Filoviridae Infections
Filoviridae
Marburg Virus Disease
Marburgvirus
Ebolavirus
Filoviral haemorrhagic fevers. (1/38)
Sensationalised accounts of wards of dying patients have fueled intense public fascination with filoviruses and highlighted the global threat of emerging and re-emerging infectious diseases. Filoviruses are the prototypical emerging pathogens: they cause a haemorrhagic disease of high case-fatality associated with explosive outbreaks due to person-to-person transmission, have no known treatment, occur unpredictably, and have an unknown reservoir. In truth, since their initial discovery in 1967, only a handful of filoviral outbreaks have occurred, mostly in remote locations. However, the documented occurrence of secondary cases in locations far from endemic areas validates the concern that filoviruses have the potential to cause unprecedented outbreaks in the future. (+info)The role of the Type I interferon response in the resistance of mice to filovirus infection. (2/38)
Adult immunocompetent mice inoculated with Ebola (EBO) or Marburg (MBG) virus do not become ill. A suckling-mouse-passaged variant of EBO Zaire '76 ('mouse-adapted EBO-Z') causes rapidly lethal infection in adult mice after intraperitoneal (i.p.) inoculation, but does not cause apparent disease when inoculated subcutaneously (s.c.). A series of experiments showed that both forms of resistance to infection are mediated by the Type I interferon response. Mice lacking the cell-surface IFN-alpha/beta receptor died within a week after inoculation of EBO-Z '76, EBO Sudan, MBG Musoke or MBG Ravn, or after s.c. challenge with mouse-adapted EBO-Z. EBO Reston and EBO Ivory Coast did not cause illness, but immunized the mice against subsequent challenge with mouse-adapted EBO-Z. Normal adult mice treated with antibodies against murine IFN-alpha/beta could also be lethally infected with i.p.-inoculated EBO-Z '76 or EBO Sudan and with s.c.-inoculated mouse-adapted EBO-Z. Severe combined immunodeficient (SCID) mice became ill 3-4 weeks after inoculation with EBO-Z '76, EBO Sudan or MBG Ravn, but not the other viruses. Treatment with anti-IFN-alpha/beta antibodies markedly accelerated the course of EBO-Z '76 infection. Antibody treatment blocked the effect of a potent antiviral drug, 3-deazaneplanocin A, indicating that successful filovirus therapy may require the active participation of the Type I IFN response. Mice lacking an IFN-alpha/beta response resemble primates in their susceptibility to rapidly progressive, overwhelming filovirus infection. The outcome of filovirus transfer between animal species appears to be determined by interactions between the virus and the innate immune response. (+info)Ecologic and geographic distribution of filovirus disease. (3/38)
We used ecologic niche modeling of outbreaks and sporadic cases of filovirus-associated hemorrhagic fever (HF) to provide a large-scale perspective on the geographic and ecologic distributions of Ebola and Marburg viruses. We predicted that filovirus would occur across the Afrotropics: Ebola HF in the humid rain forests of central and western Africa, and Marburg HF in the drier and more open areas of central and eastern Africa. Most of the predicted geographic extent of Ebola HF appear to have been observed; Marburg HF has the potential to occur farther south and east. Ecologic conditions appropriate for Ebola HF are also present in Southeast Asia and the Philippines, where Ebola Reston is hypothesized to be distributed. This first large-scale ecologic analysis provides a framework for a more informed search for taxa that could constitute the natural reservoir for this virus family. (+info)Ebola and Marburg virus-like particles activate human myeloid dendritic cells. (4/38)
The filoviruses, Ebola (EBOV) and Marburg (MARV), are potential global health threats, which cause deadly hemorrhagic fevers. Although both EBOV and MARV logarithmically replicate in dendritic cells (DCs), these viruses do not elicit DC cytokine secretion and fail to activate and mature infected DCs. Here, we employed virus-like particles (VLPs) of EBOV and MARV to investigate whether these genome-free particles maintain similar immune evasive properties as authentic filoviruses. Confocal microscopy indicated that human myeloid-derived DCs readily took up VLPs. However, unlike EBOV and MARV, VLPs induced maturation of DCs including upregulation of costimulatory molecules (CD40, CD80, CD86), major histocompatibility complex (MHC) class I and II surface antigens, and the late DC maturation marker CD83. The chemokine receptors CCR5 and CCR7 were also modulated on VLP-stimulated DCs, indicating that DC could migrate following VLP exposure. Furthermore, VLPs also elicited DC secretion of the pro-inflammatory cytokines TNF-alpha, IL-8, IL-6, and MIP-1alpha. Most significantly, in stark contrast to DC treated with intact EBOV or MARV, DC stimulated with EBOV or MARV VLPs showed enhanced ability to support human T-cell proliferation in an allogenic mixed lymphocyte response (MLR). Thus, our findings suggest that unlike EBOV and MARV, VLPs are effective stimulators of DCs and have potential in enhancing innate and adaptive immune responses. (+info)Potential mammalian filovirus reservoirs. (5/38)
Ebola and Marburg viruses are maintained in unknown reservoir species; spillover into human populations results in occasional human cases or epidemics. We attempted to narrow the list of possibilities regarding the identity of those reservoir species. We made a series of explicit assumptions about the reservoir: it is a mammal; it supports persistent, largely asymptomatic filovirus infections; its range subsumes that of its associated filovirus; it has coevolved with the virus; it is of small body size; and it is not a species that is commensal with humans. Under these assumptions, we developed priority lists of mammal clades that coincide distributionally with filovirus outbreak distributions and compared these lists with those mammal taxa that have been tested for filovirus infection in previous epidemiologic studies. Studying the remainder of these taxa may be a fruitful avenue for pursuing the identity of natural reservoirs of filoviruses. (+info)Dendritic cells in viral pathogenesis: protective or defective? (6/38)
Dendritic cells (DC) are potent antigen-presenting cells that are critical in the initiation of immune responses to control and/or eliminate viral infections. Recent studies have investigated the effects of virus infection on the biology of DC. This review summarizes these changes, focusing on both the DC parameters affected and the viral factors involved. In addition, the central role of DC biology in the pathogenesis of several viral families, including herpesviruses, paramyxoviruses and retroviruses, is explored. The field of pathogen recognition by DC is addressed, focusing on its role in protecting the host from viral infection, as well as the ability of viruses to exploit such host receptor ligation and signalling to their replicative advantage. The hypothesis is proposed that virus and host have evolved a symbiotic relationship to ensure both viral transmission and host survival. (+info)Rapid molecular strategy for filovirus detection and characterization. (7/38)
Filoviruses have the capacity to cause lethal outbreaks of hemorrhagic fever in primates. Here we present a simple consensus reverse transcription-PCR method for filovirus recognition and characterization and demonstrate its utility with all known filovirus strains. Phylogenetic assignment is achieved by automated web-based sequence analysis of amplification products. (+info)Outbreaks of filovirus hemorrhagic fever: time to refocus on the patient. (8/38)
In the 40 years since the recognition of filoviruses as agents of lethal human disease, there have been no specific advances in antiviral therapies or vaccines and few clinical studies on the efficacy of supportive care. On 20 September 2006, experts from 14 countries representing 68 institutions integrally involved in the response to outbreaks of filovirus hemorrhagic fever gathered at the National Microbiology Laboratory of the Public Health Agency of Canada in Winnipeg to discuss possible remedies for this grim situation, in a unique workshop entitled "Marburg and Ebola Hemorrhagic Fever: Feasibility of Prophylaxis and Therapy." A summary of the opportunities for and challenges to improving treatment of filovirus hemorrhagic fevers is presented here. (+info)Filoviridae infections refer to diseases caused by viruses belonging to the Filoviridae family, which includes Ebola virus and Marburg virus. These viruses are characterized by filamentous or threadlike shapes and can cause severe hemorrhagic fever in humans and primates. The infections are associated with high mortality rates, ranging from 25% to 90%, depending on the specific virus and strain.
Transmission of Filoviridae viruses occurs through direct contact with infected bodily fluids or contaminated surfaces. The initial symptoms of infection include fever, muscle pain, headache, and sore throat, followed by vomiting, diarrhea, rash, and impaired organ function. In severe cases, the disease can progress to hemorrhagic fever, characterized by internal and external bleeding, shock, and multi-organ failure.
Currently, there are no approved vaccines or antiviral treatments for Filoviridae infections, although several experimental therapies and vaccines are under development. Prevention measures include avoiding contact with infected individuals, practicing good hygiene, and using personal protective equipment when caring for sick patients.
Filoviridae is a family of negative-sense, single-stranded RNA viruses that includes three genera: Ebolavirus, Marburgvirus, and Cuevavirus. These viruses are known to cause severe hemorrhagic fever in humans and nonhuman primates, with high fatality rates. The most well-known members of this family are Ebola virus and Marburg virus.
The virions of Filoviridae are filamentous, often having a "U," "6," or "hook" shape, and can be up to 14,000 nanometers in length. The genome of these viruses is non-segmented and contains seven genes that encode for structural proteins and enzymes necessary for replication.
Transmission of Filoviridae occurs through direct contact with infected bodily fluids or contaminated surfaces, and infection can result in a range of symptoms including fever, severe headache, muscle pain, weakness, fatigue, and hemorrhage. There are currently no approved vaccines or antiviral treatments for Filoviridae infections, although several are in development.
Marburg Virus Disease (MVD) is an acute and often fatal viral hemorrhagic fever illness caused by the Marburg virus, a member of the filovirus family. It's a highly infectious disease that can be transmitted from human to human through direct contact with infected bodily fluids, tissues, or indirectly through contaminated surfaces and materials.
The incubation period for MVD ranges from 2 to 21 days, after which symptoms such as fever, chills, headache, muscle aches, severe malaise, and progressive weakness appear. Around the fifth day of illness, a maculopapular rash may occur, followed by diarrhea, nausea, vomiting, abdominal pain, and non-bloody stools. In some cases, patients may develop severe bleeding disorders, shock, liver failure, and multi-organ dysfunction, which can lead to death in 24-48 hours.
Currently, there are no approved vaccines or antiviral treatments for MVD, but supportive care is crucial for managing the symptoms of the disease. Preventive measures such as avoiding contact with infected individuals and their bodily fluids, wearing protective clothing, and practicing good hygiene can help prevent the spread of the virus.
According to the World Health Organization (WHO), Marburgviruses are toxiviral hemorrhagic fever-causing agents that belong to the Filoviridae family, which also includes Ebolaviruses. These enveloped, non-segmented, negative-stranded RNA viruses cause a severe and often fatal illness in humans and non-human primates. The Marburg virus was initially discovered in 1967, after simultaneous outbreaks occurred in laboratories in Marburg and Frankfurt, Germany, and in Belgrade, Yugoslavia (now Serbia).
The virions of Marburgviruses are typically filamentous or U-shaped and measure approximately 80 nm in diameter. The genome consists of a single non-segmented, negative-sense RNA molecule that encodes seven structural proteins: nucleoprotein (NP), polymerase cofactor protein (VP35), matrix protein (VP40), glycoprotein (GP), transcription activator protein (VP30), RNA-dependent RNA polymerase (L), and a small hydrophobic protein (sVP24 or VP80).
Marburgviruses are primarily transmitted to humans through contact with the bodily fluids of infected animals, such as bats and non-human primates. Human-to-human transmission can occur via direct contact with infected individuals' blood, secretions, organs, or other bodily fluids, as well as through contaminated surfaces and materials.
The incubation period for Marburg virus disease (MVD) typically ranges from 2 to 21 days. Initial symptoms include fever, chills, headache, muscle aches, and general malaise. As the disease progresses, patients may develop severe watery diarrhea, abdominal pain, nausea, vomiting, and unexplained bleeding or bruising. In fatal cases, MVD can cause multi-organ failure, shock, and death, often within 7 to 14 days after symptom onset.
Currently, there are no approved vaccines or antiviral treatments specifically for Marburg virus infections. However, supportive care, such as fluid replacement, electrolyte management, and treatment of secondary infections, can help improve outcomes for MVD patients. Preventive measures, including the use of personal protective equipment (PPE) and proper infection control practices, are crucial to reducing the risk of transmission during outbreaks.
Ebolavirus is a genus of viruses in the family Filoviridae, order Mononegavirales. It is named after the Ebola River in the Democratic Republic of Congo (formerly Zaire), where the virus was first identified in 1976. There are six species of Ebolavirus, four of which are known to cause disease in humans: Zaire ebolavirus, Sudan ebolavirus, Bundibugyo ebolavirus, and Tai Forest ebolavirus (formerly Cote d'Ivoire ebolavirus). The fifth species, Reston ebolavirus, is known to cause disease in non-human primates and pigs, but not in humans. The sixth and most recently identified species, Bombali ebolavirus, has not been associated with any human or animal diseases.
Ebolaviruses are enveloped, negative-sense, single-stranded RNA viruses that cause a severe and often fatal hemorrhagic fever in humans and non-human primates. The virus is transmitted to people from wild animals and spreads in the human population through human-to-human transmission. Fruit bats of the Pteropodidae family are considered to be the natural host of Ebolavirus.
The symptoms of Ebolavirus disease (EVD) typically include fever, severe headache, muscle pain, weakness, fatigue, and sore throat, followed by vomiting, diarrhea, rash, impaired kidney and liver function, and in some cases, both internal and external bleeding. The case fatality rate of EVD is variable but has been historically high, ranging from 25% to 90% in past outbreaks depending on the species and the quality of medical care. There are no licensed specific treatments or vaccines available for EVD, although several promising candidates are currently under development.
Ebola Hemorrhagic Fever (EHF) is a severe, often fatal illness in humans. It is one of the five identified subtypes of the Ebolavirus. The virus is transmitted to people from wild animals and spreads in the human population through human-to-human transmission.
The early symptoms include sudden onset of fever, fatigue, muscle pain, headache and sore throat. This is followed by vomiting, diarrhea, rash, symptoms of impaired kidney and liver function, and in some cases, both internal and external bleeding.
Laboratory findings include low white blood cell and platelet counts and elevated liver enzymes.
The virus is introduced into the human population through close contact with the blood, secretions, organs or other bodily fluids of infected animals such as fruit bats, porcupines and non-human primates. Then it spreads in communities through human-to-human transmission via direct contact (through broken skin or mucous membranes) with the blood, secretions, organs or other bodily fluids of infected people, and with surfaces and materials contaminated with these fluids.
Healthcare workers have frequently been infected while treating patients with suspected or confirmed EVD due to a lack of adequate infection prevention and control measures.
There are currently no approved specific antiviral drugs or vaccines for Ebola. Several promising treatments and vaccine candidates are being evaluated.