Marburg virus

{{See also|1967 Marburg virus outbreak in West Germany|l1=1967 Marburg virus outbreak}}

File:Marburg em1986.png. EMDB entry.{{cite web |title=CryoEM reconstruction of the Marburg virus nucleocapsid |url=https://www.ebi.ac.uk/emdb/EMD-1986 |website=Electron Microscopy Data Bank |access-date=18 February 2023}}{{cite journal | vauthors = Bharat TA, Riches JD, Kolesnikova L, Welsch S, Krähling V, Davey N, Parsy ML, Becker S, Briggs JA | display-authors = 6 | title = Cryo-electron tomography of Marburg virus particles and their morphogenesis within infected cells | journal = PLOS Biology | volume = 9 | issue = 11 | pages = e1001196 | date = November 2011 | pmid = 22110401 | pmc = 3217011 | doi = 10.1371/journal.pbio.1001196 | veditors = Rey FA | doi-access = free }}]]Marburg virus was first described in 1967.{{cite journal | vauthors = Siegert R, Shu HL, Slenczka W, Peters D, Müller G | title = [On the etiology of an unknown human infection originating from monkeys] | journal = Deutsche Medizinische Wochenschrift | volume = 92 | issue = 51 | pages = 2341–2343 | date = December 1967 | pmid = 4294540 | doi = 10.1055/s-0028-1106144 | s2cid = 116556454 }} It was discovered that year during a set of outbreaks of Marburg virus disease in the German cities of Marburg and Frankfurt and the Yugoslav capital Belgrade. Laboratory workers were exposed to tissues of infected grivet monkeys (the African green monkey, Chlorocebus aethiops) at the {{interlanguage link|Behringwerke|de}}, a major industrial plant in Marburg which was then part of Hoechst, and later part of CSL Behring. During the outbreaks, thirty-one people became infected and seven of them died.{{cite journal | vauthors = Slenczka W, Klenk HD | title = Forty years of marburg virus | journal = The Journal of Infectious Diseases | volume = 196 | issue = Suppl 2 | pages = S131–S135 | date = November 2007 | pmid = 17940940 | doi = 10.1086/520551 | doi-access = free }}

The virus is one of two members of the species Marburgvirus, which is included in the genus Marburgvirus, family Filoviridae, and order Mononegavirales. The name Marburgvirus is derived from Marburg (the city in Hesse, Germany, where the virus was first discovered) and the taxonomic suffix virus.{{cite journal |vauthors=Kuhn JH, Becker S, Ebihara H, Geisbert TW, Johnson KM, Kawaoka Y, Lipkin WI, Negredo AI, Netesov SV, Nichol ST, Palacios G, Peters CJ, Tenorio A, Volchkov VE, Jahrling PB |display-authors=6 |title = Proposal for a revised taxonomy of the family Filoviridae: classification, names of taxa and viruses, and virus abbreviations |journal = Archives of Virology |volume = 155 |issue = 12 |pages = 2083–2103 |date = December 2010 |pmid = 21046175 |pmc = 3074192 |doi = 10.1007/s00705-010-0814-x }}

Marburgvirus was first introduced under this name in 1967. The virus name was changed to Lake Victoria marburgvirus in 2005, confusingly making the only difference in distinguishing between a Marburgvirus organism and its species as a whole italicization, as in Lake Victoria marburgvirus.{{Cite book |vauthors = Feldmann H, Geisbert TW, Jahrling PB, Klenk H, Netesov SV, Peters CJ, Sanchez A, Swanepoel R, Volchkov VE |display-authors = 6 |chapter=Family Filoviridae |year=2005 |veditors = Fauquet CM, Mayo MA, Maniloff J, Desselberger U, Ball LA |title=Virus Taxonomy—Eighth Report of the International Committee on Taxonomy of Viruses |pages=645–653 |publisher=Elsevier/Academic Press |location=San Diego, US |isbn=978-0-12-370200-5}}{{cite journal |vauthors = Mayo MA |year=2002 |title = ICTV at the Paris ICV: results of the plenary session and the binomial ballot |journal = Archives of Virology |volume = 147 |issue = 11 |pages = 2254–60 |doi=10.1007/s007050200052 |s2cid=43887711 |doi-access = free}}{{cite journal |vauthors = Kuhn JH, Jahrling PB |title = Clarification and guidance on the proper usage of virus and virus species names |journal = Archives of Virology |volume = 155 |issue = 4 |pages = 445–453 |date = April 2010 |pmid = 20204430 |pmc = 2878132 |doi = 10.1007/s00705-010-0600-9 }} Still, most scientific articles continued to use the name Marburgvirus. Consequently, in 2010, the name Marburgvirus was reinstated and the species name changed.

File:Viruses-04-01878-g005.webp

Like all mononegaviruses, marburg virions contain non-infectious, linear nonsegmented, single-stranded RNA genomes of negative polarity that possess inverse-complementary 3' and 5' termini, do not possess a 5' cap, are not polyadenylated, and are not covalently linked to a protein.{{Cite book | vauthors = Pringle CR |chapter=Order Mononegavirales|year=2005| veditors = Fauquet CM, Mayo MA, Maniloff J, Desselberger U, Ball LA |title=Virus Taxonomy—Eighth Report of the International Committee on Taxonomy of Viruses|pages=609–614|publisher=Elsevier/Academic Press|location=San Diego, US|isbn=978-0-12-370200-5}} Marburgvirus genomes are approximately 19 kbp long and contain seven genes in the order 3'-UTR-NP-VP35-VP40-GP-VP30-VP24-L-5'-UTR.{{cite journal | vauthors = Kiley MP, Bowen ET, Eddy GA, Isaäcson M, Johnson KM, McCormick JB, Murphy FA, Pattyn SR, Peters D, Prozesky OW, Regnery RL, Simpson DI, Slenczka W, Sureau P, van der Groen G, Webb PA, Wulff H | display-authors = 6 | title = Filoviridae: a taxonomic home for Marburg and Ebola viruses? | journal = Intervirology | volume = 18 | issue = 1–2 | pages = 24–32 | year = 1982 | pmid = 7118520 | doi = 10.1159/000149300 | doi-access = free }}

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File:Marburg Virus Particle (30971357537).jpg

Like all filoviruses, marburgvirions are filamentous particles that may appear in the shape of a shepherd's crook or in the shape of a "U" or a "6", and they may be coiled, toroid, or branched. Marburgvirions are generally 80 nm in width, but vary somewhat in length. In general, the median particle length of marburgviruses ranges from 795 to 828 nm (in contrast to ebolavirions, whose median particle length was measured to be 974–1,086 nm), but particles as long as 14,000 nm have been detected in tissue culture.{{cite journal | vauthors = Geisbert TW, Jahrling PB | title = Differentiation of filoviruses by electron microscopy | journal = Virus Research | volume = 39 | issue = 2–3 | pages = 129–150 | date = December 1995 | pmid = 8837880 | doi = 10.1016/0168-1702(95)00080-1 | url = https://zenodo.org/record/1258399 }}

Marburgvirions consist of seven structural proteins. At the center is the helical ribonucleocapsid, which consists of the genomic RNA wrapped around a polymer of nucleoproteins (NP). Associated with the ribonucleoprotein is the RNA-dependent RNA polymerase (L) with the polymerase cofactor (VP35) and a transcription activator (VP30). The ribonucleoprotein is embedded in a matrix, formed by the major (VP40) and minor (VP24) matrix proteins. These particles are surrounded by a lipid membrane derived from the host cell membrane. The membrane anchors a glycoprotein (GP_1,2) that projects 7 to 10 nm spikes away from its surface. While nearly identical to ebolavirions in structure, marburgvirions are antigenically distinct.{{cite journal | vauthors = King LB, West BR, Schendel SL, Saphire EO | title = The structural basis for filovirus neutralization by monoclonal antibodies | journal = Current Opinion in Immunology | volume = 53 | pages = 196–202 | date = August 2018 | pmid = 29940415 | pmc = 6141344 | doi = 10.1016/j.coi.2018.05.001 }}

Niemann–Pick C1 (NPC1) cholesterol transporter protein appears to be essential for infection with both Ebola and Marburg virus. Two independent studies reported in the same issue of Nature showed that Ebola virus cell entry and replication requires NPC1.{{cite journal | vauthors = Carette JE, Raaben M, Wong AC, Herbert AS, Obernosterer G, Mulherkar N, Kuehne AI, Kranzusch PJ, Griffin AM, Ruthel G, Dal Cin P, Dye JM, Whelan SP, Chandran K, Brummelkamp TR | display-authors = 6 | title = Ebola virus entry requires the cholesterol transporter Niemann-Pick C1 | journal = Nature | volume = 477 | issue = 7364 | pages = 340–343 | date = August 2011 | pmid = 21866103 | pmc = 3175325 | doi = 10.1038/nature10348 | bibcode = 2011Natur.477..340C }}

• {{cite news | vauthors = Schaffer A |date=January 16, 2012 |title=Key Protein May Give Ebola Virus Its Opening |newspaper=The New York Times |url=https://www.nytimes.com/2012/01/17/health/npc1-protein-may-give-ebola-its-opening.html |url-access=subscription}}{{cite journal | vauthors = Côté M, Misasi J, Ren T, Bruchez A, Lee K, Filone CM, Hensley L, Li Q, Ory D, Chandran K, Cunningham J | display-authors = 6 | title = Small molecule inhibitors reveal Niemann-Pick C1 is essential for Ebola virus infection | journal = Nature | volume = 477 | issue = 7364 | pages = 344–348 | date = August 2011 | pmid = 21866101 | pmc = 3230319 | doi = 10.1038/nature10380 | bibcode = 2011Natur.477..344C }}
• {{cite news | vauthors = Schaffer A |date=January 16, 2012 |title=Key Protein May Give Ebola Virus Its Opening |newspaper=The New York Times |url=https://www.nytimes.com/2012/01/17/health/npc1-protein-may-give-ebola-its-opening.html |url-access=subscription}} When cells from patients lacking NPC1 were exposed to Ebola virus in the laboratory, the cells survived and appeared immune to the virus, further indicating that Ebola relies on NPC1 to enter cells. This might imply that genetic mutations in the NPC1 gene in humans could make some people resistant to one of the deadliest known viruses affecting humans. The same studies described similar results with Marburg virus, showing that it also needs NPC1 to enter cells. Furthermore, NPC1 was shown to be critical to filovirus entry because it mediates infection by binding directly to the viral envelope glycoprotein and that the second lysosomal domain of NPC1 mediates this binding.{{cite journal | vauthors = Miller EH, Obernosterer G, Raaben M, Herbert AS, Deffieu MS, Krishnan A, Ndungo E, Sandesara RG, Carette JE, Kuehne AI, Ruthel G, Pfeffer SR, Dye JM, Whelan SP, Brummelkamp TR, Chandran K | display-authors = 6 | title = Ebola virus entry requires the host-programmed recognition of an intracellular receptor | journal = The EMBO Journal | volume = 31 | issue = 8 | pages = 1947–1960 | date = April 2012 | pmid = 22395071 | pmc = 3343336 | doi = 10.1038/emboj.2012.53 }}

In one of the original studies, a small molecule was shown to inhibit Ebola virus infection by preventing the virus glycoprotein from binding to NPC1.{{cite journal | vauthors = Flemming A | title = Achilles heel of Ebola viral entry | journal = Nature Reviews. Drug Discovery | volume = 10 | issue = 10 | pages = 731 | date = September 2011 | pmid = 21959282 | doi = 10.1038/nrd3568 | s2cid = 26888076 | doi-access = free }} In the other study, mice that were heterozygous for NPC1 were shown to be protected from lethal challenge with mouse-adapted Ebola virus.

File:Viruses-04-01878-g007.webp

The Marburg virus life cycle begins with virion attachment to specific cell-surface receptors, followed by fusion of the virion envelope with cellular membranes and the concomitant release of the virus nucleocapsid into the cytosol.{{citation needed|date=March 2022}}

The virus RdRp partially uncoats the nucleocapsid and transcribes the genes into positive-stranded mRNAs, which are then translated into structural and nonstructural proteins. Marburgvirus L binds to a single promoter located at the 3' end of the genome. Transcription either terminates after a gene or continues to the next gene downstream. This means that genes close to the 3' end of the genome are transcribed in the greatest abundance, whereas those toward the 5' end are least likely to be transcribed. The gene order is therefore a simple but effective form of transcriptional regulation.{{cite journal | vauthors = Brauburger K, Hume AJ, Mühlberger E, Olejnik J | title = Forty-five years of Marburg virus research | journal = Viruses | volume = 4 | issue = 10 | pages = 1878–1927 | date = October 2012 | pmid = 23202446 | pmc = 3497034 | doi = 10.3390/v4101878 | doi-access = free }}

The most abundant protein produced is the nucleoprotein, whose concentration in the cell determines when L switches from gene transcription to genome replication. Replication results in full-length, positive-stranded antigenomes that are in turn transcribed into negative-stranded virus progeny genome copies. Newly synthesized structural proteins and genomes self-assemble and accumulate near the inside of the cell membrane. Virions bud off from the cell, gaining their envelopes from the cellular membrane they bud from. The mature progeny particles then infect other cells to repeat the cycle.

File:Viruses-04-01878-g001-A.jpgs]]

In 2009, the successful isolation of infectious MARV was reported from caught healthy Egyptian fruit bats (Rousettus aegyptiacus). This isolation, together with the isolation of infectious RAVV, strongly suggests that Old World fruit bats are involved in the natural maintenance of marburgviruses. Further studies are necessary to establish whether Egyptian rousettes are the actual hosts of MARV and RAVV or whether they get infected via contact with another animal and therefore serve only as intermediate hosts. In 2012 the first experimental infection study of Rousettus aegyptiacus with MARV provided further insight into the possible involvement of these bats in MARV ecology.{{cite journal | vauthors = Paweska JT, Jansen van Vuren P, Masumu J, Leman PA, Grobbelaar AA, Birkhead M, Clift S, Swanepoel R, Kemp A | display-authors = 6 | title = Virological and serological findings in Rousettus aegyptiacus experimentally inoculated with vero cells-adapted hogan strain of Marburg virus | journal = PLOS ONE | volume = 7 | issue = 9 | pages = e45479 | year = 2012 | pmid = 23029039 | pmc = 3444458 | doi = 10.1371/journal.pone.0045479 | doi-access = free | bibcode = 2012PLoSO...745479P }} {{open access}}

Experimentally infected bats developed relatively low viremia lasting at least five days, but remained healthy and did not develop any notable gross pathology. The virus also replicated to high titers in major organs (liver and spleen), and organs that might possibly be involved in virus transmission (lung, intestine, reproductive organs, salivary gland, kidney, bladder, and mammary gland). The relatively long period of viremia noted in this experiment could possibly also facilitate mechanical transmission by blood sucking arthropods in addition to infection of susceptible vertebrate hosts by direct contact with infected blood.

The viral strains fall into two clades: Ravn virus and Marburg virus.{{cite journal | vauthors = Zehender G, Sorrentino C, Veo C, Fiaschi L, Gioffrè S, Ebranati E, Tanzi E, Ciccozzi M, Lai A, Galli M | display-authors = 6 | title = Distribution of Marburg virus in Africa: An evolutionary approach | journal = Infection, Genetics and Evolution | volume = 44 | pages = 8–16 | date = October 2016 | pmid = 27282469 | doi = 10.1016/j.meegid.2016.06.014 | bibcode = 2016InfGE..44....8Z | hdl-access = free | s2cid = 1704025 | hdl = 2434/425196 }} The Marburg strains can be divided into two: A and B. The A strains were isolated from Uganda (five from 1967), Kenya (1980) and Angola (2004–2005) while the B strains were from the Democratic Republic of the Congo epidemic (1999–2000) and a group of Ugandan isolates isolated in 2007–2009.

The mean evolutionary rate of the whole genome was 3.3 × 10⁻⁴ substitutions/site/year (credibility interval 2.0–4.8). The Marburg strains had a mean root time of the most recent common ancestor of 177.9 years ago (95% highest posterior density 87–284) suggesting an origin in the mid 19th century. In contrast, the Ravn strains origin dated back to a mean 33.8 years ago (the early 1980s). The most probable location of the Marburg virus ancestor was Uganda whereas that of the RAVV ancestor was Kenya.{{citation needed|date=October 2017}}

{{Main|Marburg virus disease}}

MARV is one of two Marburg viruses that causes Marburg virus disease (MVD) in humans (in the literature also often referred to as Marburg hemorrhagic fever, MHF). The other one is Ravn virus (RAVV). Both viruses fulfill the criteria for being a member of the species Marburg marburgvirus because their genomes diverge from the prototype Marburg marburgvirus or the Marburg virus variant Musoke (MARV/Mus) by <10% at the nucleotide level.

{{expand section|date=October 2024}}

{{main|Prevention of viral hemorrhagic fever}}

As with many similar virusses, viral transmission can be reduced by taking suitable infection prevention and control measures, such as cleaning, isolation, protective clothing, safe waste disposal, and safe funeral practices for those killed by the disease.

{{main|Marburg vaccine}}

The first clinical study testing the efficacy of a Marburg virus vaccine was conducted in 2014. The study tested a DNA vaccine and concluded that individuals inoculated with the vaccine exhibited some level of antibodies. However, these vaccines were not expected to provide definitive immunity.{{cite journal | vauthors = Kibuuka H, Berkowitz NM, Millard M, Enama ME, Tindikahwa A, Sekiziyivu AB, Costner P, Sitar S, Glover D, Hu Z, Joshi G, Stanley D, Kunchai M, Eller LA, Bailer RT, Koup RA, Nabel GJ, Mascola JR, Sullivan NJ, Graham BS, Roederer M, Michael NL, Robb ML, Ledgerwood JE | display-authors = 6 | title = Safety and immunogenicity of Ebola virus and Marburg virus glycoprotein DNA vaccines assessed separately and concomitantly in healthy Ugandan adults: a phase 1b, randomised, double-blind, placebo-controlled clinical trial | language = English | journal = Lancet | volume = 385 | issue = 9977 | pages = 1545–1554 | date = April 2015 | pmid = 25540891 | doi = 10.1016/S0140-6736(14)62385-0 | s2cid = 205975536 | doi-access = free }} Several animal models have shown to be effective in the research of Marburg virus, such as hamsters, mice, and non-human primates (NHPs). Mice are useful in the initial phases of vaccine development as they are ample models for mammalian disease, but their immune systems are still different enough from humans to warrant trials with other mammals.{{cite journal | vauthors = Shifflett K, Marzi A | title = Marburg virus pathogenesis - differences and similarities in humans and animal models | journal = Virology Journal | volume = 16 | issue = 1 | pages = 165 | date = December 2019 | pmid = 31888676 | pmc = 6937685 | doi = 10.1186/s12985-019-1272-z | doi-access = free }} Of these models, the infection in macaques seems to be the most similar to the effects in humans.{{cite journal | vauthors = Ewers EC, Pratt WD, Twenhafel NA, Shamblin J, Donnelly G, Esham H, Wlazlowski C, Johnson JC, Botto M, Hensley LE, Goff AJ | display-authors = 6 | title = Natural History of Aerosol Exposure with Marburg Virus in Rhesus Macaques | journal = Viruses | volume = 8 | issue = 4 | pages = 87 | date = March 2016 | pmid = 27043611 | pmc = 4848582 | doi = 10.3390/v8040087 | doi-access = free }} A variety of other vaccines have been considered. Virus replicon particles (VRPs) were shown to be effective in guinea pigs, but lost efficacy once tested on NHPs. Additionally, an inactivated virus vaccine proved ineffective. DNA vaccines showed some efficacy in NHPs, but all inoculated individuals showed signs of infection.{{cite journal | vauthors = Suschak JJ, Schmaljohn CS | title = Vaccines against Ebola virus and Marburg virus: recent advances and promising candidates | journal = Human Vaccines & Immunotherapeutics | volume = 15 | issue = 10 | pages = 2359–2377 | date = 2019-10-03 | pmid = 31589088 | pmc = 6816442 | doi = 10.1080/21645515.2019.1651140 }}

Because Marburg virus and Ebola virus belong to the same family, Filoviridae, some scientists have attempted to create a single-injection vaccine for both viruses. This would both make the vaccine more practical and lower the cost for developing countries.{{cite journal | vauthors = Geisbert TW, Geisbert JB, Leung A, Daddario-DiCaprio KM, Hensley LE, Grolla A, Feldmann H | title = Single-injection vaccine protects nonhuman primates against infection with marburg virus and three species of ebola virus | journal = Journal of Virology | volume = 83 | issue = 14 | pages = 7296–7304 | date = July 2009 | pmid = 19386702 | pmc = 2704787 | doi = 10.1128/JVI.00561-09 }} Using a single-injection vaccine has shown to not cause any adverse reactogenicity, which the possible immune response to vaccination, in comparison to two separate vaccinations.

There is a candidate vaccine against the Marburg virus called rVSV-MARV. It was developed alongside vaccines for closely-related Ebolaviruses by the Canadian government in the early 2000s, twenty years before the outbreak. Production and testing of rVSV-MARV is blocked by legal monopolies held by the Merck Group. Merck acquired rights to all the closely-related candidate vaccines in 2014, but declined to work on most of them, including the Marburg vaccine, for economic reasons. While Merck returned the rights to the abandoned vaccines to the Public Health Agency of Canada, the vital rVSV vaccine production techniques which Merck had gained (while bringing the closely-related rVSV-ZEBOV vaccine into commercial use in 2019, with GAVI funding) remain Merck's, and cannot be used by anyone else wishing to develop a rVSV vaccine.{{Cite web |date=September 25, 2018 |title=MSF's response to CEPI's policy regarding equitable access |url=https://msfaccess.org/msfs-response-cepis-policy-regarding-equitable-access |url-status=live |archive-url=https://web.archive.org/web/20210321163753/https://msfaccess.org/msfs-response-cepis-policy-regarding-equitable-access |archive-date=March 21, 2021 |access-date=April 10, 2020 |website=Médecins Sans Frontières Access Campaign |language=en |quote=In vaccine development, access to know how is important. Knowledge and expertise including but not limited to purification techniques, cell lines, materials, software codes and their transfer of this to alternative manufacturers in the event the awardee discontinues development of a promising vaccine is critically important. The recent example of Merck abandoning the development of rVSV vaccines for Marburg (rVSV-MARV) and for Sudan-Ebola (rVSV-SUDV) is a case in point. Merck continues to retain vital know-how on the rVSV platform as it developed the rVSV vaccine for Zaire-Ebola (rVSV-ZEBOV) with funding support from GAVI. While it has transferred the rights on these vaccines back to Public Health Agency of Canada, there is no mechanism to share know how on the rVSV platform with other vaccine developers who would like to also use rVSV as a vector against other pathogens.}}{{Cite news |date=November 24, 2014 |title=Merck & Co. Licenses NewLink's Ebola Vaccine Candidate |url=http://www.genengnews.com/gen-news-highlights/merck-co-licenses-newlink-s-ebola-vaccine-candidate/81250631 |url-status=dead |archive-url=https://web.archive.org/web/20180518055647/https://www.genengnews.com/gen-news-highlights/merck-co-licenses-newlink-s-ebola-vaccine-candidate/81250631 |archive-date=May 18, 2018 |access-date=January 20, 2016 |work=Genetic Engineering & Biotechnology News}}{{Cite news |date=November 24, 2014 |title=Canadian Ebola vaccine development taken over by Merck |url=https://www.cbc.ca/news/health/canadian-ebola-vaccine-development-taken-over-by-merck-1.2847128 |url-status=live |archive-url=https://web.archive.org/web/20180402075111/http://www.cbc.ca/news/health/canadian-ebola-vaccine-development-taken-over-by-merck-1.2847128 |archive-date=April 2, 2018 |access-date=January 10, 2020 |agency=Reuters}}{{Cite press release |title=First FDA-approved vaccine for the prevention of Ebola virus disease, marking a critical milestone in public health preparedness and response |date=December 19, 2019 |publisher=U.S. Food and Drug Administration (FDA) |url=https://www.fda.gov/news-events/press-announcements/first-fda-approved-vaccine-prevention-ebola-virus-disease-marking-critical-milestone-public-health |access-date=December 19, 2019 |url-status=live |archive-url=https://web.archive.org/web/20191220052152/https://www.fda.gov/news-events/press-announcements/first-fda-approved-vaccine-prevention-ebola-virus-disease-marking-critical-milestone-public-health |archive-date=December 20, 2019}} {{PD-notice}}

As of June 23, 2022, researchers working with the Public Health Agency of Canada conducted a study which showed promising results of a recombinant vesicular stomatitis virus (rVSV) vaccine in guinea pigs, entitled PHV01. According to the study, inoculation with the vaccine approximately one month prior to infection with the virus provided a high level of protection.{{cite journal | vauthors = Zhu W, Liu G, Cao W, He S, Leung A, Ströher U, Fairchild MJ, Nichols R, Crowell J, Fusco J, Banadyga L | display-authors = 6 | title = A Cloned Recombinant Vesicular Stomatitis Virus-Vectored Marburg Vaccine, PHV01, Protects Guinea Pigs from Lethal Marburg Virus Disease | journal = Vaccines | volume = 10 | issue = 7 | pages = 1004 | date = June 2022 | pmid = 35891170 | pmc = 9324024 | doi = 10.3390/vaccines10071004 | doi-access = free }}

Even though there is much experimental research on Marburg virus, there is still no prominent vaccine. Human vaccination trials are either ultimately unsuccessful or are missing data specifically regarding Marburg virus.{{cite journal | vauthors = Dulin N, Spanier A, Merino K, Hutter JN, Waterman PE, Lee C, Hamer MJ | title = Systematic review of Marburg virus vaccine nonhuman primate studies and human clinical trials | journal = Vaccine | volume = 39 | issue = 2 | pages = 202–208 | date = January 2021 | pmid = 33309082 | doi = 10.1016/j.vaccine.2020.11.042 | s2cid = 229178658 }} Due to the cost needed to handle Marburg virus at qualified facilities, the relatively few number of fatalities, and lack of commercial interest, the possibility of a vaccine has simply not come to fruition{{cite journal | vauthors = Reynolds P, Marzi A | title = Ebola and Marburg virus vaccines | journal = Virus Genes | volume = 53 | issue = 4 | pages = 501–515 | date = August 2017 | pmid = 28447193 | pmc = 7089128 | doi = 10.1007/s11262-017-1455-x }} (see also economics of vaccines).

The Soviet Union had an extensive offensive and defensive biological weapons program that included MARV.{{Cite book| vauthors = Alibek K, Handelman S |title= Biohazard: The Chilling True Story of the Largest Covert Biological Weapons Program in the World—Told from Inside by the Man Who Ran It|publisher=Random House|location=New York |isbn=978-0-385-33496-9|url=https://books.google.com/books?id=eDTaCwAAQBAJ|year=1999}} At least three Soviet research institutes had MARV research programs during the Cold War: The Virology Center of the Scientific Research Institute for Microbiology in Zagorsk (today Sergiev Posad), the Scientific-Production Association "Vektor" (today the State Research Center of Virology and Biotechnology "Vektor") in Koltsovo, and the Irkutsk Scientific-Research Anti-Plague Institute of Siberia and the Far East in Irkutsk.

As most performed research was highly classified, it remains unclear how successful the MARV program was. However, Soviet defector Ken Alibek claimed that a weapon filled with MARV was tested at the Stepnogorsk Scientific Experimental and Production Base in Stepnogorsk, Kazakh Soviet Socialist Republic (today Kazakhstan), suggesting that the development of a MARV biological weapon had reached advanced stages. Independent confirmation for this claim is lacking. At least one laboratory accident with MARV, resulting in the death of Koltsovo researcher Nikolai Ustinov, occurred during the Cold War in the Soviet Union and was first described in detail by Alibek.

MARV is a select agent under US law.{{cite web|url=http://www.selectagents.gov|title=National Select Agent Registry (NSAR)|access-date=2011-10-16|last=US Animal and Plant Health Inspection Service (APHIS) and US Centers for Disease Control and Prevention (CDC)}}

{{Reflist|30em}}

{{Refbegin}}

• {{Cite book | vauthors = Klenk HD |title=Marburg and Ebola Viruses |series=Current Topics in Microbiology and Immunology |volume=235|year=1999|publisher=Springer-Verlag|location=Berlin, Germany|isbn=978-3-540-64729-4|url=https://books.google.com/books?id=2ltWAAAAYAAJ}}
• {{Cite book |vauthors = Klenk HD, Feldmann H |title=Ebola and Marburg Viruses: Molecular and Cellular Biology|year=2004|publisher=Horizon Bioscience|location=Wymondham, Norfolk, UK|isbn=978-1-904933-49-6}}
• {{Cite book | vauthors = Kuhn JH |title=Filoviruses: A Compendium of 40 Years of Epidemiological, Clinical, and Laboratory Studies. | series = Archives of Virology Supplement | volume = 20 |year=2008 |publisher=Springer |location=Vienna, Austria|isbn=978-3-211-20670-6|url=https://books.google.com/books?id=ArZtuAEACAAJ}}
• {{Cite book | vauthors = Martini GA, Siegert R |title=Marburg Virus Disease|year=1971|publisher=Springer-Verlag|location=Berlin, Germany|isbn=978-0-387-05199-4|url=https://books.google.com/books?id=SoFrAAAAMAAJ}}
• {{Cite book | vauthors = Ryabchikova EI, Price BB | title = Ebola and Marburg Viruses: A View of Infection Using Electron Microscopy | year = 2004 | publisher = Battelle Press | location = Columbus, Ohio, US | isbn = 978-1-57477-131-2 | url = https://books.google.com/books?id=3PhqAAAAMAAJ }}

{{Refend}}

{{Commons category|Marburgvirus}}

• [https://ictv.global/ International Committee on Taxonomy of Viruses (ICTV)]
• [http://www.filovir.com FILOVIR—scientific resources for research on filoviruses] {{Webarchive|url=https://web.archive.org/web/20200730224033/http://www.filovir.com/ |date=2020-07-30 }}

{{Filoviridae}}

{{Taxonbar|from=Q6755280}}

Category:Animal viruses

Category:Human viruses

Category:Species described in 1967

Category:Viruses described in the 20th century

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Category:Arthropod-borne viral fevers and viral haemorrhagic fevers

Category:Biological agents

Category:Biosafety level 4 pathogens

Category:Hemorrhagic fevers

Category:Tropical diseases

Category:Primate diseases

Category:Zoonoses

Category:Filoviridae

Category:Negative-sense single-stranded RNA viruses