Arenaviruses, New World
Hemorrhagic Fever, American
Hemorrhagic Fevers, Viral
Hemorrhagic Fever, Crimean
Hemorrhagic Fever Virus, Crimean-Congo
Hemorrhagic Fever, Ebola
Hemorrhagic Fever with Renal Syndrome
Marburg Virus Disease
Experimental infection of the cane mouse Zygodontomys brevicauda (family Muridae) with guanarito virus (Arenaviridae), the etiologic agent of Venezuelan hemorrhagic fever. (1/73)Chronic infections in specific rodents appear to be crucial to the long-term persistence of arenaviruses in nature. The cane mouse, Zygodontomys brevicauda, is a natural host of Guanarito virus (family Arenaviridae), the etiologic agent of Venezuelan hemorrhagic fever. The purpose of this study was to elucidate the natural history of Guanarito virus infection in Z. brevicauda. Thirty-nine laboratory-reared cane mice each were inoculated subcutaneously with 3.0 log10 plaque-forming units of the Guanarito virus prototype strain INH-95551. No lethality was associated with infection in any animal, regardless of age at inoculation. The 13 newborn, 14 weanling, and 8 of the 12 adult animals developed chronic viremic infections characterized by persistent shedding of infectious virus in oropharyngeal secretions and urine. These findings indicate that Guanarito virus infection in Z. brevicauda can be chronic and thus support the concept that this rodent species is the natural reservoir of Guanarito virus. (+info)
Lassa and Mopeia virus replication in human monocytes/macrophages and in endothelial cells: different effects on IL-8 and TNF-alpha gene expression. (2/73)Cells of the mononuclear and endothelial lineages are targets for viruses which cause hemorrhagic fevers (HF) such as the filoviruses Marburg and Ebola, and the arenaviruses Lassa and Junin. A recent model of Marburg HF pathogenesis proposes that virus directly causes endothelial cell damage and macrophage release of TNF-alpha which increases the permeability of endothelial monolayers [Feldmann et al. , 1996]. We show that Lassa virus replicates in human monocytes/macrophages and endothelial cells without damaging them. Human endothelial cells (HUVEC) are highly susceptible to infection by both Lassa and Mopeia (a non-pathogenic Lassa-related arenavirus). Whereas monocytes must differentiate into macrophages before supporting even low level production of these viruses, the virus yields in the culture medium of infected HUVEC cells reach more than 7 log10 PFU/ml without cellular damage. In contrast to filovirus, Lassa virus replication in monocytes/macrophages fails to stimulate TNF-alpha gene expression and even down-regulates LPS-stimulated TNF-alpha mRNA synthesis. The expression of IL-8, a prototypic proinflammatory CXC chemokine, was also suppressed in Lassa virus infected monocytes/macrophages and HUVEC on both the protein and mRNA levels. This contrasts with Mopeia virus infection of HUVEC in which neither IL-8 mRNA nor protein are reduced. The cumulative down-regulation of TNF-alpha and IL-8 expression could explain the absence of inflammatory and effective immune responses in severe cases of Lassa HF. (+info)
Genetic diversity among Lassa virus strains. (3/73)The arenavirus Lassa virus causes Lassa fever, a viral hemorrhagic fever that is endemic in the countries of Nigeria, Sierra Leone, Liberia, and Guinea and perhaps elsewhere in West Africa. To determine the degree of genetic diversity among Lassa virus strains, partial nucleoprotein (NP) gene sequences were obtained from 54 strains and analyzed. Phylogenetic analyses showed that Lassa viruses comprise four lineages, three of which are found in Nigeria and the fourth in Guinea, Liberia, and Sierra Leone. Overall strain variation in the partial NP gene sequence was found to be as high as 27% at the nucleotide level and 15% at the amino acid level. Genetic distance among Lassa strains was found to correlate with geographic distance rather than time, and no evidence of a "molecular clock" was found. A method for amplifying and cloning full-length arenavirus S RNAs was developed and used to obtain the complete NP and glycoprotein gene (GP1 and GP2) sequences for two representative Nigerian strains of Lassa virus. Comparison of full-length gene sequences for four Lassa virus strains representing the four lineages showed that the NP gene (up to 23.8% nucleotide difference and 12.0% amino acid difference) is more variable than the glycoprotein genes. Although the evolutionary order of descent within Lassa virus strains was not completely resolved, the phylogenetic analyses of full-length NP, GP1, and GP2 gene sequences suggested that Nigerian strains of Lassa virus were ancestral to strains from Guinea, Liberia, and Sierra Leone. Compared to the New World arenaviruses, Lassa and the other Old World arenaviruses have either undergone a shorter period of diverisification or are evolving at a slower rate. This study represents the first large-scale examination of Lassa virus genetic variation. (+info)
Extreme genetic diversity among Pirital virus (Arenaviridae) isolates from western Venezuela. (4/73)Pirital-like virus isolates from rodents collected in a variety of habitats within a six-state area of central Venezuela were analyzed genetically by amplifying a portion of the nucleocapsid protein gene using RT-PCR. Comparisons of the sequences from 30 selected Pirital-like virus isolates demonstrated up to 26% divergence in nucleotide sequences and up to 16% divergence in deduced amino acid sequences. Within the Pirital monophyletic group, 14 distinct lineages or genotypes, differing by at least 6% in nucleotide sequences, were identified. Although sample sizes were small for some lineages, many of the different genotypes were sampled in only one region or locality, suggesting allopatric divergence. Complement fixation tests with representatives of the most divergent Pirital virus lineages failed to delineate multiple species or subtypes within the Pirital clade. These results indicate that the previously proposed 12% nucleocapsid protein amino acid sequence divergence cutoff value for delineating arenavirus species is not appropriate for the entire family. When individual clones were examined from PCR amplicons, a mean of 0.17% sequence diversity vs the consensus sequences was detected, suggesting diverse quasispecies populations within infected rodent hosts. Possible explanations for the extreme genetic diversity within and among Pirital virus populations in infected rodents are discussed. (+info)
Generation of "natural killer cell-escape" variants of Pichinde virus during acute and persistent infections. (5/73)Pichinde virus (PV) strain AN 3739 was determined to be sensitive to natural killer (NK) cells in vivo by enhanced replication in NK-cell-depleted mice. An NK-sensitive subclone (PV-NKs1) was serially passed in mice whose NK cells had previously been activated by an interferon inducer, and two plaque isolates were shown to be resistant to NK cells but not to interferon. Inoculation of severe-combined-immunodeficient mice with PV-NKs1 led to a persistent infection resulting in an NK-resistant viral population. This is the first demonstration of the isolation of viral "NK-escape" variants, as defined by the ability of the virus to replicate in vivo. (+info)
Posttranslational modification of alpha-dystroglycan, the cellular receptor for arenaviruses, by the glycosyltransferase LARGE is critical for virus binding. (6/73)The receptor for lymphocytic choriomeningitis virus (LCMV), the human pathogenic Lassa fever virus (LFV), and clade C New World arenaviruses is alpha-dystroglycan (alpha-DG), a cell surface receptor for proteins of the extracellular matrix (ECM). Specific posttranslational modification of alpha-DG by the glycosyltransferase LARGE is critical for its function as an ECM receptor. In the present study, we show that LARGE-dependent modification is also crucial for alpha-DG's function as a cellular receptor for arenaviruses. Virus binding involves the mucin-type domain of alpha-DG and depends on modification by LARGE. A crucial role of the LARGE-dependent glycosylation of alpha-DG for virus binding is found for several isolates of LCMV, LFV, and the arenaviruses Mobala and Oliveros. Since the posttranslational modification by LARGE is crucial for alpha-DG recognition by both arenaviruses and the host-derived ligand laminin, it also influences competition between virus and laminin for alpha-DG. Hence, LARGE-dependent glycosylation of alpha-DG has important implications for the virus-host cell interaction and the pathogenesis of LFV in humans. (+info)
Molecular organization of Junin virus S RNA: complete nucleotide sequence, relationship with other members of the Arenaviridae and unusual secondary structures. (7/73)In this study, overlapping cDNA clones covering the entire S RNA molecule of Junin virus, an arenavirus that causes Argentine haemorrhagic fever, were generated. The complete sequence of this 3400 nucleotide RNA was determined using the dideoxynucleotide chain termination method. The nucleocapsid protein (N) and the glycoprotein precursor (GPC) genes were identified as two non-overlapping open reading frames of opposite polarity, encoding primary translation products of 564 and 481 amino acids, respectively. Intracellular processing of the latter yields the glycoproteins found in the viral envelope. Comparison of the Junin virus N protein with the homologous proteins of other arenaviruses indicated that amino acid sequences are conserved, the identity ranging from 46 to 76%. The N-terminal half of GPC exhibits an even higher degree of conservation (54 to 82%), whereas the C-terminal half is less conserved (21 to 50%). In all comparisons the highest level of amino acid sequence identity was seen when Junin virus and Tacaribe virus sequences were aligned. The nucleotide sequence at the 5' end of Junin virus S RNA is not identical to that determined of the other sequenced arenaviruses. However, it is complementary to the 3'-terminal sequences and may form a very stable panhandle structure (delta G-242.7 kJ/mol) involving the complete non-coding regions upstream from both the N and GPC genes. In addition, a distinct secondary structure was identified in the intergenic region, downstream from the coding sequences; Junin virus S RNA shows a potential secondary structure consisting of two hairpin loops (delta G -163.2 and -239.3 kJ/mol) instead of the single hairpin loop that is usually found in other arenaviruses. The analysis of the arenavirus S RNA nucleotide sequences and their encoded products is discussed in relation to structure and function. (+info)
Receptor use by pathogenic arenaviruses. (8/73)The arenavirus family contains several important human pathogens including Lassa fever virus (LASV), lymphocytic choriomeningitis virus (LCMV) and the New World clade B viruses Junin (JUNV) and Machupo (MACV). Previously, alpha-dystroglycan (alpha-DG) was identified as a receptor recognized by LASV and certain strains of LCMV. However, other studies have suggested that alpha-DG is probably not used by the clade B viruses, and the receptor(s) for these pathogens is currently unknown. Using pseudotyped retroviral vectors displaying arenavirus glycoproteins (GPs), we are able to explore the role played by the GP in viral entry in the absence of other viral proteins. By examining the ability of the vectors to transduce DG knockout murine embryonic stem (ES) cells, we have confirmed that LASV has an absolute requirement for alpha-DG in these cells. However, the LCMV GP can still direct substantial entry into murine ES cells in the absence of alpha-DG, even when the GP from the clone 13 variant is used that has previously been reported to be highly dependent on alpha-DG for entry. We also found that neither LASV or LCMV pseudotyped vectors were able to transduce human or murine lymphocytes, presumably due to the glycosylation state of alpha-DG in these cells. In contrast, the JUNV and MACV GPs displayed broad tropism on human, murine and avian cell types, including lymphocytes, and showed no requirement for alpha-DG in murine ES cells. These findings highlight the importance of molecules other than alpha-DG for arenavirus entry. An alternate receptor is present on murine ES cells that can be used by LCMV but not by LASV, and which is not available on human or murine lymphocytes, while a distinct and widely expressed receptor(s) is used by the clade B viruses. (+info)
Arenaviridae is a family of viruses that includes several species known to cause disease in humans and animals. The name "Arenaviridae" comes from the Latin word "arena," meaning "sand," due to the sandy appearance of these viruses when viewed under an electron microscope.
The virions (complete virus particles) of Arenaviridae are typically enveloped, spherical or pleomorphic in shape, and measure between 50-300 nanometers in diameter. The genome of Arenaviridae viruses is composed of two single-stranded, negative-sense RNA segments called the L (large) segment and the S (small) segment. These segments encode for several viral proteins, including the glycoprotein (GP), nucleoprotein (NP), and the RNA-dependent RNA polymerase (L).
Arenaviridae viruses are primarily transmitted to humans through contact with infected rodents or their excreta. Some of the most well-known human pathogens in this family include Lassa fever virus, Junín virus, Machupo virus, and Guanarito virus, which can cause severe hemorrhagic fevers. Other Arenaviridae viruses, such as lymphocytic choriomeningitis virus (LCMV), can cause milder illnesses in humans, including fever, rash, and meningitis.
Prevention and control of Arenaviridae infections typically involve reducing exposure to infected rodents and their excreta, as well as the development of vaccines and antiviral therapies for specific viruses in this family.
Arenaviridae infections are viral illnesses caused by members of the Arenaviridae family of viruses, which include several Old World and New World arenaviruses. These viruses are primarily transmitted to humans through contact with infected rodents or their excreta.
Old World arenaviruses include Lassa fever virus, Lymphocytic choriomeningitis virus (LCMV), and Lujo virus, among others. They are endemic in Africa and can cause severe hemorrhagic fever with high mortality rates.
New World arenaviruses, found mainly in the Americas, include Junin virus, Machupo virus, Guanarito virus, and Sabia virus. These viruses can cause hemorrhagic fever as well, although their severity varies.
In general, Arenaviridae infections can present with a wide range of symptoms, from mild flu-like illness to severe hemorrhagic fever, depending on the specific virus and the individual's immune status. Treatment typically involves supportive care, while some viruses have specific antiviral therapies available. Prevention measures include avoiding contact with rodents and their excreta, as well as implementing public health interventions to control rodent populations in endemic areas.
Arenaviruses, New World, are a group of viruses in the Arenaviridae family that primarily infect rodents and can cause disease in humans. They are named after the Latin word "arena" which means "sand" because of the sandy-like appearance of their virions when viewed under an electron microscope.
New World arenaviruses include several different species, such as Junín virus, Machupo virus, Guanarito virus, and Sabia virus, among others. These viruses are endemic to certain regions in the Americas, particularly in South America. They are transmitted to humans through close contact with infected rodents or their excreta, and can cause severe hemorrhagic fever with high fatality rates if left untreated.
Some New World arenaviruses, such as Junín virus and Machupo virus, have been associated with outbreaks of human disease in the past, while others, like Guanarito virus and Sabia virus, have caused sporadic cases of illness. There are currently no vaccines available for most New World arenaviruses, although research is ongoing to develop effective countermeasures against these viruses.
Arenavirus is a type of virus that belongs to the family Arenaviridae. These viruses are enveloped and have a single-stranded, bi-segmented RNA genome. They are named after the Latin word "arena" which means "sand" because their virions contain ribosomes which resemble sand granules when viewed under an electron microscope.
Arenaviruses are primarily associated with rodents and can cause chronic infection in their natural hosts. Some arenaviruses can also infect humans and other animals, causing severe hemorrhagic fevers. Examples of human diseases caused by arenaviruses include Lassa fever, Argentine hemorrhagic fever, Bolivian hemorrhagic fever, and Venezuelan hemorrhagic fever.
These viruses are typically transmitted to humans through contact with infected rodents or their excreta, but some can also be spread from person to person through close contact with an infected individual's blood or other bodily fluids. There are currently no vaccines available for most arenaviruses, and treatment is primarily supportive, focusing on managing symptoms and complications.
Hemorrhagic fever, American is a group of viral diseases that are transmitted to humans by infected ticks, mosquitoes or rodents. The most common types of American hemorrhagic fevers include:
1. Hantavirus Pulmonary Syndrome (HPS): It is caused by Sin Nombre virus and is transmitted to humans through inhalation of aerosolized urine, droppings or saliva of infected rodents.
2. Colorado Tick Fever (CTF): It is caused by a Coltivirus and is transmitted to humans through the bite of an infected tick.
3. Venezuelan Equine Encephalitis (VEE): It is caused by an Alphavirus and is transmitted to humans through the bite of an infected mosquito.
4. Eastern Equine Encephalitis (EEE) and Western Equine Encephalitis (WEE): They are also caused by Alphaviruses and are transmitted to humans through the bite of an infected mosquito.
These diseases are called hemorrhagic fevers because they are characterized by bleeding disorders, high fever, muscle and joint pain, headache, and fatigue. In severe cases, they can lead to shock, organ failure, and death. There are no specific treatments for these diseases, but early detection and supportive care can improve outcomes. Prevention measures include avoiding contact with rodents, using insect repellent, and wearing protective clothing in areas where the diseases are common.
**Hemorrhagic fevers, viral** are a group of severe, potentially fatal illnesses caused by viruses that affect the body's ability to regulate its blood vessels and clotting abilities. These viruses belong to several different families including *Filoviridae* (e.g., Ebola, Marburg), *Arenaviridae* (e.g., Lassa, Machupo), *Bunyaviridae* (e.g., Hantavirus, Crimean-Congo hemorrhagic fever virus) and *Flaviviridae* (e.g., Dengue, Yellow Fever).
The initial symptoms are non-specific and include sudden onset of fever, fatigue, muscle aches, joint pains, headache, and vomiting. As the disease progresses, it may lead to capillary leakage, internal and external bleeding, and multi-organ failure resulting in shock and death in severe cases.
The transmission of these viruses can occur through various means depending on the specific virus. For example, some are transmitted via contact with infected animals or their urine/feces (e.g., Hantavirus), others through insect vectors like ticks (Crimean-Congo hemorrhagic fever) or mosquitoes (Dengue, Yellow Fever), and yet others through direct contact with infected body fluids (Ebola, Marburg).
There are no specific treatments for most viral hemorrhagic fevers. However, some experimental antiviral drugs have shown promise in treating certain types of the disease. Supportive care, such as maintaining blood pressure, replacing lost fluids and electrolytes, and managing pain, is critical to improving outcomes. Prevention measures include avoiding areas where the viruses are common, using personal protective equipment when caring for infected individuals or handling potentially contaminated materials, and controlling insect vectors.
Sources: Centers for Disease Control and Prevention (CDC), World Health Organization (WHO).
Lassa virus is an arenavirus that causes Lassa fever, a type of hemorrhagic fever. It is primarily transmitted to humans through contact with infected rodents or their urine and droppings. The virus can also be spread through person-to-person transmission via direct contact with the blood, urine, feces, or other bodily fluids of an infected person.
The virus was first discovered in 1969 in the town of Lassa in Nigeria, hence its name. It is endemic to West Africa and is a significant public health concern in countries such as Sierra Leone, Liberia, Guinea, and Nigeria. The symptoms of Lassa fever can range from mild to severe and may include fever, sore throat, muscle pain, chest pain, and vomiting. In severe cases, the virus can cause bleeding, organ failure, and death.
Prevention measures for Lassa fever include avoiding contact with rodents, storing food in rodent-proof containers, and practicing good hygiene. There is no vaccine available to prevent Lassa fever, but ribavirin, an antiviral drug, has been shown to be effective in treating the disease if administered early in the course of illness.
Junin virus is a type of arenavirus that causes Argentine hemorrhagic fever, a severe and often fatal disease endemic to Argentina. The virus is primarily transmitted to humans through contact with the excreta of infected rodents, particularly the dryland vole (Microtus parvulus).
The Junin virus has a lipid envelope and a single-stranded RNA genome that encodes for four structural proteins and several nonstructural proteins. The viral glycoproteins are responsible for receptor binding, membrane fusion, and host immune response evasion.
Argentine hemorrhagic fever caused by Junin virus is characterized by fever, muscle pain, headache, and gastrointestinal symptoms, which can progress to severe bleeding, shock, and multi-organ failure in severe cases. The virus has a high case fatality rate if left untreated, but antiviral therapy with ribavirin and immune plasma from convalescent patients has significantly improved survival rates.
Prevention measures include avoiding contact with rodents, using personal protective equipment during high-risk activities, and implementing rodent control programs in endemic areas. Vaccination with the Candid #1 vaccine has also been shown to be effective in preventing Argentine hemorrhagic fever caused by Junin virus.
I'm sorry for any confusion, but "Venezuela" is not a medical term. It is the name of a country located in South America, known officially as the Bolivarian Republic of Venezuela. If you have any questions about medical terms or health-related topics, I would be happy to try and help answer those for you!
Sigmodontinae is a subfamily of rodents, more specifically within the family Cricetidae. This group is commonly known as the New World rats and mice, and it includes over 300 species that are primarily found in North, Central, and South America. The members of Sigmodontinae vary greatly in size and habits, with some being arboreal while others live on the ground or burrow. Some species have specialized diets, such as eating insects or seeds, while others are more generalist feeders. This subfamily is also notable for its high degree of speciation and diversity, making it an interesting subject for evolutionary biologists and ecologists.
Lassa fever is an acute viral hemorrhagic fever caused by the Lassa virus. It is primarily transmitted to humans through contact with infected rodents or their excreta, and it can also spread from person to person via bodily fluids. The symptoms of Lassa fever typically include fever, sore throat, muscle pain, chest pain, headache, and vomiting. In severe cases, the disease can cause bleeding from the mouth and nose, as well as complications such as deafness and encephalitis. Lassa fever is endemic to West Africa, particularly in Nigeria, Guinea, Liberia, and Sierra Leone.
Pichinde virus (PICV) is an enveloped, negative-sense, single-stranded RNA virus that belongs to the family Arenaviridae. It is primarily found in rodents, specifically the Pichinde deer mouse (Oligoryzomys fulvescens), which are endemic to South America, particularly Colombia.
PICV is not known to cause disease in humans and is often used as a model organism for studying arenaviral pathogenesis and immunity. However, accidental laboratory infections have been reported, resulting in mild febrile illness or seroconversion without symptoms. Therefore, it is recommended that appropriate biosafety measures be taken when handling this virus.
Nucleocapsid proteins are structural proteins that are associated with the viral genome in many viruses. They play a crucial role in the formation and stability of the viral particle, also known as the virion. In particular, nucleocapsid proteins bind to the viral RNA or DNA genome and help to protect it from degradation by host cell enzymes. They also participate in the assembly and disassembly of the virion during the viral replication cycle.
In some viruses, such as coronaviruses, the nucleocapsid protein is also involved in regulating the transcription and replication of the viral genome. The nucleocapsid protein of SARS-CoV-2, for example, has been shown to interact with host cell proteins that are involved in the regulation of gene expression, which may contribute to the virus's ability to manipulate the host cell environment and evade the immune response.
Overall, nucleocapsid proteins are important components of many viruses and are often targeted by antiviral therapies due to their essential role in the viral replication cycle.
Phylogeny is the evolutionary history and relationship among biological entities, such as species or genes, based on their shared characteristics. In other words, it refers to the branching pattern of evolution that shows how various organisms have descended from a common ancestor over time. Phylogenetic analysis involves constructing a tree-like diagram called a phylogenetic tree, which depicts the inferred evolutionary relationships among organisms or genes based on molecular sequence data or other types of characters. This information is crucial for understanding the diversity and distribution of life on Earth, as well as for studying the emergence and spread of diseases.
Crimean hemorrhagic fever (CHF) is a tick-borne disease caused by the virus named Crimean-Congo hemorrhagic fever virus (CCHFV). It is a severe and often fatal illness. The disease is characterized by sudden onset of high fever, muscle pain, severe headache, soreness in the eyes, fatigue, and dizziness. After two to four days, there may be evidence of hemorrhage (bleeding) from the mouth, gums, nose, or other sites. The virus is primarily transmitted to people from ticks that feed on domestic animals such as cattle, sheep, and goats. It can also be transmitted through contact with infected animal blood or tissues during and after slaughtering. Human-to-human transmission can occur resulting from close contact with the blood, secretions, organs or other bodily fluids of infected persons. Healthcare workers are at risk if they are not wearing appropriate personal protective equipment. There is no specific treatment for CHF yet, but early supportive care and symptomatic treatment improve survival rates.
Crimean-Congo Hemorrhagic Fever (CCHF) is a viral disease transmitted to humans through tick bites or contact with infected animal blood or tissues during and after slaughter. The virus belongs to the Nairovirus genus in the Bunyaviridae family. The disease was first identified in Crimea in 1944 and later in the Congo in 1956, hence the name Crimean-Congo Hemorrhagic Fever.
The CCHF virus causes severe illness with a case fatality rate of up to 40% in hospitalized patients. The symptoms include sudden onset of fever, muscle pain, headache, dizziness, neck pain and stiffness, back pain, sore eyes, and sensitivity to light. After a few days, patients may develop nausea, vomiting, diarrhea, abdominal pain, and bleeding from the mouth, nose, gums, and private parts.
There is no specific treatment or vaccine available for CCHF, but early supportive care with oral or intravenous fluids, analgesics, and antipyretics can significantly reduce mortality. Ribavirin has been used in the treatment of severe cases, but its efficacy is not fully proven. Preventive measures include avoiding tick bites, using protective clothing and gloves while handling animals or their tissues, and practicing good hygiene and food safety.
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.
Hemorrhagic Fever with Renal Syndrome (HFRS) is a group of clinically similar diseases caused by several distinct but related orthohantaviruses. The viruses are primarily transmitted to humans through inhalation of aerosols contaminated with excreta of infected rodents.
The clinical presentation of HFRS includes four phases: febrile, hypotensive, oliguric (decreased urine output), and polyuric (increased urine output). The febrile phase is characterized by fever, headache, myalgia, and abdominal pain. In the hypotensive phase, patients may experience a sudden drop in blood pressure, shock, and acute kidney injury leading to oliguria. The oliguric phase can last for days to weeks, followed by a polyuric phase where urine output increases significantly.
Additional symptoms of HFRS may include nausea, vomiting, conjunctival injection (redness), photophobia (sensitivity to light), and petechial rash (small red or purple spots on the skin caused by bleeding under the skin). In severe cases, HFRS can lead to acute renal failure, hypovolemic shock, and even death.
The severity of HFRS varies depending on the specific virus causing the infection. The most severe form of HFRS is caused by the Hantaaan virus, which has a mortality rate of up to 15%. Other viruses that can cause HFRS include Dobrava-Belgrade, Seoul, and Puumala viruses, with lower mortality rates ranging from less than 1% to about 5%.
Prevention measures for HFRS include reducing exposure to rodents and their excreta through proper food storage, waste disposal, and rodent control. Vaccines are available in some countries to prevent HFRS caused by specific viruses.
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.
A Mass Casualty Incident (MCI) is a situation in which the number of injured or deceased individuals exceeds the local resources available to respond and manage the incident. It typically involves multiple victims, often resulting from natural disasters, transportation accidents, terrorist attacks, or industrial incidents. The severity and scale of injuries require additional resources, coordination, and response from regional, national, or international emergency management and healthcare systems.
Bear Canyon mammarenavirus
Whitewater Arroyo mammarenavirus
Brazilian hemorrhagic fever
Viral hemorrhagic fever
Bolivian hemorrhagic fever
Virus Pathogen Database and Analysis Resource
Venezuelan hemorrhagic fever
List of MeSH codes (B04)
Arenaviruses (Arenaviridae) | Viral Hemorrhagic Fevers (VHFs) | CDC
British Library EThOS: Comparative studies on Mopeia viruses and other Arenaviridae, particularly Lassa virus
CBRNE - Viral Hemorrhagic Fevers: Practice Essentials, Pathophysiology, Etiology
Cell Culture and Electron Microscopy for Identifying Viruses in Diseases of Unknown Cause - Volume 19, Number 6-June 2013 -...
Arboviruses, Arenaviridae, and Filoviridae - MSD Manual Professional Edition
Lymphocytic choriomeningitis virus (LCMV) (Arenaviridae, Mammarenavirus) - Molecular diagnosis (PCR). - IVAMI
Lujo mammarenavirus - Wikipedia
ArboCat Virus: Ippy (IPPYV)
Electron microscopy and antigenic studies of uncharacterized viruses. I. Evidence suggesting the placement of viruses in...
Search Results | AJTMH
Hemorrhagic Fevers: MedlinePlus
Graphic Guide to Infectious Disease Elsevier eBook on VitalSource (Retail Access Card), 1st Edition - 9780323442169
Advanced Search Results - Public Health Image Library(PHIL)
Advanced Search Results - Public Health Image Library(PHIL)
Lujo Hemorrhagic Fever (LUHF) | CDC
KEGG Selected Viruses
Infectious Diseases - MSD Manual Professional Edition
Lassa Fever | WHO | Regional Office for Africa
Chikungunya Disease - Infectious Diseases - Merck Manuals Professional Edition
BR112020000524A2 - method for liquid incubation and virus inactivation - Google Patents
Arenaviruses | 72 | Molecular Detection of Animal Viral Pathogens | Do
Nonparametric methods for the analysis of single-color pathogen microarrays | BMC Bioinformatics | Full Text
Management of Patients With Suspected Viral Hemorrhagic Fever
Viruses | Free Full-Text | Mutagenic Effects of Ribavirin on Hepatitis E Virus-Viral Extinction versus Selection of Fitness...
Meet the 2021-2022 DGH Research Assistants and Fellows | University of Washington - Department of Global Health
- Lassa fever is a potentially severe viral infection caused by Lassa virus (family Arenaviridae , genus Arenavirus ), with an overall case-fatality rate of 1%-2% and a case-fatality rate of 15%-20% for hospitalized patients ( 1 , 2 ). (cdc.gov)
- The 12 distinct enveloped RNA viruses that cause most viral hemorrhagic fever (VHF) cases are members of 4 families: Arenaviridae, Bunyaviridae, Filoviridae, and Flaviviridae. (medscape.com)
- Other viruses, principally from the families Arenaviridae, Bunyaviridae, Flaviviridae, Filoviridae, and Herpesviridae , also cause hepatitis as part of systemic diseases, but these are generally not grouped with the hepatitis viruses. (nationalacademies.org)
- We study how viruses belonging to families Arenaviridae and Bunyaviridae infect their host cells. (ox.ac.uk)
- Lassa virus, named after a small town in northeastern Nigeria, is an enveloped, single-stranded, bisegmented ribonucleic acid (RNA) virus classified in the family Arenaviridae. (cdc.gov)
- According to the World Health Organization, Lassa fever is an acute viral haemorrhagic illness caused by a virus belonging to the family Arenaviridae that can last between two and 21 days. (kyra-info.com)
- Lassa fever is caused by a virus that belongs to the family Arenaviridae (WHO). (kyra-info.com)
- It is caused by Lassa virus (LASV), a single stranded RNA virus of the Arenaviridae family. (jenner.ac.uk)
- Viruses in the family Arenaviridae are generally spread by rodents, with each virus associated with one, or a few, closely related rodent species that serve as the virus' natural reservoir. (cdc.gov)
- citation needed] Viruses from the Arenaviridae family, to which Lujo virus belongs, almost always have a rodent reservoir, with one virus in the family having a bat reservoir. (wikipedia.org)
- Three viruses were found to have morphologic and morphogenetic characteristics consistent with those of members of the family Arenaviridae: Quaranfil virus, a human pathogen, Johnston Atoll virus, isolated from birds and ticks, and Araguari virus, isolated from an opossum. (utmb.edu)
- This, the first in a series of three papers, described methods used for these investigations and also presents descriptions of viruses provisionally placed in the families Arenaviridae, Paramyxoviridae, or Poxviridae. (utmb.edu)
- The Arenaviridae family comprises of a diverse group of single-stranded RNA viruses. (taylorfrancis.com)
- Lujo hemorrhagic fever (LUHF) is caused by Lujo virus, a single-stranded virus of the Arenaviridae family. (cdc.gov)
- The virus is a single-stranded RNA virus belonging to the virus family Arenaviridae . (who.int)
- The virus, a member of the virus family Arenaviridae , is a single-stranded RNA virus, and is zoonotic, or animal-borne that can be transmitted to humans. (outbreaknewstoday.com)
- Lujo is a bisegmented RNA virus-a member of the family Arenaviridae-and a known cause of viral hemorrhagic fever (VHF) in humans. (wikipedia.org)
- An un for sik is en Virus also en Nukleinsüer , wo de Informatschoon to'n Stüern vun den Stoffwessel in de Zellen vun en Weert in afspiekert is, sunnerlich to'n Vermehren vun de Virus-Nukleinsüer un um de Viruspartikels (Virionen) alles mit to geven, wat se bruken doot. (wikipedia.org)
- Vundeswegen kann de Virus sik bloß in de Zell vun en Weert vermehren. (wikipedia.org)
- Although the specifics of the mechanism might vary between bunyaviruses (e.g., families Hantaviridae, Peribunyaviridae, Phenuiviridae, Arenaviridae ), a constant feature in their genome transcription is the Cap-ENDO responsible for the host cellular mRNA cleavage. (bnitm.de)
- It is the most widely distributed of the Arenaviridae, being found worldwide in the house mouse (Mus musculus). (taylorfrancis.com)
Single-stranded RNA virus2
- The discovery of Bear Canyon virus is the first unequivocal evidence that the virus family Arenaviridae is naturally associated with the rodent genus Peromyscus and that a Tacaribe serocomplex virus occurs in California. (medscape.com)
- Arenaviridae" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (ouhsc.edu)
- This graph shows the total number of publications written about "Arenaviridae" by people in this website by year, and whether "Arenaviridae" was a major or minor topic of these publications. (ouhsc.edu)
- Below are the most recent publications written about "Arenaviridae" by people in Profiles. (ouhsc.edu)