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At least 19 recordsLinked to original sources
PubMed1976

Marburg virus.

Marburg virus disease, which produced 20 per cent mortality when it first occured during 1967 in Germany and Yugoslavia, recently appeared again in South Africa. The source of the first outbreak was monkeys shipped from Africa; the origin of the second episode is unclear. Because distribution of the virus in nature is unknown, its threat to man cannot be readily determined. Differential laboratory diagnoses of hemorrhagic fevers should be encouraged in order to learn more about the epidemiology of these diseases and to better assess the risks which their etiologic agents may pose for attending medical personnel.

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PubMed2025

Transcription- and Replication-Competent Virus-like Particle Systems for Marburg Virus.

Here, we describe the transcription- and replication-competent virus-like particle (trVLP) system for Marburg virus (MARV), which recapitulates transcription and replication of the viral genome in addition to viral particle assembly, egress, and entry. This protocol includes instructions for transfections for producer and acceptor cells and the use of trVLPs for infection.

Marburgvirus↗
PubMed2025

Generation of Biologically Contained Marburg Virus.

Wild-type Marburg virus (MARV) can only be handled in biosafety level 4 facilities. By removing an essential gene from the virus genome, deficient virus particles can be generated that are only capable of replication if the missing gene product is provided in trans. As a result, these viruses are restricted to specific cell lines, making them safe to handle at lower biosafety levels. Here, we provide a detailed overview of how to generate MARV in which the VP30 gene has been replaced by a green fluorescent reporter gene, as well as how to use lentiviral transduction to create stable cell lines expressing MARV VP30. These cell lines can be used for the propagation and confinement of the resulting reporter virus.

Marburgvirus↗
PubMed1975

Outbreake of Marburg virus disease in Johannesburg.

The first recognised outbreak of Marburg virus disease in Africa, and the first since the original epidemic in West Germany and Yugoslavia in 1967, occurred in South Africa in February 1975. The primary case was in a young Australian man , who was admitted to the Johannesburg Hospital after having toured Rhodesia. Two secondary cases occurred, one being in the first patient's travelling companion, and the other in a nurse. Features of the illness included high fever, myalgia, vomiting and diarrhoea, hepatitis, a characteristic maculopapular rash, leucopenia, thrombocytopenia, and a bleeding tendency. The first patient died on the seventh day from haemorrhage resulting from a combination of disseminated intravascular coagulation and hepatic failure. The other two patients were given vigorous supportive treatment and prophylactic heparin and recovered after an acute phase lasting about seven days. During this period on developed pancreatitis, the serum amylase remaining raised until the 32nd day after the onset of the illness. The other developed unilateral uveitis after having been asymptomatic for two months. This persisted for several weeks and Marburg virus was cultured from the anterior chamber of the eye.

Adult↗
PubMed2026

Re-emerging Marburg virus disease in Africa: spillover ecology, geographic expansion, and surveillance vulnerabilities.

Marburg virus disease (MVD) is re-emerging across Africa as a high-consequence zoonosis shaped by expanding ecological suitability, repeated spillover, and uneven surveillance capacity. This review synthesizes current evidence on the ecological, epidemiological, and operational determinants of contemporary Marburg virus (MARV) emergence. We conceptualize MVD as an ecological-emergence system produced by interactions among reservoir-host biology, environmental change, human exposure, health-system readiness, and mobility, rather than as a series of isolated outbreaks. Recent detections in multiple African regions indicate wider enzootic circulation than previously recognized and support repeated, reservoir-associated introductions from distributed ecological foci. Spillover risk is heightened where mining, land-use change, agricultural encroachment, settlement growth, climate-sensitive habitat disruption, and population movement increase contact with Egyptian rousette bats (Rousettus aegyptiacus) and contaminated roost environments. Following primary spillover, diagnostic delays, fragmented surveillance, limited laboratory decentralization, healthcare-associated transmission, and mobility-linked exposure can enable outbreak amplification and delayed recognition. Serological findings further suggest possible "shadow epidemiology," with unrecognized or mild MARV infections occurring outside confirmed outbreak chains. Critical preparedness gaps persist in ecological risk mapping, longitudinal reservoir surveillance, decentralized molecular diagnostics, genomic sequencing, data integration, and cross-border early warning. Future preparedness should move beyond reactive containment toward integrated One Health approach combining predictive ecological surveillance, rapid community-level detection, real-time genomics, infection prevention, risk communication, and regional coordination to identify spillover early and prevent human transmission.

Animals↗
PubMed1978

Early detection of antigen and estimation of virus yield in specimens from patients with Marburg virus disease.

Autopsy specimens from patients with Marburg disease having at least 10(4.5) TCID(50) of virus per gram of tissue were found to contain sufficient fluorescent antigen-positive cells to make a specific diagnosis possible in less than 3 h. Liver, heart, spleen, and kidney tissues were found to contain significant amounts of virus. Tissue suspensions, as well as blood or serum samples, inoculated into Vero cell cultures produced virus-specific immunofluorescence within 2-5 days. At least one specimen of all virus-positive persons yielded Marburg virus-specific antigen on day 2 or 3 after inoculation. Furthermore, tissues with at least 10(5.5) TCID(50) of virus/g had Marburg antigen of sufficient titre to be used in complement fixation tests.

Animals↗
PubMed1979

Ebola and Marburg viruses: I. Some ultrastructural differences between strains when grown in Vero cells.

A strain of Marburg virus and two strains of Ebola virus grown in Vero cells were compared by electron microscopy. The outer coat of the Marburg virion appeared to be more resistant to erosion by negative staining techniques than that of the Epbola strains. Marburg virus commonly produced "torus" forms and short filaments; the Zaire strain of Ebola produced extensive branched forms and very long filaments; the Sudan strain of Ebola produced shorter, less branched structures but very many aberrant forms. The mechanism for the production of these aberrant forms is described.

Animals↗
PubMed1978

Epidemiologic investigation of Marburg virus disease, Southern Africa, 1975.

During the first 10 days of February 1975, an Australian hitchhiker contracted Marburg virus disease while traveling through Rhodesia and died; the infection was subsequently passed to two other persons, who recovered. Investigators retraced the hitchhiker's steps in March and again in June 1975 in an effort to uncover the natural reservoir of the virus and determine how it was transmitted. Serum samples were collected from humans and animals wherever the patient had come in close contact with animals or insects. Arthropods of various types were collected in June 1975 and again in February 1976 for virus isolation attempts; at no time did the patient come in direct contact with nonhuman primates of any kind, or any other animals. Indirect contact with bats, monkeys, and birds through aerosols was possible, though at some distance. Direct contact with arthropods occurred throughout the trip; on several occasions it was notably severe. We believe that during this outbreak the first Marburg virus infection occurred by vector-borne transmission from an arthropod yet to be identified, and that patients 2 and 3 acquired the disease by exposure to the oropharyngeal secretions of patients 1 and 2, respectively. Studies are underway to identify the species of arthropod involved in this transmission.

Adult↗
PubMed2025

Marburg Virus Minigenome Assays.

This chapter describes minigenome systems for Marburg virus (MARV), which reconstitute the viral polymerase complex functions of gene expression and genome replication. Procedures covered herein include passage and seeding of cells, transfection, sample collection, and reporter gene assays.

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PubMed1979

Immunoglobulin M and G responses measured by immunofluorescence in patients with Lassa or Marburg virus infections.

Immunoglobulin M antibodies can be measured by indirect immunofluorescence in sera of patients suffering from Lassa fever or Marburg virus disease 4-7 days after onset of illness. Titres reach a peak 1-2 weeks later. These antibodies disappear, or titres decrease considerably, 1-2 months after onset of illness. Antiviral IgG antibodies can be detected at the same time as, or a little later than, IgM antibodies, but they persist much longer. None of the three patients discussed in this paper who died of Lassa fever developed IgG antibodies and only one developed IgM antibodies.

Animals↗
PubMed1979

Ebola and Marburg viruses: II. Thier development within Vero cells and the extra-cellular formation of branched and torus forms.

The development of Marburg virus and the Sudanese and Zaire strains of Ebola virus in Vero cells as visualized by electron microscopy is described. Despite differences in timing, all three strains appear to pass through identical stages of development. Initially there is a large increase in nucleolus material, and viral precursor material arranges itself in spirals and then into tubes. The cells fill with core material, which passes to the plasmalemma, which often proliferates. Each virion passes through the plasmalemma, acquiring a coat of host material. The formation of torus forms is discussed; the branched appearance that is often seen is believed to be an aberrant form. The reasons for this view are put forward.

Animals↗
PubMed1975

[Viral contamination in laboratories and hospital units].

Viral contamination is at least as important in hospital laboratories and wards as contamination by bacteria or microscopic fungi, but it is much more insidious and sometimes unrecognized. There are two main types: The first has a purely technical effect and only interest the virologist. This is contamination of reagents, reference strains, cell cultures, etc.., by foreign viral agents. It may be the cause of errors on diagnosis or regrettable errors of interpretation of certain experimental data. It is most difficult to detect, if not to avoid. The second is much more worrying as it is liable to cause disease in man, which may induce severe, and even fatal infections in patients or in the medical, para-medical and technical personnel. This is the case with type B hepatitis virus which tends to invade surgical units using extra-corporeal circulation, hemodialysis units and transplantation units, blood transfusion centres, dental units and even causes victims in routine laboratories. However, type B hepatitis is not the only virus which may lead to severe infections; other viruses include: poxvirus, cytomegalovirus, arbovirus, etc. Finally, other often severe accidents may occur in research laboratories and in the pharmaceutical industry, owing to manipulation of dangerous viruses or by contact with experimental animals, e.g. rodents, or monkeys, which contain the virus in a latent state, e.g. lymphocytic choriomeningitis, Sabin virus, Marburg virus, type A hepatitis virus, etc. With regard to such accidents, we are almost completely powerless from the therapeutic point of view and, even poorly equipped, from the point of view of prophylaxis.

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