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At least 19 recordsLinked to original sources
PubMed2000

Infections by viruses of the families Bunyaviridae and Filoviridae.

Rift Valley fever is the most important bunyaviral disease of animals in Africa. The virus, transmitted by mosquitoes, causes abortions and mortality in young animals in addition to haemorrhagic fevers in humans. Although vaccines against this virus are available, the uses of these vaccines are limited because of deleterious effects or incomplete protection, justifying further studies to improve the existing vaccines or to develop others. Nairobi sheep disease is transmitted by ticks. The disease is endemic in East Africa and sporadic cases are reported in India and Sri Lanka. Other viruses transmitted by mosquitoes or midges are teratogenic in cattle or sheep, these include Akabane and related viruses in Asia, Australia and the Middle East, and Cache Valley in North America. The Marburg and Ebola viruses of the genus Filovirus are associated with epidemics in Central Africa with high fatality rates in humans; some outbreaks were related to contact with monkeys. Another subtype of Ebola virus was first described in a quarantine facility in the United States of America among cynomolgus monkeys (Macaca fascicularis) from the Philippines. The reservoir of these viruses remains unknown.

Animals↗
PubMed1999

Characteristics of Filoviridae: Marburg and Ebola viruses.

Filoviruses are enveloped, nonsegmented negative-stranded RNA viruses. The two species, Marburg and Ebola virus, are serologically, biochemically, and genetically distinct. Marburg virus was first isolated during an outbreak in Europe in 1967, and Ebola virus emerged in 1976 as the causative agent of two simultaneous outbreaks in southern Sudan and northern Zaire. Although the main route of infection is known to be person-to-person transmission by intimate contact, the natural reservoir for filoviruses still remains a mystery.

Animals↗
PubMed1995

Detection of Ebola-Reston (Filoviridae) virus antibody by dot-immunobinding assay.

Thirty human and nonhuman primate sera tested at the Centers for Disease Control by enzyme-linked immunosorbent assay (ELISA), immunofluorescent antibody assay (IFA), and Western blotting were retested at the Virus Reference Laboratory, Inc. by the dot-immunobinding assay (DIA). The Ebola-Reston strain of virus received from the Centers for Disease Control was prepared into a suitable DIA antigen as described for other antigens. All six Western blotting-positive sera were also positive by DIA, as were the five ELISA-positive sera. Testing by IFA, the original test of choice, indicated an additional four seropositives, all negative by the other test systems. Of 288 randomly selected macaque sera, 19 were also found to be Ebola-Reston virus-positive by DIA.

Animals↗
PubMed1997

Haemorrhagic fevers and ecological perturbations.

Hemorrhagic fever is a clinical and imprecise definition for several different diseases. Their main common point is to be zoonoses. These diseases are due to several viruses which belong to different families. The Flaviviridae have been known for the longest time. They include the Amaril virus that causes yellow fever and is transported by mosquitoes. Viruses that have come to light more recently belong to three other families: Arenaviridae, Bunyaviridae, and Filoviridae. They are transmitted by rodents (hantaviruses and arenaviruses) or from unknown reservoirs (Ebola Marburg). The primary cause of most outbreaks of hemorrhagic fever viruses is ecological disruption resulting from human activities. The expansion of the world population perturbs ecosystems that were stable a few decades ago and facilitates contacts with animals carrying viruses pathogenic to humans. Another dangerous human activity is the development of hospitals with poor medical hygiene. Lassa, Crimean-Congo or Ebola outbreaks are mainly nosocomial. There are also natural environmental changes: the emergence of Sin Nombre in the U.S. resulted from heavier than usual rain and snow during spring 1993 in the Four Corners. Biological industries also present risks. In 1967, collection of organs from monkeys allowed the discovery in Marburg of a new family of viruses, the Filoviridae. Hemorrhagic fever viruses are cause for worry, and the avenues to reduce their toll are still limited.

Animals↗
PubMed1993

Molecular biology and evolution of filoviruses.

The family Filoviridae contains extremely pathogenic human viruses causing a fulminating, febrile hemorrhagic disease. Filoviruses are enveloped, filamentous particles with a nonsegmented negative-strand RNA genome showing the gene arrangement 3'-NP-VP35-VP40-GP-VP30-VP24-L-5'. Genes are flanked by highly conserved transcriptional signals and are generally separated by variable intergenic regions. They are transcribed into monocistronic polyadenylated messenger RNAs which contain relatively long 5' and 3' untranslated regions. Seven structural proteins are encoded by the genome of which four form the helical nucleocapsid (NP-VP35-VP30-L), two are membrane-associated (VP40-VP24), and one is a transmembrane glycoprotein (GP). Comparison of filovirus genomes with those of other nonsegmented negative-strand RNA viruses suggest comparable mechanisms of transcription and replication and a common evolutionary lineage for all these viruses. Sequence analyses of single genes, however, showed that filoviruses are more closely related to paramyxoviruses, particularly human respiratory syncytial virus. These data support the concept of the taxonomic order Mononegavirales for all nonsegmented negative-strand RNA viruses and the classification of Marburg virus, Ebola virus, and Reston virus in the family Filoviridae, separate from the families Paramyxoviridae and Rhabdoviridae.

Animals↗
PubMed1998

A novel P/V/C gene in a new member of the Paramyxoviridae family, which causes lethal infection in humans, horses, and other animals.

In 1994, a new member of the family Paramyxoviridae isolated from fatal cases of respiratory disease in horses and humans was shown to be distantly related to morbilliviruses and provisionally called equine morbillivirus (K. Murray et al., Science 268:94-97, 1995). To facilitate characterization and classification, the virus was purified, viral proteins were identified, and the P/V/C gene was cloned and sequenced. The coding strategy of the gene is similar to that of Sendai and measles viruses, members of the Paramyxovirus and Morbillivirus genera, respectively, in the subfamily Paramyxovirinae. The P/V/C gene contains four open reading frames, three of which, P, C, and V, have Paramyxovirinae counterparts. The P and C proteins are larger and smaller, respectively, than are cognate proteins in members of the subfamily, and the V protein is made as a result of a single G insertion during transcription. The P/V/C gene has two unique features. (i) A fourth open reading frame is located between those of the C and V proteins and potentially encodes a small basic protein similar to those found in some members of the Rhabdoviridae and Filoviridae families. (ii) There is also a long untranslated 3' sequence, a feature common in Filoviridae members. Sequence comparisons confirm that although the virus is a member of the Paramyxovirinae subfamily, it displays only low levels of homology with paramyxoviruses and morbilliviruses and negligible homologies with rubulaviruses.

Amino Acid Sequence↗
PubMed2005

The role of reverse genetics systems in determining filovirus pathogenicity.

The family Filoviridae is comprised of two genera: Marburgvirus and Ebolavirus. To date minigenome systems have been developed for two Ebola viruses (Reston ebolavirus and Zaire ebolavirus [ZEBOV]) as well as for Lake Victoria marburgvirus, the sole member of the Marburgvirus genus. The use of these minigenome systems has helped characterize functions for many viral proteins in both genera and have provided valuable insight towards the development of an infectious clone system in the case of ZEBOV. The recent development of two such infectious clone systems for ZEBOV now allow effective strategies for experimental mutagenesis to study the biology and pathogenesis of one of the most lethal human pathogens.

Animals↗
PubMed2003

Vaccine research efforts for filoviruses.

Ebola and Marburg viruses belong to the family Filoviridae, and cause acute, frequently fatal, haemorrhagic fever in humans and non-human primates. No vaccines are available for human use. This review describes the status of research efforts to develop vaccines for these viruses and to identify the immune mechanisms of protection. The vaccine approaches discussed include DNA-based vaccines, and subunit vaccines vectored by adenovirus, alphavirus replicons, and vaccinia virus.

Animals↗
PubMed2005

Filovirus-like particles as vaccines and discovery tools.

Ebola and Marburg viruses are members of the family Filoviridae, which cause severe hemorrhagic fevers in humans. Filovirus outbreaks have been sporadic, with mortality rates currently ranging from 30 to 90%. Unfortunately, there is no efficacious human therapy or vaccine available to treat disease caused by either Ebola or Marburg virus infection. Expression of the filovirus matrix protein, VP40, is sufficient to drive spontaneous production and release of virus-like particles (VLPs) that resemble the distinctively filamentous infectious virions. The addition of other filovirus proteins, including virion proteins (VP)24, 30 and 35 and glycoprotein, increases the efficiency of VLP production and results in particles containing multiple filovirus antigens. Vaccination with Ebola or Marburg VLPs containing glycoprotein and VP40 completely protects rodents from lethal challenge with the homologous virus. These candidate vaccines are currently being tested for immunogenicity and efficacy in nonhuman primates. Furthermore, the Ebola and Marburg VLPs are being used as a surrogate model to further understand the filovirus life cycle, with the goal of developing rationally designed vaccines and therapeutics. Thus, in addition to their use as a vaccine, VLPs are currently being used as tools to learn lessons about filovirus pathogenesis, immunology, replication and assembly requirements.

Animals↗
PubMed1995

Differentiation of filoviruses by electron microscopy.

Cultured monolayers of MA-104, Vero 76, SW-13, and DBS-FRhL-2 cells were infected with Marburg (MBG), Ebola-Sudan (EBO-S), Ebola-Zaire (EBO-Z), and Ebola-Reston (EBO-R) viruses (Filoviridae, Filovirus) and examined by electron microscopy to provide ultrastructural details of morphology and morphogenesis of these potential human pathogens. Replication of each filovirus was seen in all cell systems employed. Filoviral particles appeared to enter host cells by endocytosis. Filoviruses showed a similar progression of morphogenic events, from the appearance of nascent intracytoplasmic viral inclusions to formation of mature virions budded through plasma membranes, regardless of serotype or host cell. However, ultrastructural differences were demonstrated between MBG and other filoviruses. MBG virions recovered from culture fluids were uniformly shorter in mean unit length than EBO-S, EBO-Z, or EBO-R particles. Examination of filovirus-infected cells revealed that intermediate MBG inclusions were morphologically distinct from EBO-S, EBO-Z, and EBO-R inclusions. No structural difference of viral inclusion material was observed among EBO-S, EBO-Z, and EBO-R. Immunoelectron microscopy showed that the filoviral matrix protein (VP40) and nucleoprotein (NP) accumulated in EBO-Z inclusions, and were closely associated during viral morphogenesis. These details facilitate the efficient and definitive diagnosis of filoviral infections by electron microscopy.

Animals↗
PubMed2004

Filovirus budding.

Family Filoviridae, which includes Ebola virus (EBOV) and Marburg virus (MARV), is a growing threat to human and non-human primate populations in central Africa. Although many facets of the filovirus life cycle remain to be deciphered, a great deal has been learned in recent years. In particular, a clearer understanding of the roles played by viral, as well as cellular, proteins in the assembly and budding processes has been achieved. This review will discuss the current state of filovirus budding research, with especial emphasis placed on the viral matrix protein VP40 and its relationship with the cellular vesicular sorting pathway. Possible budding functions of the viral glycoprotein (GP), as well as the membrane-associated viral protein 24 (VP24), will also be described, and a model for filovirus budding will be proposed.

Animals↗
PubMed1997

Filovirus-like particles detected in the leafhopper Psammotettix alienus.

Filamentous particles were detected by negative contrast electron microscopy of extracts from the leafhopper Psammotettix alienus (Dahlbom) reared on healthy Festuca gigantea plants. The particles were straight, slightly curved or flexuous, sometimes with the one end curled into a ring with an outer diameter of about 200 nm. Length distribution of 280 particles showed a minor and a major group with median length of about 600 and 1,100 nm, respectively. Projections, 8-10 nm long and about 10 nm apart, were evenly distributed on the surface. The diameter of particles, including projections, was 55-70 nm. Partly disintegrated revealed an internal structure about 30 nm in diameter and with cross-striation with a periodicity of 5-5.5 nm. In some particles, a central canal, 5-10 nm in diameter, could be seen at one end. Ultramicrotomy of leafhopper heads showed that some cells contained intracytoplasmic clusters of particles together with filamentous structures. The particles described in this paper resemble virions in the virus family Filoviridae, but can be distinguished by having a smaller particle diameter. The name Taastrup virus is suggested for the putative virus from Psammotettix alienus, according to the place it was first detected.

Animals↗
PubMed2005

[Haemorrhagic fever viruses, possible bioterrorist use].

The majority of haemorrhagic fever viruses are responsible for various clinical manifestations, the mutual characteristics of which are fever and haemorrhage in 5 to 70% of cases. All degrees of severity can be observed, ranging from isolated fever to multi-organ failure and death. These viruses belong to one of the following families: filoviridae, arenaviridae, bunyaviridae, and flaviviridae. They must be considered as dangerous biological weapons that could potentially be used. Most of the viruses responsible for haemorrhagic fever can be transmitted to humans through the air in spray form, except the dengue virus and the agents of haemorrhagic fever from the Congo Crimea and the haemorrhagic fever with renal syndrome that are difficult to handle in cell culture. In the event of a bioterrorist act, the management of persons infected or suspected of being so will be made by the referent departments of infectious diseases, defined by the French Biotox plan. Management includes isolation, confirmation or invalidation of the diagnosis and rapid initiation of treatment with ribavirin. Ribavirin is recommended for the treatment and prophylaxis of arenavirus and bunyavirus infections; it is not effective for the other families of virus. Except for yellow fever, there is no vaccination for the other forms of viral haemorrhagic fever.

Antiviral Agents↗
PubMed2000

Hemorrhagic fever virus-induced changes in hemostasis and vascular biology.

Viral hemorrhagic fever (VHF) denotes a virus-induced acute febrile, hemorrhagic disease reported from wide areas of the world. Hemorrhagic fever (HF) viruses are encapsulated, single-stranded RNA viruses that are associated with insect or rodent vectors whose interaction with humans defines the mode of disease transmission. There are 14 HF viruses, which belong to four viral families: Arenaviridae, Bunyaviridae, Filoviridae and Flaviviridae. This review presents, in order, the following aspects of VHF: (1) epidemiology, (2) anomalies of platelets and coagulation factors, (3) vasculopathy, (4) animal models of VHFs, (5) pathogenic mechanisms, and (6) treatment and future studies. HF viruses produce the manifestations of VHFs either by direct effects on cellular functions or by activation of immune and inflammatory pathways. In Lassa fever, Rift Valley fever and Crimean-Congo HF, the main feature of fatal illness appears to be impaired/delayed cellular immunity, which leads to unchecked viremia. However, in HF with renal syndrome and dengue HF, the immune response plays an active role in disease pathogenesis. The interplay of hemostasis, immune response, and inflammation is very complex. Molecular biologic techniques and the use of animal models have helped to unravel some of these interactions.

Animals↗
PubMed2025

Conserved Filovirus Proteins as Targets of Broad-Spectrum Antivirals.

Filoviruses are enveloped, non-segmented, negative-strand RNA viruses belonging to the Filoviridae family, which includes five genera: Ebolavirus, Marburgvirus, Cuevavirus, Striavirus, and Thamnovirus. Members of this family cause severe and, often, fatal hemorrhagic fevers in humans and non-human primates, with high mortality rates. To date, only two filoviruses, Ebola virus (EBOV) and Marburg virus (MARV), are known to infect humans and are listed as priority pathogens by the World Health Organization due to their potential for re-emergence and the current lack of effective vaccines and antiviral treatments. In this study, we identify and characterize conserved binding sites within key filoviral proteins to support the development of broad-spectrum, direct-acting antiviral agents. We validated the significance of these conserved regions for drug discovery using existing experimental data. Our analysis revealed notably high sequence similarity among proteins from filoviruses capable of infecting humans (EBOV, TAFV, BDBV, SUDV, MARV, and RAVV) compared to those from non-zoonotic species, with the highest conservation observed in the L and VP40 proteins-both critical for viral genome transcription and replication. Furthermore, we compiled and analyzed available experimental data on known antiviral compounds targeting these proteins, identifying several agents with cross-filovirus activity, including Galidesivir, Remdesivir, and Favipiravir. The integrated approach described here-combining sequence and structural conservation analysis with chemical structure and antiviral activity data-demonstrates a strategy that could be extended to the development of broad-spectrum therapeutics across multiple viral families.

Broad Spectrum Antiviral↗
PubMed1998

Zoonoses and haemorrhagic fever.

Virus zoonoses causing haemorrhagic fever have been recognized in three major families: Arenaviridae, Bunyaviridae and Filoviridae. All are negative-stranded RNA viruses, with genomes in two segments, three segments, or non-segmented, respectively. Acquisition of haemorrhagic fever in man generally requires close contact with a vertebrate vector species, usually rodents, for the arenaviruses and bunyaviruses. In the case of filoviruses, the vector is currently unknown, but these viruses may infect monkeys, and may contaminate cell cultures prepared from them. Both bunyavirus and arenavirus haemorrhagic fevers have arisen in humans following exposure to rodents, and in the case of Hantaan, a virus causing haemorrhagic fever with renal syndrome (HFRS), there have been numerous laboratory-acquired infections among animal care workers. As the technology to differentiate virus species has improved, it has become clear that there are numerous potentially hazardous viruses capable of causing HFRS or hantavirus pulmonary syndrome (HPS) within the feral rodent population. In many cases it would be desirable to introduce screening methods for such viruses before preparing cell cultures from these rodent or simian species that will be used to prepare biological products for human use.

Africa↗