Marburg virus. We then separately tested viral persistence on fruit varieties commonly cultivated in sub-Saharan Africa using a recombinant Marburg virus expressing the fluorescent ZsGreen1. Marburg virus RNA was repeatedly detected on fruit in the food bowls of the infected bats and viable MARV was recovered from inoculated fruit for up to 6 h.

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Bebell, Lisa M., and Laura E. Riley. "Ebola Virus Disease and Marburg Disease in Pregnancy." Obstetrics & Gynecology 125, no. 6 (June 2015): 1293–98. http://dx.doi.org/10.1097/aog.0000000000000853.

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Markin, Vladimir A. "Marburg virus and the disease it causes." Journal of microbiology, epidemiology and immunobiology 99, no. 5 (December 7, 2022): 605–18. http://dx.doi.org/10.36233/0372-9311-273.

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Over the 50 years since its discovery, many properties of the Marburg virus have been studied, but no reliable medical remedies of preventing and treating the infection it causes have been developed, although it can potentially cause large-scale epidemics. Marburg fever is relevant due to the risk of importation to other countries. The source of infection in nature is bats (reservoir) and monkeys (intermediate host), and the routes of transmission are aerosol, contact and alimentary. The mortality rate in recent outbreaks has reached 90%. In convalescents the causative agent was identified in tears, semen, and liver biopsies weeks and months after recovery. The lack of therapeutic and prophylactic antiviral drugs, high rates of mortality, infectivity, the ability of aerosol contamination, and a high epidemic potential all together define Marburg fever as a serious global threat to international health. The development of medical protection against this infection should be an urgent task of ensuring the biological safety of the population of the Russian Federation. The most promising ways to develop vaccines against Marburg fever are the construction of recombinants based on adenovirus, vesicular stomatitis virus or alphavirus replicon, DNA vaccines. A reliable protective effect of the chemotherapy drug remdesivir in combination with human antibodies, as well as an etiotropic drug with an antisense mechanism of action and an interferon inducer has been shown. In model experiments with pseudovirus, fundamentally new ways of developing pathogen inhibitors were found preventing its exit from cells, as well as the construction of anti-gene-binding Fab fragments that inhibit the synthesis of viral RNA.

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Koundouno, Fara R., Liana E. Kafetzopoulou, Martin Faye, Annick Renevey, Barrè Soropogui, Kékoura Ifono, Emily V. Nelson, et al. "Detection of Marburg Virus Disease in Guinea." New England Journal of Medicine 386, no. 26 (June 30, 2022): 2528–30. http://dx.doi.org/10.1056/nejmc2120183.

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Kortepeter, Mark G., Kerry Dierberg, Erica S. Shenoy, and Theodore J. Cieslak. "Marburg virus disease: A summary for clinicians." International Journal of Infectious Diseases 99 (October 2020): 233–42. http://dx.doi.org/10.1016/j.ijid.2020.07.042.

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Knust, Barbara, Ilana J. Schafer, Joseph Wamala, Luke Nyakarahuka, Charles Okot, Trevor Shoemaker, Kimberly Dodd, et al. "Multidistrict Outbreak of Marburg Virus Disease—Uganda, 2012." Journal of Infectious Diseases 212, suppl 2 (July 23, 2015): S119—S128. http://dx.doi.org/10.1093/infdis/jiv351.

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Volkova, N. V., E. I. Kazachinskaya, and D. N. Shcherbakov. "Experimental Vaccines for Prevention of Marburg Hemorrhagic Fever and Animal Models for Studying Pathogenesis." Problems of Particularly Dangerous Infections, no. 3 (October 5, 2018): 8–15. http://dx.doi.org/10.21055/0370-1069-2018-3-8-15.

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Marburg fever is an acute natural-focal disease characterized by severe course, hemorrhagic syndrome, high level of contagiousness and lethality. The causative agent of the disease is the RNA-containing virus belonging to the family of filoviruses (Filoviridae). The main problem faced by doctors and scientists involved in the fight against Marburg fever is the lack of vaccines and preventive drugs against this disease. The development of effective vaccines against filovirus infection is relevant for protecting the population living in natural foci and medical personnel during epidemic outbreaks, as well as for ensuring safe research work in BSL-4 laboratories. In this regard, this review considers biomodels suitable for studying the pathogenesis of filovirus infections, preclinical studies of specific activity and harmlessness of prototype Marburg virus vaccines and variants of these vaccines.

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Nakayama, Eri, and Ayato Takada. "Ebola and Marburg Viruses." Journal of Disaster Research 6, no. 4 (August 1, 2011): 381–89. http://dx.doi.org/10.20965/jdr.2011.p0381.

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Ebola and Marburg viruses, members of the filovirus family, cause severe hemorrhagic fever in human and nonhuman primates and are classified as biosafety level 4 agents. No effective filovirus-specific prophylaxis or treatment is yet commercially available. Filovirus species vary genetically, with one in the Marburg virus group and five in the Ebola virus group. Epidemiological efforts to prevent outbreaks lie mainly in identifying natural animal reservoirs. Increasingly frequent outbreaks in Africa and concerns about bioterrorism and imported cases in nonendemic areas point to the importance of public health in two ways – finding strategies to control disease outbreak and developing effective vaccines and drugs.

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Zhu, Wenjun, Guodong Liu, Wenguang Cao, Shihua He, Anders Leung, Ute Ströher, Michael Fairchild, et al. "A Cloned Recombinant Vesicular Stomatitis Virus-Vectored Marburg Vaccine, PHV01, Protects Guinea Pigs from Lethal Marburg Virus Disease." Vaccines 10, no. 7 (June 23, 2022): 1004. http://dx.doi.org/10.3390/vaccines10071004.

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Marburg virus (MARV) is a negative-sense, single-stranded RNA virus that belongs to the Filoviridae family. Despite having caused numerous outbreaks of severe hemorrhagic fever with high case fatality rates, there are still no clinically approved therapeutics or vaccines to treat or prevent MARV disease. Recombinant vesicular stomatitis viruses (rVSVs) expressing heterologous viral glycoproteins have shown remarkable promise as live-attenuated vaccine vectors, with an rVSV-based Ebola virus vaccine having received regulatory approval in the United States and numerous other countries. Analogous rVSV vaccine vectors have also been developed for MARV and have shown efficacy in several preclinical studies conducted in nonhuman primates. Here, we used a guinea pig model to confirm the protective efficacy of a cloned, rVSV-based candidate vaccine, termed PHV01, expressing the MARV variant Angola glycoprotein. Our results demonstrated that a single dose (2 × 106 PFU) of vaccine administered 28 days prior to challenge with a uniformly lethal dose of guinea-pig-adapted MARV variant Angola provided complete protection from death and disease. Moreover, protection was robust, with as little as 200 PFU of vaccine conferring significant protection. Not only does this study highlight the potential predictive value of the guinea pig model in the evaluation of MARV countermeasures, but it also demonstrates consistent and reproducible protection afforded by a clonal vaccine candidate. Indeed, this study identifies PHV01 as a suitable vaccine candidate for advanced development.

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Porter, Danielle P., Jessica M. Weidner, Laura Gomba, Roy Bannister, Christiana Blair, Robert Jordan, Jay Wells, et al. "Remdesivir (GS-5734) Is Efficacious in Cynomolgus Macaques Infected With Marburg Virus." Journal of Infectious Diseases 222, no. 11 (June 1, 2020): 1894–901. http://dx.doi.org/10.1093/infdis/jiaa290.

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Abstract Marburg virus (MARV) is a filovirus with documented human case-fatality rates of up to 90%. Here, we evaluated the therapeutic efficacy of remdesivir (GS-5734) in nonhuman primates experimentally infected with MARV. Beginning 4 or 5 days post inoculation, cynomolgus macaques were treated once daily for 12 days with vehicle, 5 mg/kg remdesivir, or a 10-mg/kg loading dose followed by 5 mg/kg remdesivir. All vehicle-control animals died, whereas 83% of animals receiving a 10-mg/kg loading dose of remdesivir survived, as did 50% of animals receiving a 5-mg/kg remdesivir regimen. Remdesivir-treated animals exhibited improved clinical scores, lower plasma viral RNA, and improved markers of kidney function, liver function, and coagulopathy versus vehicle-control animals. The small molecule remdesivir showed therapeutic efficacy in this Marburg virus disease model with treatment initiation 5 days post inoculation, supporting further assessment of remdesivir for the treatment of Marburg virus disease in humans.

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Nyakarahuka, Luke, Joseph Ojwang, Alex Tumusiime, Stephen Balinandi, Shannon Whitmer, Simon Kyazze, Sam Kasozi, et al. "Isolated Case of Marburg Virus Disease, Kampala, Uganda, 2014." Emerging Infectious Diseases 23, no. 6 (June 2017): 1001–4. http://dx.doi.org/10.3201/eid2306.170047.

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A, Khanifar. "The Effect of Ezetimibe in the Treatment of Ebola." Virology & Immunology Journal 5, no. 3 (August 2, 2021): 1–7. http://dx.doi.org/10.23880/vij-16000281.

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Background: In this article, we are looking for treatment for Ebola virus. We will do it using a cholesterol-lowering drug called Ezetimibe. Methods: Marburg and Ebola hemorrhagic fevers are severe, systemic viral diseases affecting humans and non-human primates. They are characterized by multiple symptoms such as hemorrhages, fever, headache, muscle and abdominal pain, chills, sore throat, nausea, vomiting and diarrhea. Elevated liver-associated enzyme levels and coagulopathy are also associated with these diseases. Marburg and Ebola hemorrhagic fevers are caused by (Lake Victoria) Marburg virus and different species of Ebola viruses, respectively. They are enveloped, single-stranded RNA viruses and belong to the family of filoviridae. Case fatality rates of filovirus disease outbreaks are among the highest reported for any human pathogen, ranging from 25 to 90% or more. But when Ezetimibe is given to patients with the Ebola virus, we see that the drug blocks the transmission of the virus to the body by delivering the virus to the immune system. Results: In this article are paid to effect of drug Ezetimibe in the treatment of disease Ebola.NPC1L1 carry Ebola virus that by Ezetimibe, NPC1L1 disabled and cannot carry the virus with you. In fact, this drug (Ezetimibe) is a supplier of antigen to antibodies. We will also look at the function of the NPC1L1 and NPC1 receptors and the drug Ezetimibe. Conclusions: Ezetimibe has a higher affinity for NPC1L1 receptor than cholesterol, and cholesterol has a higher affinity for NPC1L1 receptor than Ebola virus. In fact, if we want to show the percentage of desire for NPC1L1 receptor, it is as follows: Ezetimibe> Cholesterol> Ebola virus

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Connor, John H., Judy Yen, Ignacio S. Caballero, Sara Garamszegi, Shikha Malhotra, Kenny Lin, Lisa Hensley, and Arthur J. Goff. "Transcriptional Profiling of the Immune Response to Marburg Virus Infection." Journal of Virology 89, no. 19 (July 22, 2015): 9865–74. http://dx.doi.org/10.1128/jvi.01142-15.

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ABSTRACTMarburg virus is a genetically simple RNA virus that causes a severe hemorrhagic fever in humans and nonhuman primates. The mechanism of pathogenesis of the infection is not well understood, but it is well accepted that pathogenesis is appreciably driven by a hyperactive immune response. To better understand the overall response to Marburg virus challenge, we undertook a transcriptomic analysis of immune cells circulating in the blood following aerosol exposure of rhesus macaques to a lethal dose of Marburg virus. Using two-color microarrays, we analyzed the transcriptomes of peripheral blood mononuclear cells that were collected throughout the course of infection from 1 to 9 days postexposure, representing the full course of the infection. The response followed a 3-stage induction (early infection, 1 to 3 days postexposure; midinfection, 5 days postexposure; late infection, 7 to 9 days postexposure) that was led by a robust innate immune response. The host response to aerosolized Marburg virus was evident at 1 day postexposure. Analysis of cytokine transcripts that were overexpressed during infection indicated that previously unanalyzed cytokines are likely induced in response to exposure to Marburg virus and further suggested that the early immune response is skewed toward a Th2 response that would hamper the development of an effective antiviral immune response early in disease. Late infection events included the upregulation of coagulation-associated factors. These findings demonstrate very early host responses to Marburg virus infection and provide a rich data set for identification of factors expressed throughout the course of infection that can be investigated as markers of infection and targets for therapy.IMPORTANCEMarburg virus causes a severe infection that is associated with high mortality and hemorrhage. The disease is associated with an immune response that contributes to the lethality of the disease. In this study, we investigated how the immune cells circulating in the blood of infected primates respond following exposure to Marburg virus. Our results show that there are three discernible stages of response to infection that correlate with presymptomatic, early, and late symptomatic stages of infection, a response format similar to that seen following challenge with other hemorrhagic fever viruses. In contrast to the ability of the virus to block innate immune signalingin vitro, the earliest and most sustained response is an interferon-like response. Our analysis also identifies a number of cytokines that are transcriptionally upregulated during late stages of infection and suggest that there is a Th2-skewed response to infection. When correlated with companion data describing the animal model from which our samples were collected, our results suggest that the innate immune response may contribute to overall pathogenesis.

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Schuh, Amy J., Brian R. Amman, and Jonathan S. Towner. "Filoviruses and bats." Microbiology Australia 38, no. 1 (2017): 12. http://dx.doi.org/10.1071/ma17005.

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While Reston and Lloviu viruses have never been associated with human disease, the other filoviruses cause outbreaks of hemorrhagic fever characterised by person-to-person transmission and high case fatality ratios. Cumulative evidence suggests that bats are the most likely reservoir hosts of the filoviruses. Ecological investigations following Marburg virus disease outbreaks associated with entry into caves inhabited by Rousettus aegyptiacus bats led to the identification of this bat species as the natural reservoir host of the marburgviruses. Experimental infection of R. aegyptiacus with Marburg virus has provided insight into the natural history of filovirus infection in bats that may help guide the search for the reservoir hosts of the ebolaviruses.

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McLaren, C. A. B. "Green Monkeys—Red Herrings??" Prehospital and Disaster Medicine 2, no. 1-4 (1986): 189–90. http://dx.doi.org/10.1017/s1049023x00030788.

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In 1967 an apparently new viral hemorrhagic disease appeared in research workers in the cities of Marburg and Frankfurt in West Germany, and in Belgrade in Yugoslavia. In all, 35 workers became ill, of whom 9 died. The only common factor between the three centers was a batch of green monkeys, imported from Uganda. These animals had been used throughout the world to provide tissue cultures with up to 12,000 being imported annually into the USA, with no previous disease noted. Eventually a virus was isolated and called the Marburg virus, but as yet it has not been detected to give any symptoms in the monkeys.

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Pigott, David M., Nick Golding, Adrian Mylne, Zhi Huang, Daniel J. Weiss, Oliver J. Brady, Moritz U. G. Kraemer, and Simon I. Hay. "Mapping the zoonotic niche of Marburg virus disease in Africa." Transactions of The Royal Society of Tropical Medicine and Hygiene 109, no. 6 (March 27, 2015): 366–78. http://dx.doi.org/10.1093/trstmh/trv024.

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Cross, Robert W., Ira M. Longini, Stephan Becker, Karin Bok, David Boucher, Miles W. Carroll, Janet V. Díaz, et al. "An introduction to the Marburg virus vaccine consortium, MARVAC." PLOS Pathogens 18, no. 10 (October 13, 2022): e1010805. http://dx.doi.org/10.1371/journal.ppat.1010805.

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The emergence of Marburg virus (MARV) in Guinea and Ghana triggered the assembly of the MARV vaccine “MARVAC” consortium representing leaders in the field of vaccine research and development aiming to facilitate a rapid response to this infectious disease threat. Here, we discuss current progress, challenges, and future directions for MARV vaccines.

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Jones, Megan, Brian Amman, Tara Sealy, Luke Uebelhoer, Amy Schuh, Timothy Flietstra, Brian Bird, et al. "Clinical, Histopathologic, and Immunohistochemical Characterization of Experimental Marburg Virus Infection in A Natural Reservoir Host, the Egyptian Rousette Bat (Rousettus aegyptiacus)." Viruses 11, no. 3 (March 2, 2019): 214. http://dx.doi.org/10.3390/v11030214.

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Egyptian rousette bats (Rousettus aegyptiacus) are natural reservoir hosts of Marburg virus (MARV), and Ravn virus (RAVV; collectively called marburgviruses) and have been linked to human cases of Marburg virus disease (MVD). We investigated the clinical and pathologic effects of experimental MARV infection in Egyptian rousettes through a serial euthanasia study and found clear evidence of mild but transient disease. Three groups of nine, captive-born, juvenile male bats were inoculated subcutaneously with 10,000 TCID50 of Marburg virus strain Uganda 371Bat2007, a minimally passaged virus originally isolated from a wild Egyptian rousette. Control bats (n = 3) were mock-inoculated. Three animals per day were euthanized at 3, 5–10, 12 and 28 days post-inoculation (DPI); controls were euthanized at 28 DPI. Blood chemistry analyses showed a mild, statistically significant elevation in alanine aminotransferase (ALT) at 3, 6 and 7 DPI. Lymphocyte and monocyte counts were mildly elevated in inoculated bats after 9 DPI. Liver histology revealed small foci of inflammatory infiltrate in infected bats, similar to lesions previously described in wild, naturally-infected bats. Liver lesion severity scores peaked at 7 DPI, and were correlated with both ALT and hepatic viral RNA levels. Immunohistochemical staining detected infrequent viral antigen in liver (3–8 DPI, n = 8), spleen (3–7 DPI, n = 8), skin (inoculation site; 3–12 DPI, n = 20), lymph nodes (3–10 DPI, n = 6), and oral submucosa (8–9 DPI, n = 2). Viral antigen was present in histiocytes, hepatocytes and mesenchymal cells, and in the liver, antigen staining co-localized with inflammatory foci. These results show the first clear evidence of very mild disease caused by a filovirus in a reservoir bat host and provide support for our experimental model of this virus-reservoir host system.

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Wolfe, Daniel N., Carol L. Sabourin, Michael J. Merchlinsky, William C. Florence, Larry A. Wolfraim, Kimberly L. Taylor, and Lucy A. Ward. "Selection of Filovirus Isolates for Vaccine Development Programs." Vaccines 9, no. 9 (September 19, 2021): 1045. http://dx.doi.org/10.3390/vaccines9091045.

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The continuing outbreaks of ebola virus disease highlight the ongoing threat posed by filoviruses. Fortunately, licensed vaccines and therapeutics are now available for Zaire ebolavirus. However, effective medical countermeasures, such as vaccines for other filoviruses such as Sudan ebolavirus and the Marburg virus, are presently in early stages of development and, in the absence of a large outbreak, would require regulatory approval via the U.S. Food and Drug Administration (FDA) Animal Rule. The selection of an appropriate animal model and virus challenge isolates for nonclinical studies are critical aspects of the development program. Here, we have focused on the recommendation of challenge isolates for Sudan ebolavirus and Marburg virus. Based on analyses led by the Filovirus Animal and Nonclinical Group (FANG) and considerations for strain selection under the FDA Guidance for the Animal Rule, we propose prototype virus isolates for use in nonclinical challenge studies.

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&NA;. "Postexposure vaccination with a recombinant virus vector prevents Marburg virus (MARV) disease in primates,." Inpharma Weekly &NA;, no. 1536 (May 2006): 19. http://dx.doi.org/10.2165/00128413-200615360-00046.

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Shrivastava, PrateekSaurabh, and SaurabhRamBihariLal Shrivastava. "2022 outbreak of Marburg virus disease in Ghana: Public health alert." Environmental Disease 7, no. 3 (2022): 80. http://dx.doi.org/10.4103/ed.ed_17_22.

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Borchert, Matthias, Jean Jacques Muyembe-Tamfum, Robert Colebunders, Modeste Libande, Mulangu Sabue, and Patrick Van der Stuyft. "Short communication: A cluster of Marburg virus disease involving an infant*." Tropical Medicine and International Health 7, no. 10 (October 2002): 902–6. http://dx.doi.org/10.1046/j.1365-3156.2002.00945.x.

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Thi, Emily P., Chad E. Mire, Amy C. H. Lee, Joan B. Geisbert, Raul Ursic-Bedoya, Krystle N. Agans, Marjorie Robbins, et al. "siRNA rescues nonhuman primates from advanced Marburg and Ravn virus disease." Journal of Clinical Investigation 127, no. 12 (November 6, 2017): 4437–48. http://dx.doi.org/10.1172/jci96185.

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Ströher, Ute, Elmar West, Harald Bugany, Hans-Dieter Klenk, Hans-Joachim Schnittler, and Heinz Feldmann. "Infection and Activation of Monocytes by Marburg and Ebola Viruses." Journal of Virology 75, no. 22 (November 15, 2001): 11025–33. http://dx.doi.org/10.1128/jvi.75.22.11025-11033.2001.

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ABSTRACT In this study we investigated the effects of Marburg virus and Ebola virus (species Zaire and Reston) infections on freshly isolated suspended monocytes in comparison to adherent macrophages under culture conditions. Our data showed that monocytes are permissive for both filoviruses. As is the case in macrophages, infection resulted in the activation of monocytes which was largely independent of virus replication. The activation was triggered similarly by Marburg and Ebola viruses, species Zaire and Reston, as indicated by the release of the proinflammatory cytokines interleukin-1β (IL-1β), tumor necrosis factor α, and IL-6 as well as the chemokines IL-8 and gro-α. Our data suggest that infected monocytes may play an important role in the spread of filoviruses and in the pathogenesis of filoviral hemorrhagic disease.

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Rausch, Andreas, and Thomas Schanze. "Fractal Dimensions of Subviral Particle Movement." Current Directions in Biomedical Engineering 4, no. 1 (September 1, 2018): 79–82. http://dx.doi.org/10.1515/cdbme-2018-0020.

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AbstractThe development of new medicines against virus infections like the Marburg virus disease requires an accurate knowledge of the respective pathogens. Conventionally, this process is very time expensive. In cooperation with the Virology of the Philipps-University in Marburg an automatic tracking algorithm for subviral particles in fluorescence image sequences was developed and programmed. To expand the benefit for the pharmaceutical researchers, also the trackevaluations need to be widely automated. In this work, a new parameterizing-method facing the fractal dimensions of spline interpolated subviral particle tracks is presented and tested with simulated and real data. The results reveal a good potential to classify tracks and, thus, types of subviral particles in infected cells.

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Comer, Jason E., Trevor Brasel, Shane Massey, David W. Beasley, Chris M. Cirimotich, Daniel C. Sanford, Ying-Liang Chou, et al. "Natural History of Marburg Virus Infection to Support Medical Countermeasure Development." Viruses 14, no. 10 (October 18, 2022): 2291. http://dx.doi.org/10.3390/v14102291.

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The Biomedical Advanced Research and Development Authority, part of the Administration for Strategic Preparedness and Response within the U.S. Department of Health and Human Services, recognizes that the evaluation of medical countermeasures under the Animal Rule requires well-characterized and reproducible animal models that are likely to be predictive of clinical benefit. Marburg virus (MARV), one of two members of the genus Marburgvirus, is characterized by a hemorrhagic fever and a high case fatality rate for which there are no licensed vaccines or therapeutics available. This natural history study consisted of twelve cynomolgus macaques challenged with 1000 PFU of MARV Angola and observed for body weight, temperature, viremia, hematology, clinical chemistry, and coagulation at multiple time points. All animals succumbed to disease within 8 days and exhibited signs consistent with those observed in human cases, including viremia, fever, systemic inflammation, coagulopathy, and lymphocytolysis, among others. Additionally, this study determined the time from exposure to onset of disease manifestations and the time course, frequency, and magnitude of the manifestations. This study will be instrumental in the design and development of medical countermeasures to Marburg virus disease.

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Yen, Benjamin C., and Christopher F. Basler. "Effects of Filovirus Interferon Antagonists on Responses of Human Monocyte-Derived Dendritic Cells to RNA Virus Infection." Journal of Virology 90, no. 10 (March 9, 2016): 5108–18. http://dx.doi.org/10.1128/jvi.00191-16.

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ABSTRACTDendritic cells (DCs) are major targets of filovirus infectionin vivo. Previous studies have shown that the filoviruses Ebola virus (EBOV) and Marburg virus (MARV) suppress DC maturationin vitro. Both viruses also encode innate immune evasion functions. The EBOV VP35 (eVP35) and the MARV VP35 (mVP35) proteins each can block RIG-I-like receptor signaling and alpha/beta interferon (IFN-α/β) production. The EBOV VP24 (eVP24) and MARV VP40 (mVP40) proteins each inhibit the production of IFN-stimulated genes (ISGs) by blocking Jak-STAT signaling; however, this occurs by different mechanisms, with eVP24 blocking nuclear import of tyrosine-phosphorylated STAT1 and mVP40 blocking Jak1 function. MARV VP24 (mVP24) has been demonstrated to modulate host cell antioxidant responses. Previous studies demonstrated that eVP35 is sufficient to strongly impair primary human monocyte-derived DC (MDDC) responses upon stimulation induced through the RIG-I-like receptor pathways. We demonstrate that mVP35, like eVP35, suppresses not only IFN-α/β production but also proinflammatory responses after stimulation of MDDCs with RIG-I activators. In contrast, eVP24 and mVP40, despite suppressing ISG production upon RIG-I activation, failed to block upregulation of maturation markers or T cell activation. mVP24, although able to stimulate expression of antioxidant response genes, had no measurable impact of DC function. These data are consistent with a model where filoviral VP35 proteins are the major suppressors of DC maturation during filovirus infection, whereas the filoviral VP24 proteins and mVP40 are insufficient to prevent DC maturation.IMPORTANCEThe ability to suppress the function of dendritic cells (DCs) likely contributes to the pathogenesis of disease caused by the filoviruses Ebola virus and Marburg virus. To clarify the basis for this DC suppression, we assessed the effect of filovirus proteins known to antagonize innate immune signaling pathways, including Ebola virus VP35 and VP24 and Marburg virus VP35, VP40, and VP24, on DC maturation and function. The data demonstrate that the VP35s from Ebola virus and Marburg virus are the major suppressors of DC maturation and that the effects on DCs of the remaining innate immune inhibitors are minor.

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Tiemessen, Machteld M., Laura Solforosi, Liesbeth Dekking, Dominika Czapska-Casey, Jan Serroyen, Nancy J. Sullivan, Ariane Volkmann, et al. "Protection against Marburg Virus and Sudan Virus in NHP by an Adenovector-Based Trivalent Vaccine Regimen Is Correlated to Humoral Immune Response Levels." Vaccines 10, no. 8 (August 5, 2022): 1263. http://dx.doi.org/10.3390/vaccines10081263.

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The Marburg virus (MARV) and Sudan virus (SUDV) belong to the filovirus family. The sporadic human outbreaks occur mostly in Africa and are characterized by an aggressive disease course with high mortality. The first case of Marburg virus disease in Guinea in 2021, together with the increased frequency of outbreaks of Ebola virus (EBOV), which is also a filovirus, accelerated the interest in potential prophylactic vaccine solutions against multiple filoviruses. We previously tested a two-dose heterologous vaccine regimen (Ad26.Filo, MVA-BN-Filo) in non-human primates (NHP) and showed a fully protective immune response against both SUDV and MARV in addition to the already-reported protective effect against EBOV. The vaccine-induced glycoprotein (GP)-binding antibody levels appear to be good predictors of the NHP challenge outcome as indicated by the correlation between antibody levels and survival outcome as well as the high discriminatory capacity of the logistic model. Moreover, the elicited GP-specific binding antibody response against EBOV, SUDV, and MARV remains stable for more than 1 year. Overall, the NHP data indicate that the Ad26.Filo, MVA-BN-Filo regimen may be a good candidate for a prophylactic vaccination strategy in regions at high risk of filovirus outbreaks.

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Wong, Gary, Zirui Zhang, Shihua He, Marc-Antoine de La Vega, Kevin Tierney, Geoff Soule, Kaylie Tran, Lisa Fernando, and Xiangguo Qiu. "Marburg and Ravn Virus Infections Do Not Cause Observable Disease in Ferrets." Journal of Infectious Diseases 218, suppl_5 (June 8, 2018): S471—S474. http://dx.doi.org/10.1093/infdis/jiy245.

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Natesan, Mohan, Stig M. Jensen, Sarah L. Keasey, Teddy Kamata, Ana I. Kuehne, Spencer W. Stonier, Julius Julian Lutwama, Leslie Lobel, John M. Dye, and Robert G. Ulrich. "Human Survivors of Disease Outbreaks Caused by Ebola or Marburg Virus Exhibit Cross-Reactive and Long-Lived Antibody Responses." Clinical and Vaccine Immunology 23, no. 8 (June 22, 2016): 717–24. http://dx.doi.org/10.1128/cvi.00107-16.

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ABSTRACTA detailed understanding of serological immune responses to Ebola and Marburg virus infections will facilitate the development of effective diagnostic methods, therapeutics, and vaccines. We examined antibodies from Ebola or Marburg survivors 1 to 14 years after recovery from disease, by using a microarray that displayed recombinant nucleoprotein (NP), viral protein 40 (VP40), envelope glycoprotein (GP), and inactivated whole virions from six species of filoviruses. All three outbreak cohorts exhibited significant antibody responses to antigens from the original infecting species and a pattern of additional filoviruses that varied by outbreak. NP was the most cross-reactive antigen, while GP was the most specific. Antibodies from survivors of infections byMarburg marburgvirus(MARV) species were least cross-reactive, while those from survivors of infections bySudan virus(SUDV) species exhibited the highest cross-reactivity. Based on results revealed by the protein microarray, persistent levels of antibodies to GP, NP, and VP40 were maintained for up to 14 years after infection, and survival of infection caused by one species imparted cross-reactive antibody responses to other filoviruses.

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Crozier, Ian, Kyla A. Britson, Daniel N. Wolfe, John D. Klena, Lisa E. Hensley, John S. Lee, Larry A. Wolfraim, et al. "The Evolution of Medical Countermeasures for Ebola Virus Disease: Lessons Learned and Next Steps." Vaccines 10, no. 8 (July 29, 2022): 1213. http://dx.doi.org/10.3390/vaccines10081213.

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The Ebola virus disease outbreak that occurred in Western Africa from 2013–2016, and subsequent smaller but increasingly frequent outbreaks of Ebola virus disease in recent years, spurred an unprecedented effort to develop and deploy effective vaccines, therapeutics, and diagnostics. This effort led to the U.S. regulatory approval of a diagnostic test, two vaccines, and two therapeutics for Ebola virus disease indications. Moreover, the establishment of fieldable diagnostic tests improved the speed with which patients can be diagnosed and public health resources mobilized. The United States government has played and continues to play a key role in funding and coordinating these medical countermeasure efforts. Here, we describe the coordinated U.S. government response to develop medical countermeasures for Ebola virus disease and we identify lessons learned that may improve future efforts to develop and deploy effective countermeasures against other filoviruses, such as Sudan virus and Marburg virus.

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Finch, Courtney L., Thomas H. King, Kendra J. Alfson, Katie A. Albanese, Julianne N. P. Smith, Paul Smock, Jocelyn Jakubik, et al. "Single-Shot ChAd3-MARV Vaccine in Modified Formulation Buffer Shows 100% Protection of NHPs." Vaccines 10, no. 11 (November 15, 2022): 1935. http://dx.doi.org/10.3390/vaccines10111935.

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Marburg virus (MARV) is a virus of high human consequence with a case fatality rate of 24–88%. The global health and national security risks posed by Marburg virus disease (MVD) underscore the compelling need for a prophylactic vaccine, but no candidate has yet reached regulatory approval. Here, we evaluate a replication-defective chimpanzee adenovirus type 3 (ChAd3)-vectored MARV Angola glycoprotein (GP)-expressing vaccine against lethal MARV challenge in macaques. The ChAd3 platform has previously been reported to protect against the MARV-related viruses, Ebola virus (EBOV) and Sudan virus (SUDV), and MARV itself in macaques, with immunogenicity demonstrated in macaques and humans. In this study, we present data showing 100% protection against MARV Angola challenge (versus 0% control survival) and associated production of GP-specific IgGs generated by the ChAd3-MARV vaccine following a single dose of 1 × 1011 virus particles prepared in a new clinical formulation buffer designed to enhance product stability. These results are consistent with previously described data using the same vaccine in a different formulation and laboratory, demonstrating the reproducible and robust protective efficacy elicited by this promising vaccine for the prevention of MVD. Additionally, a qualified anti-GP MARV IgG ELISA was developed as a critical pre-requisite for clinical advancement and regulatory approval.

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Prugar, Laura I., Danielle Dorosky, Frederick Holtsberg, Sergey Shulenin, Hong Vu, Katy Howell, Russell Bakken, Jennifer Brannan, John M. Dye, and M. Javad Aman. "Pan-filovirus monoclonal antibody cocktail protects against lethal challenge with Marburg virus in non-human primates." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 180.13. http://dx.doi.org/10.4049/jimmunol.200.supp.180.13.

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Abstract While disregarded in the past, the use of antibody therapeutics in the treatment of filovirus infection has been gaining traction in recent years. Early studies in our lab with the treatment of non-human primates (NHPs) with polyclonal antibodies from convalescent NHPs demonstrated protection against challenges with a lethal dose of Ebola virus (EBOV). Successes with monoclonal antibody (mAb) cocktails such as ZMapp™ have encouraged the development of a cocktail that may be protective against multiple species of filovirus. This may ultimately allow for the prepositioning of a single cocktail in filovirus prone locations, rather than storing and maintaining multiple cocktails at each location. We have previously described three antibodies, FVM04 and CA45, which can neutralize multiple species of ebolavirus, and MR191, which can neutralize marburgviruses, and have shown efficacy in rodent and NHP models of filovirus disease. In this study, we evaluated the efficacy of a pan-ebolavirus cocktail (FVM04+CA45) in combination with the Marburg virus specific mAb MR191 in a pan-filovirus cocktail (FVM04+CA45+MR191), in the NHP model of Marburg virus disease. Both the pan-ebolavirus and pan-filovirus cocktails have been shown to be efficacious against lethal challenge with Sudan virus (SUDV) or EBOV in the rhesus macaque model. These data are the first to demonstrate protective efficacy of MR191 as part of a pan-filovirus cocktail against MARV in the NHP model of disease.

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Clarke, Elizabeth C., and Steven Bradfute. "The impact of glycoyslation on filovirus vaccine immunogenicity in mice." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 247.20. http://dx.doi.org/10.4049/jimmunol.204.supp.247.20.

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Abstract Filoviruses are highly virulent pathogens which cause severe hemorrhagic fevers, including Ebola virus disease (EVD). There is currently an ongoing large outbreak in the Democratic Republic of Congo, and while investigational vaccines have been used in trials during the outbreak, there are no licensed vaccines to EVD, or the related Marburg virus disease (MVD). The glycoproteins of filoviruses are the only virally expressed proteins on the virion surface and are required for receptor binding and as such, they are the main candidate vaccine antigen. A major component of the glycoprotein are the N- and O-linked glycans, but these glycans vary in number, distribution and type depending on the cell type producing the glycoprotein. Both mammalian and insect cell lines are commonly used to produce filovirus proteins used in vaccine development, but produce proteins with very different glycosylation. Here, we describe the impact of the filovirus glycoprotein glycans on the immunogenicity of the transmembrane-deleted glycoprotein (GPdTM) vaccine in mice using insect-produced, mammalian-produced, and deglycosylated filovirus glycoproteins. Results suggest differences in antibody titer and T cell epitopes induced between glycoproteins with different glycosylation patterns. Studies are underway to test how these changes affect survival against live virus challenge with mouse-adapted Ebola and Marburg.

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Nyakarahuka, Luke, Trevor R. Shoemaker, Stephen Balinandi, Godfrey Chemos, Benon Kwesiga, Sophia Mulei, Jackson Kyondo, et al. "Marburg virus disease outbreak in Kween District Uganda, 2017: Epidemiological and laboratory findings." PLOS Neglected Tropical Diseases 13, no. 3 (March 18, 2019): e0007257. http://dx.doi.org/10.1371/journal.pntd.0007257.

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Blair, Paul, Maryam Keshtkar-Jahromi, Kevin Psoter, and Anthony Cardile. "2493. Marburg Virus Disease: Virulence of Angola vs. Musoke Strain in Cynomolgus Macaques." Open Forum Infectious Diseases 5, suppl_1 (November 2018): S748. http://dx.doi.org/10.1093/ofid/ofy210.2145.

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Al-Halhouli, Ala’aldeen, Ahmed Albagdady, Ja’far Alawadi, and Mahmoud Abu Abeeleh. "Monitoring Symptoms of Infectious Diseases: Perspectives for Printed Wearable Sensors." Micromachines 12, no. 6 (May 27, 2021): 620. http://dx.doi.org/10.3390/mi12060620.

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Infectious diseases possess a serious threat to the world’s population, economies, and healthcare systems. In this review, we cover the infectious diseases that are most likely to cause a pandemic according to the WHO (World Health Organization). The list includes COVID-19, Crimean-Congo Hemorrhagic Fever (CCHF), Ebola Virus Disease (EBOV), Marburg Virus Disease (MARV), Lassa Hemorrhagic Fever (LHF), Middle East Respiratory Syndrome (MERS), Severe Acute Respiratory Syndrome (SARS), Nipah Virus diseases (NiV), and Rift Valley fever (RVF). This review also investigates research trends in infectious diseases by analyzing published research history on each disease from 2000–2020 in PubMed. A comprehensive review of sensor printing methods including flexographic printing, gravure printing, inkjet printing, and screen printing is conducted to provide guidelines for the best method depending on the printing scale, resolution, design modification ability, and other requirements. Printed sensors for respiratory rate, heart rate, oxygen saturation, body temperature, and blood pressure are reviewed for the possibility of being used for disease symptom monitoring. Printed wearable sensors are of great potential for continuous monitoring of vital signs in patients and the quarantined as tools for epidemiological screening.

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Imran, Muhammad, Muhammad Touqeer Hanif, Waseem Abbas, and Amjad Bilal. "Bat Borne Diseases." BioMedica 36, no. 2S (June 24, 2020): 194–200. http://dx.doi.org/10.51441/biomedica//biomedica/5-440.

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<p>A bat-borne disease is any infectious disease whose primary reservoir is any species of bat. It is not a coincidence that some of the deadly viral disease outbreaks in recent years like severe acute respiratory syndrome (SARS), Middle East respiratory disorder (MERS), Ebola, Marburg and the new 2019-nCoV virus are speculated to be originated in bats. Rarely some bacterial and fungal diseases are also related to certain species of bats. Such illnesses are part of Zoonosis, which refers to the human diseases of animal origin. In this review we highlight some of the bat-borne diseases with emphasis on the viral outbreaks as bats world-wide harbor a greater proportion of viruses than several other groups of mammals.</p>

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Dorosky, Danielle, Laura I. Prugar, Szuyan Pu, Cecilia O’Brien, Russell Bakken, Steven De Jonghe, Piet Herdewijn, Jennifer Brannan, John M. Dye, and Shirit Einav. "AAK1 and GAK inhibitors demonstrate activity against Filoviruses." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 50.7. http://dx.doi.org/10.4049/jimmunol.200.supp.50.7.

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Abstract Ebola virus (EBOV) and Marburg virus (MARV) are highly pathogenic members of the family filoviridae. The recent West Africa epidemic of Ebola virus disease was a grave reminder of the unmet need for post exposure therapeutics to combat filovirus infection. Our group has reported that multiple unrelated viruses, including EBOV, commandeer host kinases AP2-associated protein kinase-1 (AAK1) and cyclin G-associated kinase (GAK) during viral entry, assembly, and/or egress. This shared attribute makes AAK1 and GAK desirable broad-spectrum targets for the treatment of multiple viral infections without necessitating species identification. As the targets of these inhibitors are host cell factors, this may allow for the reduction in the likelihood that the virus will develop drug resistance. We have demonstrated that treatment with sunitinib and erlotinib, approved anticancer drugs with anti-AAK1 or GAK activity, is effective in inhibiting replication of Ebola, Hepatitis C and Dengue (DENV) viruses in vitro. Additionally, the combination of sunitinib and erlotinib has demonstrated efficacy in reducing morbidity and mortality following challenge with EBOV and DENV in the relevant mouse models. In an effort to improve toxicity and survival, we are developing novel, chemically distinct, more selective inhibitors of AAK1 and GAK. Here we describe the capability of these next generation AAK1 and GAK inhibitors to reduce in vitro infection of Ebola virus and Marburg virus.

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Lin, Kenny L., Nancy A. Twenhafel, John H. Connor, Kathleen A. Cashman, Joshua D. Shamblin, Ginger C. Donnelly, Heather L. Esham, et al. "Temporal Characterization of Marburg Virus Angola Infection following Aerosol Challenge in Rhesus Macaques." Journal of Virology 89, no. 19 (July 22, 2015): 9875–85. http://dx.doi.org/10.1128/jvi.01147-15.

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ABSTRACTMarburg virus (MARV) infection is a lethal hemorrhagic fever for which no licensed vaccines or therapeutics are available. Development of appropriate medical countermeasures requires a thorough understanding of the interaction between the host and the pathogen and the resulting disease course. In this study, 15 rhesus macaques were sequentially sacrificed following aerosol exposure to the MARV variant Angola, with longitudinal changes in physiology, immunology, and histopathology used to assess disease progression. Immunohistochemical evidence of infection and resulting histopathological changes were identified as early as day 3 postexposure (p.e.). The appearance of fever in infected animals coincided with the detection of serum viremia and plasma viral genomes on day 4 p.e. High (>107PFU/ml) viral loads were detected in all major organs (lung, liver, spleen, kidney, brain, etc.) beginning day 6 p.e. Clinical pathology findings included coagulopathy, leukocytosis, and profound liver destruction as indicated by elevated liver transaminases, azotemia, and hypoalbuminemia. Altered cytokine expression in response to infection included early increases in Th2 cytokines such as interleukin 10 (IL-10) and IL-5 and late-stage increases in Th1 cytokines such as IL-2, IL-15, and granulocyte-macrophage colony-stimulating factor (GM-CSF). This study provides a longitudinal examination of clinical disease of aerosol MARV Angola infection in the rhesus macaque model.IMPORTANCEIn this study, we carefully analyzed the timeline of Marburg virus infection in nonhuman primates in order to provide a well-characterized model of disease progression following aerosol exposure.

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Stonier, Spencer, Andrew Herbert, Ariel Sobarzo, Ana Kuehne, Yael Eskira, Julius Lutwaama, Leslie Lobel, and John Dye. "T and B cell memory responses in 2012 filovirus outbreak survivors (VIR7P.1060)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 208.12. http://dx.doi.org/10.4049/jimmunol.192.supp.208.12.

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Abstract From 2011 to the present, there have been four confirmed filovirus outbreaks with a fifth case involving a single patient. Four outbreaks/cases were attributed to the Ebolavirus genus, with Marburgvirus responsible for one. With the high lethality rates seen in these outbreaks (generally ~40-90%), and the potentially dramatic disease sequelae, filovirus outbreaks can devastate local communities and present great health risks for affected regions. These issues obviate the need for effective vaccines and therapeutics to limit and manage future outbreaks. In 2012 alone, three outbreaks occurred in Uganda - two of Sudan virus and one Marburg virus. We collected PBMC and serum samples from survivors from each outbreak to evaluate the presence of immune memory and its composition. Serum antibodies displayed broad specificity to Marburg virus and Sudan virus glycoprotein in addition to other proteins. Virtually all serum samples displayed neutralizing activity. PBMCs stimulated with viral and recombinant antigen were evaluated by flow cytometry for functional parameters as well as level of antigen-responsive T cells. Cytokines in the supernatants of these cultures were determined by multiplex ELISA. Cytokine responses were largely pro-inflammatory produced predominantly by CD4 T cells. Establishing immune memory parameters and the nature thereof gives us targets for vaccine development and opens avenues for development of immune-based therapeutics.

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Pavlin, Boris I. "Calculation of incubation period and serial interval from multiple outbreaks of Marburg virus disease." BMC Research Notes 7, no. 1 (2014): 906. http://dx.doi.org/10.1186/1756-0500-7-906.

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Languon, Sylvester, and Osbourne Quaye. "Filovirus Disease Outbreaks: A Chronological Overview." Virology: Research and Treatment 10 (January 2019): 1178122X1984992. http://dx.doi.org/10.1177/1178122x19849927.

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Filoviruses cause outbreaks which lead to high fatality in humans and non-human primates, thus tagging them as major threats to public health and species conservation. In this review, we give account of index cases responsible for filovirus disease outbreaks that have occurred over the past 52 years in a chronological fashion, by describing the circumstances that led to the outbreaks, and how each of the outbreaks broke out. Since the discovery of Marburg virus and Ebola virus in 1967 and 1976, respectively, more than 40 filovirus disease outbreaks have been reported; majority of which have occurred in Africa. The chronological presentation of this review is to provide a concise overview of filovirus disease outbreaks since the discovery of the viruses, and highlight the patterns in the occurrence of the outbreaks. This review will help researchers to better appreciate the need for surveillance, especially in areas where there have been no filovirus disease outbreaks. We conclude by summarizing some recommendations that have been proposed by health and policy decision makers over the years.

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Woolsey, Courtney, Robert W. Cross, Krystle N. Agans, Viktoriya Borisevich, Daniel J. Deer, Joan B. Geisbert, Cheryl Gerardi, et al. "A highly attenuated Vesiculovax vaccine rapidly protects nonhuman primates against lethal Marburg virus challenge." PLOS Neglected Tropical Diseases 16, no. 5 (May 27, 2022): e0010433. http://dx.doi.org/10.1371/journal.pntd.0010433.

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Background Marburg virus (MARV), an Ebola-like virus, remains an eminent threat to public health as demonstrated by its high associated mortality rate (23–90%) and recent emergence in West Africa for the first time. Although a recombinant vesicular stomatitis virus (rVSV)-based vaccine (Ervebo) is licensed for Ebola virus disease (EVD), no approved countermeasures exist against MARV. Results from clinical trials indicate Ervebo prevents EVD in 97.5–100% of vaccinees 10 days onwards post-immunization. Methodology/Findings Given the rapid immunogenicity of the Ervebo platform against EVD, we tested whether a similar, but highly attenuated, rVSV-based Vesiculovax vector expressing the glycoprotein (GP) of MARV (rVSV-N4CT1-MARV-GP) could provide swift protection against Marburg virus disease (MVD). Here, groups of cynomolgus monkeys were vaccinated 7, 5, or 3 days before exposure to a lethal dose of MARV (Angola variant). All subjects (100%) immunized one week prior to challenge survived; 80% and 20% of subjects survived when vaccinated 5- and 3-days pre-exposure, respectively. Lethality was associated with higher viral load and sustained innate immunity transcriptional signatures, whereas survival correlated with development of MARV GP-specific antibodies and early expression of predicted NK cell-, B-cell-, and cytotoxic T-cell-type quantities. Conclusions/Significance These results emphasize the utility of Vesiculovax vaccines for MVD outbreak management. The highly attenuated nature of rVSV-N4CT1 vaccines, which are clinically safe in humans, may be preferable to vaccines based on the same platform as Ervebo (rVSV “delta G” platform), which in some trial participants induced vaccine-related adverse events in association with viral replication including arthralgia/arthritis, dermatitis, and cutaneous vasculitis.

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Blair, Paul, Maryam Keshtkar-Jahromi, Kevin Psoter, Ronald Reisler, Travis Warren, Sara Johnston, Arthur Goff, Lydia Downey, Sina Bavari, and Anthony Cardile. "Virulence of Marburg Virus Angola Compared to Mt. Elgon (Musoke) in Macaques: A Pooled Survival Analysis." Viruses 10, no. 11 (November 21, 2018): 658. http://dx.doi.org/10.3390/v10110658.

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Angola variant (MARV/Ang) has replaced Mt. Elgon variant Musoke isolate (MARV/MtE-Mus) as the consensus standard variant for Marburg virus research and is regarded as causing a more aggressive phenotype of disease in animal models; however, there is a dearth of published evidence supporting the higher virulence of MARV/Ang. In this retrospective study, we used data pooled from eight separate studies in nonhuman primates experimentally exposed with either 1000 pfu intramuscular (IM) MARV/Ang or MARV/MtE-Mus between 2012 and 2017 at the United States Army Medical Research Institute of Infectious Diseases (USAMRIID). Multivariable Cox proportional hazards regression was used to evaluate the association of variant type with time to death, the development of anorexia, rash, viremia, and 10 select clinical laboratory values. A total of 47 cynomolgus monkeys were included, of which 18 were exposed to MARV/Ang in three separate studies and 29 to MARV/MtE-Mus in five studies. Following universally fatal Marburg virus exposure, compared to MARV/MtE-Mus, MARV/Ang was associated with an increased risk of death (HR = 22.10; 95% CI: 7.08, 68.93), rash (HR = 5.87; 95% CI: 2.76, 12.51) and loss of appetite (HR = 35.10; 95% CI: 7.60, 162.18). Our data demonstrate an increased virulence of MARV/Ang compared to MARV/MtE-Mus variant in the 1000 pfu IM cynomolgus macaque model.

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Rojek, Amanda M., and Peter W. Horby. "Offering patients more: how the West Africa Ebola outbreak can shape innovation in therapeutic research for emerging and epidemic infections." Philosophical Transactions of the Royal Society B: Biological Sciences 372, no. 1721 (April 10, 2017): 20160294. http://dx.doi.org/10.1098/rstb.2016.0294.

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Although, after an epidemic of over 28 000 cases, there are still no licensed treatments for Ebola virus disease (EVD), significant progress was made during the West Africa outbreak. The pace of pre-clinical development was exceptional and a number of therapeutic clinical trials were conducted in the face of considerable challenges. Given the on-going risk of emerging infectious disease outbreaks in an era of unprecedented population density, international travel and human impact on the environment it is pertinent to focus on improving the research and development landscape for treatments of emerging and epidemic-prone infections. This is especially the case since there are no licensed therapeutics for some of the diseases considered by the World Health Organization as most likely to cause severe outbreaks—including Middle East respiratory syndrome coronavirus, Marburg virus, Crimean Congo haemorrhagic fever and Nipah virus. EVD, therefore, provides a timely exemplar to discuss the barriers, enablers and incentives needed to find effective treatments in advance of health emergencies caused by emerging infectious diseases. This article is part of the themed issue ‘The 2013–2016 West African Ebola epidemic: data, decision-making and disease control’.

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Vanmechelen, Bert, Joren Stroobants, Kurt Vermeire, and Piet Maes. "Development of a T7-Independent MARV Minigenome System." Proceedings 50, no. 1 (June 9, 2020): 27. http://dx.doi.org/10.3390/proceedings2020050027.

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Marburg virus (MARV) is the only known pathogenic filovirus that does not belong to the genus Ebolavirus. It causes a severe hemorrhagic fever that is associated with a high mortality rate (>80%). The potential for filoviruses to cause devastating outbreaks, in combination with the lack of licensed therapeutics and vaccines for Marburg virus disease, illustrates the need for more MARV research. However, research involving MARV is hindered by its dependency on access to high-containment laboratories. Virus alternatives such as minigenomes have proven to be a useful tool to study virus replication and transcription at lower biosafety levels, and can be used for antiviral compound screening. All currently available MARV minigenomes are dependent on the addition of an ectopic T7 RNA polymerase that can drive minigenome expression. While this allows for high expression levels, the ectopic expression of a T7 polymerase is not feasible in all cell types, and acts as a confounding factor in compound screening assays. We have developed an alternative MARV minigenome system that is controlled by an RNA polymerase II promoter, which is natively expressed in most mammalian cell types. We show here that this novel minigenome can be used in a wide range of cell types, and can be easily amended to a 96-well format to be used for high-throughput compound screening, thereby providing a valuable alternative to previously developed MARV minigenomes.

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Jaskaran Singh, Thapa Komal, Sandeep Arora, Amarjot Kaur, and Thakur Gurjeet Singh. "Ebola Hemorrhagic Fever: Recent Update On Disease Status, Current Therapies And Advances In Treatment." Journal of Pharmaceutical Technology, Research and Management 5, no. 2 (November 2, 2017): 217–34. http://dx.doi.org/10.15415/jptrm.2017.52013.

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Swiftly growing viruses are a major intimidation to human health. Such viruses are extremely pathogenic like Ebola virus, influenza virus, HIV virus, Zika virus etc . Ebola virus, a type of Filovirus, is an extremely infectious, single-stranded ribonucleic acid virus that infects both humans and apes, prompting acute fever with hemorrhagic syndrome. The high infectivity, severity and mortality of Ebola has plagued the world for the past fifty years with its first outbreak in 1976 in Marburg, Germany, and Frankfurt along with Belgrade and Serbia. The world has perceived about 28,000 cases and over 11,000 losses. The high lethality of Ebola makes it a candidate for use in bioterrorism thereby arising more concern. New guidelines have been framed for providing best possible care to the patients suffering from Ebola virus i.e Grading of Recommendation Assessment, Development And Evaluation (GRADE) methodology to develop evidence-based strategy for the treatment in future outbreak of Ebola virus. No drugs have been approved, while many potent drugs like rVSV-EBOV, Favipiravir, ZMapp are on clinical test for human safety. In this review we will discover and discuss perspective aspects that lead to the evolution of different Ebola variants as well as advances in various drugs and vaccines for treatment of the disease.

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Journal articles on the topic 'Marburg virus disease'

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