Forty Years of Marburg Virus

Slenczka, Werner; Klenk, Hans Dieter

doi:10.1086/520551

Cited by 88 publications

(70 citation statements)

References 14 publications

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“…Five spillover events involved tourists with defined dates of visitation to caves containing R. aegyptiacus , in the weeks just before the onset of MHF symptoms. The original 1967 outbreak was also included, and for that, a date was chosen that was one incubation period (three weeks) prior to the first shipment of infected monkeys that arrived in Frankfurt, Germany on 21 July 1967 (via London Heathrow airport) and further distributed within Germany (Marburg and Frankfurt) and to Belgrade, Yugoslavia [19]. When all 13 Marburg virus spillover events are listed by month of occurrence, the data show a temporal clustering of human infections, coinciding with the summer (mid-June through mid-September) and winter months (mid-December through mid-March) of the northern hemisphere.…”

Section: Resultsmentioning

confidence: 99%

Seasonal Pulses of Marburg Virus Circulation in Juvenile Rousettus aegyptiacus Bats Coincide with Periods of Increased Risk of Human Infection

et al. 2012

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Marburg virus (family Filoviridae) causes sporadic outbreaks of severe hemorrhagic disease in sub-Saharan Africa. Bats have been implicated as likely natural reservoir hosts based most recently on an investigation of cases among miners infected in 2007 at the Kitaka mine, Uganda, which contained a large population of Marburg virus-infected Rousettus aegyptiacus fruit bats. Described here is an ecologic investigation of Python Cave, Uganda, where an American and a Dutch tourist acquired Marburg virus infection in December 2007 and July 2008. More than 40,000 R. aegyptiacus were found in the cave and were the sole bat species present. Between August 2008 and November 2009, 1,622 bats were captured and tested for Marburg virus. Q-RT-PCR analysis of bat liver/spleen tissues indicated ∼2.5% of the bats were actively infected, seven of which yielded Marburg virus isolates. Moreover, Q-RT-PCR-positive lung, kidney, colon and reproductive tissues were found, consistent with potential for oral, urine, fecal or sexual transmission. The combined data for R. aegyptiacus tested from Python Cave and Kitaka mine indicate low level horizontal transmission throughout the year. However, Q-RT-PCR data show distinct pulses of virus infection in older juvenile bats (∼six months of age) that temporarily coincide with the peak twice-yearly birthing seasons. Retrospective analysis of historical human infections suspected to have been the result of discrete spillover events directly from nature found 83% (54/65) events occurred during these seasonal pulses in virus circulation, perhaps demonstrating periods of increased risk of human infection. The discovery of two tags at Python Cave from bats marked at Kitaka mine, together with the close genetic linkages evident between viruses detected in geographically distant locations, are consistent with R. aegyptiacus bats existing as a large meta-population with associated virus circulation over broad geographic ranges. These findings provide a basis for developing Marburg hemorrhagic fever risk reduction strategies.

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Section: Resultsmentioning

confidence: 99%

Seasonal Pulses of Marburg Virus Circulation in Juvenile Rousettus aegyptiacus Bats Coincide with Periods of Increased Risk of Human Infection

et al. 2012

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“…The genus Marburgvirus is composed of a single species, Marburg marburgvirus, which includes the subspecies MARV and Ravn virus. The first outbreak of MARV occurred simultaneously in Germany and the former Yugoslavia in August 1967, when laboratory personnel were exposed to the virus through contact with infected tissues from African green monkeys imported from Uganda (2,3). Seven of the 32 confirmed human cases (mostly primary exposures) succumbed to infection (4,5).…”

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confidence: 99%

Temporal Characterization of Marburg Virus Angola Infection following Aerosol Challenge in Rhesus Macaques

Lin

Twenhafel

Connor

et al. 2015

J Virol

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Marburg 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 (>10 7 PFU/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 wellcharacterized model of disease progression following aerosol exposure. Marburg virus (MARV) is a single-stranded negative-sense RNA virus that belongs to the family Filoviridae (1). The genus Marburgvirus is composed of a single species, Marburg marburgvirus, which includes the subspecies MARV and Ravn virus. The first outbreak of MARV occurred simultaneously in Germany and the former Yugoslavia in August 1967, when laboratory personnel were exposed to the virus through contact with infected tissues from African green monkeys imported from Uganda (2, 3). Seven of the 32 confirmed human cases (mostly primary exposures) succumbed to infection (4,5). From 1975 to 1998, subsequent MARV infections were limited to sporadic cases in selected areas of Africa, until the occurrence of two large outbreaks in the Democratic Republic of the Congo from 1998 to 2000 and Angola from 2004 to 2005 (6, 7). The case fatality rates for these outbreaks were 83% (128/154) and 90% (227/252), respectively, and established MARV disease as an important public health threat (8, 9).There are currently no licensed medical countermeasures to combat infections with filoviruses such as MARV. Due to the high pathogenicity of MARV, it is classified as a biological select agent by the U.S. Department of Health and Human Services (HHS) and a category A bioterrorism agent by the Centers for Disease Control and Prevention (CDC) (1). As such, any MARV research ...

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“…Uveitis and retinitis have been described in Rift Valley fever [16]. Marburg virus has been associated with uveitis, orchitis and hepatitis [17], and has been isolated and cultured from aqueous humor in a patient who suffered from acute anterior uveitis 3 months after infection [18].…”

Section: Pathogenesismentioning

confidence: 99%

Post-Ebolavirus disease syndrome: what do we know?

Carod-Artal

2015

Expert Review of Anti-infective Therapy

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Forty Years of Marburg Virus

Cited by 88 publications

References 14 publications

Seasonal Pulses of Marburg Virus Circulation in Juvenile Rousettus aegyptiacus Bats Coincide with Periods of Increased Risk of Human Infection

Seasonal Pulses of Marburg Virus Circulation in Juvenile Rousettus aegyptiacus Bats Coincide with Periods of Increased Risk of Human Infection

Temporal Characterization of Marburg Virus Angola Infection following Aerosol Challenge in Rhesus Macaques

Post-Ebolavirus disease syndrome: what do we know?

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