Arteritis Virus, Equine
Takayasu Arteritis
Giant Cell Arteritis
Arterivirus
Horses
Temporal Arteries
Togaviridae
Polymyalgia Rheumatica
Vaccines, Marker
Open Reading Frames
Viral Structural Proteins
Virus Replication
Lactate dehydrogenase-elevating virus
Neutralization Tests
Molecular Sequence Data
RNA Replicase
Semen
Viral Envelope Proteins
Vaccinia virus
Porcine respiratory and reproductive syndrome virus
Cricetinae
Viral Plaque Assay
Virion
Amino Acid Sequence
Receptors, Virus
Polyarteritis Nodosa
Virus Shedding
Viral Nonstructural Proteins
HLA-B52 Antigen
Aortic Arch Syndromes
Simian virus 40
Virus Assembly
Defective Viruses
Viral Matrix Proteins
Carrier State
Sindbis Virus
Genetic diversity of equine arteritis virus. (1/128)
Equine arteritis viruses (EAV) from Europe and America were compared by phylogenetic analysis of 43 isolates obtained over four decades. An additional 22 virus sequences were retrieved from GenBank. Fragments of the glycoprotein G(L) and the replicase genes were amplified by RT-PCR, prior to sequencing and construction of phylogenetic trees. The trees revealed many distinctive lineages, consistent with prolonged diversification within geographically separated host populations. Two large groups and five subgroups were distinguished. Group I consisted mainly of viruses from North America, whilst group II consisted mainly of European isolates. In most instances, where the geographic origin of the viruses appeared to be at variance with the phylogenetically predicted relationships, the horses from which the viruses were recovered had been transported between Europe and America or vice versa. Analysis of the replicase gene revealed similar phylogenetic relationships although not all of the groups were as clearly defined. Virus strains CH1 (Switzerland, 1964) and S1 (Sweden, 1989) represented separate 'outgroups' based on analysis of both genomic regions. The results of this study confirm the value of the G(L) gene of EAV for estimating virus genetic diversity and as a useful tool for tracing routes by which EAV is spread. In addition, computer-assisted predictions of antigenic sites on the G(L) protein revealed considerable variability among the isolates, especially with respect to regions associated with neutralization domains. (+info)Genetic divergence with emergence of novel phenotypic variants of equine arteritis virus during persistent infection of stallions. (2/128)
The persistently infected carrier stallion is the critical natural reservoir of equine arteritis virus (EAV), as venereal infection of mares frequently occurs after breeding to such stallions. Two Thoroughbred stallions that were infected during the 1984 outbreak of equine viral arteritis in central Kentucky subsequently became long-term EAV carriers. EAV genomes amplified from the semen of these two stallions were compared by sequence analysis of the six 3' open reading frames (ORFs 2 through 7), which encode the four known structural proteins and two uncharacterized glycoproteins. The major variants of the EAV population that sequentially arose within the reproductive tract of each carrier stallion varied by approximately 1% per year, and the heterogeneity of the viral quasispecies increased during the course of long-term persistent infection. The various ORFs of the dominant EAV variants evolved independently, and there was apparently strong selective pressure on the uncharacterized GP3 protein during persistent infection. Amino acid changes also occurred in the V1 variable region of the GL protein. This region has been previously identified as a crucial neutralization domain, and selective pressures exerted on the V1 region during persistent EAV infection led to the emergence of virus variants with distinct neutralization properties. Thus, evolution of the EAV quasispecies that occurs during persistent infection of the stallion clearly can influence viral phenotypic properties such as neutralization and perhaps virulence. (+info)Characterization of an equine arteritis virus replicase mutant defective in subgenomic mRNA synthesis. (3/128)
Equine arteritis virus (EAV) is a positive-stranded RNA virus that synthesizes a 5'- and 3'-coterminal nested set of six subgenomic mRNAs. These mRNAs all contain a common leader sequence which is derived from the 5' end of the genome. Subgenomic mRNA transcription and genome replication are directed by the viral replicase, which is expressed in the form of two polyproteins and subsequently processed into smaller nonstructural proteins (nsps). During the recent construction of an EAV infectious cDNA clone (pEAV030 [L. C. van Dinten, J. A. den Boon, A. L. M. Wassenaar, W. J. M. Spaan, and E. J. Snijder, Proc. Natl. Acad. Sci. USA 94:991-996, 1997]), a mutant cDNA clone (pEAV030F) which carries a single replicase point mutation was obtained. This substitution (Ser-2429-->Pro) is located in the nsp10 subunit and renders the EAV030F virus deficient in subgenomic mRNA synthesis. To obtain more insight into the role of nsp10 in transcription and the nature of the transcriptional defect, we have now analyzed the EAV030F mutant in considerable detail. The Ser-2429-->Pro mutation does not affect the proteolytic processing of the replicase but apparently affects the function of nsp10 in transcription. Furthermore, our study showed that EAV030F still produces subgenomic positive and negative strands, albeit at a very low level. Both subgenomic positive-strand synthesis and negative-strand synthesis are equally affected by the Ser-2429-->Pro mutation, suggesting that nsp10 plays an important role in an early step of EAV mRNA transcription. (+info)Identification of a novel structural protein of arteriviruses. (4/128)
Arteriviruses are positive-stranded RNA viruses with an efficiently organized, polycistronic genome. A short region between the replicase gene and open reading frame (ORF) 2 of the equine arteritis virus (EAV) genome was previously assumed to be untranslated. However, here we report that this segment of the EAV genome contains the 5' part of a novel gene (ORF 2a) which is conserved in all arteriviruses. The 3' part of EAV ORF 2a overlaps with the 5' part of the former ORF 2 (now renamed ORF 2b), which encodes the GS glycoprotein. Both ORF 2a and ORF 2b appear to be expressed from mRNA 2, which thereby constitutes the first proven example of a bicistronic mRNA in arteriviruses. The 67-amino-acid protein encoded by EAV ORF 2a, which we have provisionally named the envelope (E) protein, is very hydrophobic and has a basic C terminus. An E protein-specific antiserum was raised and used to demonstrate the expression of the novel gene in EAV-infected cells. The EAV E protein proved to be very stable, did not form disulfide-linked oligomers, and was not N-glycosylated. Immunofluorescence and immunoelectron microscopy studies showed that the E protein associates with intracellular membranes both in EAV-infected cells and upon independent expression. An analysis of purified EAV particles revealed that the E protein is a structural protein. By using reverse genetics, we demonstrated that both the EAV E and GS proteins are essential for the production of infectious progeny virus. (+info)Equine arteritis virus derived from an infectious cDNA clone is attenuated and genetically stable in infected stallions. (5/128)
Virus derived from an infectious cDNA clone of equine arteritis virus (EAV030H) was intranasally inoculated into two stallions, neither of which subsequently developed clinical manifestations of equine viral arteritis (EVA). Virus was isolated from nasal swabs and mononuclear cells collected from both stallions +info)Genetic stability of equine arteritis virus during horizontal and vertical transmission in an outbreak of equine viral arteritis. (6/128)
An imported carrier stallion (A) from Europe was implicated in causing an extensive outbreak of equine viral arteritis (EVA) on a Warmblood breeding farm in Pennsylvania, USA. Strains of equine arteritis virus (EAV) present in the semen of two carrier stallions (A and G) on the farm were compared to those in tissues of foals born during the outbreak, as well as viruses present in the semen of two other stallions that became persistently infected carriers of EAV following infection during the outbreak. The 2822 bp segment encompassing ORFs 2-7 (nt 9807-12628; which encode the G(S), GP3, GP4, G(L), M and N proteins, respectively) was directly amplified by RT-PCR from semen samples and foal tissues. Nucleotide and phylogenetic analyses confirmed that virus present in the semen of stallion A initiated the outbreak. The genomes of viruses present in most foal tissues (10/11) and serum from an acutely infected mare collected during the outbreak were identical to that of virus present in the lung of the first foal that died of EVA. Virus in the placenta of one foal differed by one nucleotide (99.9% identity) from the predominant outbreak virus. The relative genetic stability of viruses that circulated during the outbreak contrasts markedly with the heterogeneous virus populations variously present in the semen of persistently infected stallions on the farm. These findings are consistent with the hypothesis that the carrier stallion can be a source of genetic diversity of EAV, and that outbreaks of EVA can be initiated by the horizontal aerosol transmission of specific viral variants that occur in the semen of particular carrier stallions. (+info)The open reading frame 3 of equine arteritis virus encodes an immunogenic glycosylated, integral membrane protein. (7/128)
Open reading frame 3 (ORF 3) of equine arteritis virus (EAV) is predicted to encode a glycosylated membrane protein (GP3) that is uncharacterized. ORF 3 of the American Type Culture Collection strain of EAV was in vitro transcribed and the encoded GP3 protein was in vitro translated with and without canine microsomal membranes. The GP3 protein was approximately 17 kDa after in vitro translation without canine microsomal membranes whereas the glycosylated form, after translation with microsomal membranes, was a diffuse band of 36-42 kDa, indicating that the GP3 protein is extensively glycosylated. Deglycosylation reduced the GP3 protein to approximately 17 kDa, the same size as that translated without microsomal membranes, indicating that the signal sequence was not cleaved. The EAV GP3 protein was membrane associated and not released as a soluble protein, in marked contrast to the ORF 3-encoded proteins of some other arteriviruses. The GP3 protein was protected from protease digestion in closed membrane vesicles, suggesting that the protein extends into the membrane vesicles and is anchored by the N-terminal signal sequence, a C-terminal hydrophobic domain, or both, but does not span the membrane three times. A GP3 protein lacking the C-terminal transmembrane domain remained membrane associated, indicating that this terminus is not a necessary membrane anchor. Sera from stallions persistently infected with EAV and horses immunized repeatedly with the modified live EAV vaccine contained antibodies specific for the GP3 protein. The data indicate that the GP3 protein is an extensively glycosylated membrane protein that is immunogenic during some EAV infections. (+info)Effects of chlorine, iodine, and quaternary ammonium compound disinfectants on several exotic disease viruses. (8/128)
The effects of three representative disinfectants, chlorine (sodium hypochlorite), iodine (potassium tetraglicine triiodide), and quaternary ammonium compound (didecyldimethylammonium chloride), on several exotic disease viruses were examined. The viruses used were four enveloped viruses (vesicular stomatitis virus, African swine fever virus, equine viral arteritis virus, and porcine reproductive and respiratory syndrome virus) and two non-enveloped viruses (swine vesicular disease virus (SVDV) and African horse sickness virus (AHSV)). Chlorine was effective against all viruses except SVDV at concentrations of 0.03% to 0.0075%, and a dose response was observed. Iodine was very effective against all viruses at concentrations of 0.015% to 0.0075%, but a dose response was not observed. Quaternary ammonium compound was very effective in low concentration of 0.003% against four enveloped viruses and AHSV, but it was only effective against SVDV with 0.05% NaOH. Electron microscopic observation revealed the probable mechanism of each disinfectant. Chlorine caused complete degeneration of the viral particles and also destroyed the nucleic acid of the viruses. Iodine destroyed mainly the inner components including nucleic acid of the viruses. Quaternary ammonium compound induced detachment of the envelope of the enveloped viruses and formation of micelle in non-enveloped viruses. According to these results, chlorine and iodine disinfectants were quite effective against most of the viruses used at adequately high concentration. The effective concentration of quaternary ammonium compound was the lowest among the disinfectants examined. (+info)Arteriviruses are characterized by their ability to infect cells in the blood vessels, particularly endothelial cells, which line the inside of blood vessels. This allows the virus to cause widespread damage to the cardiovascular system and can lead to severe illness and death.
Arterivirus infections are a significant concern for public health, as they have the potential to spread rapidly and cause large outbreaks. In addition, many arteriviruses are zoonotic, meaning that they can be transmitted between animals and humans, which can make it difficult to control outbreaks.
There is currently no specific treatment or vaccine available for arterivirus infections, although supportive care such as intravenous fluids and oxygen therapy may be provided to manage symptoms. Research is ongoing to develop effective treatments and vaccines against these viruses.
The exact cause of Takayasu arteritis is not known, but it is believed to be an autoimmune disorder, meaning the immune system mistakenly attacks healthy tissue in the body. The disease primarily affects women of childbearing age, although it can occur at any age.
The symptoms of Takayasu arteritis can vary depending on the location and severity of the inflammation. Common symptoms include:
* Fatigue
* Weakness
* Joint pain
* Fever
* Headaches
* Muscle wasting
* Decreased vision
If the disease affects the aorta, it can cause:
* Aortic regurgitation
* Aortic stenosis
* Aortic aneurysm
Diagnosis of Takayasu arteritis is based on a combination of clinical findings, laboratory tests, and imaging studies. Laboratory tests may include:
* Erythrocyte sedimentation rate (ESR)
* C-reactive protein (CRP)
* Antineutrophil cytoplasmic antibodies (ANCA)
* Anti-citrullinated protein antibodies (ACPA)
Imaging studies may include:
* Ultrasonography (US)
* Computed tomography (CT)
* Magnetic resonance angiography (MRA)
* Positron emission tomography (PET)
Treatment for Takayasu arteritis typically involves a combination of medications and surgery. Medications may include:
* Glucocorticoids
* Immunosuppressive drugs
* Antibiotics
Surgical interventions may include:
* Aortic root replacement
* Aortic grafting
* Bypass surgery
The prognosis for Takayasu arteritis is generally good if the disease is diagnosed and treated early, with a 5-year survival rate of approximately 80%. However, if left untreated, the disease can progress to severe complications such as aortic dissection, myocardial infarction, or stroke, which can be fatal.
Prevention of Takayasu arteritis is not possible, as the exact cause of the disease is not fully understood. However, early diagnosis and treatment can help to prevent complications and improve outcomes.
Current research is focused on identifying specific biomarkers that can aid in the diagnosis of Takayasu arteritis, as well as developing new treatments that can more effectively target the underlying immune mechanisms of the disease.
Arteritis can lead to a range of symptoms including fever, fatigue, joint pain, skin rashes, and difficulty speaking or swallowing. In severe cases, it can also cause cardiovascular complications such as heart attack, stroke, or organ failure.
There are several types of arteritis, each with different causes and symptoms. Some common forms of arteritis include:
1. Giant cell arteritis (GCA): This is the most common form of arteritis and primarily affects older adults. It is caused by inflammation of the medium-sized arteries, particularly those in the head and neck. Symptoms may include headaches, vision loss, and pain in the face and jaw.
2. Takayasu arteritis (TA): This is a rare form of arteritis that affects the aorta and its branches. It is more common in women than men and typically affects young adults. Symptoms may include high blood pressure, chest pain, and weakness or numbness in the limbs.
3. Polyarteritis nodosa (PAN): This is a rare form of arteritis that affects multiple arteries throughout the body. It can cause symptoms such as fever, fatigue, joint pain, and skin rashes.
4. Kawasaki disease: This is a rare inflammatory disease that primarily affects children under the age of 5. It causes inflammation in the blood vessels, particularly those in the heart and can lead to cardiovascular complications if left untreated.
Arteritis can be diagnosed through various tests such as blood tests, imaging studies like CT or MRI scans, and biopsies. Treatment options vary depending on the type of arteritis and its severity but may include corticosteroids, immunosuppressive medications, and antibiotics. Early diagnosis and treatment are crucial to prevent long-term damage and improve outcomes.
* Headache
* Weakness or numbness in the limbs
* Vision problems such as blurred vision or blind spots
* Pain in the jaw, shoulder, or tongue
* Fatigue
* Low-grade fever
* Loss of appetite
The exact cause of GCA is not known, but it is believed to be an autoimmune disorder. This means that the immune system mistakenly attacks healthy tissues in the blood vessels, leading to inflammation and damage. The condition can be diagnosed through a combination of physical examination, laboratory tests, and imaging studies such as ultrasound or CT scans.
Treatment for GCA usually involves high doses of corticosteroids, which can help reduce inflammation and prevent further damage to the blood vessels. In some cases, immunosuppressive medications may also be prescribed to suppress the immune system and prevent the condition from returning. If left untreated, GCA can lead to serious complications such as stroke or blindness, so it is important to seek medical attention if symptoms persist or worsen over time.
Here are some of the key points of the definition of giant cell arteritis:
* A type of vasculitis that affects medium and large arteries
* Typically occurs in people over the age of 50
* More common in women than men
* Symptoms can include headache, vision problems, pain in the jaw or tongue, fatigue, and low-grade fever
* Autoimmune disorder
* Can lead to serious complications if left untreated
* Treatment typically involves corticosteroids and immunosuppressive medications.
Some common horse diseases include:
1. Equine Influenza (EI): A highly contagious respiratory disease caused by the equine influenza virus. It can cause fever, coughing, and nasal discharge.
2. Strangles: A bacterial infection of the lymph nodes, which can cause swelling of the neck and difficulty breathing.
3. West Nile Virus (WNV): A viral infection that can cause fever, weakness, and loss of coordination. It is transmitted by mosquitoes and can be fatal in some cases.
4. Tetanus: A bacterial infection caused by Clostridium tetani, which can cause muscle stiffness, spasms, and rigidity.
5. Rabies: A viral infection that affects the central nervous system and can be fatal if left untreated. It is transmitted through the saliva of infected animals, usually through a bite.
6. Cushing's Disease: A hormonal disorder caused by an overproduction of cortisol, which can cause weight gain, muscle wasting, and other health issues.
7. Laminitis: An inflammation of the laminae, the tissues that connect the hoof to the bone. It can be caused by obesity, overeating, or excessive exercise.
8. Navicular Syndrome: A condition that affects the navicular bone and surrounding tissue, causing pain and lameness in the foot.
9. Pneumonia: An inflammation of the lungs, which can be caused by bacteria, viruses, or fungi.
10. Colic: A general term for abdominal pain, which can be caused by a variety of factors, including gas, impaction, or twisting of the intestines.
These are just a few examples of the many potential health issues that can affect horses. Regular veterinary care and proper management can help prevent many of these conditions, and early diagnosis and treatment can improve the chances of a successful outcome.
The exact cause of PMR is not known, but it is believed to be related to an abnormal immune response. The condition often occurs in conjunction with another inflammatory disorder called giant cell arteritis (GCA), which affects the blood vessels.
Symptoms of PMR include:
* Pain and stiffness in the shoulders, hips, and other joints
* Fatigue
* Fever
* Loss of appetite
* Sleep disturbances
* Weight loss
The diagnosis of PMR is based on a combination of symptoms, physical examination findings, and laboratory test results. Laboratory tests may include blood tests to check for inflammatory markers, such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP).
Treatment for PMR typically involves a combination of medications, including:
* Corticosteroids to reduce inflammation
* Pain relievers, such as nonsteroidal anti-inflammatory drugs (NSAIDs) or narcotics
* Anti-inflammatory medications, such as disease-modifying anti-rheumatic drugs (DMARDs) or biologic response modifiers
In addition to medication, physical therapy and exercise may be helpful in managing the symptoms of PMR. In some cases, surgery may be necessary to repair joint damage.
The prognosis for PMR is generally good, with most people experiencing significant improvement within a few months of starting treatment. However, the condition can be challenging to diagnose and treat, and it is important to work closely with a healthcare provider to find the most effective treatment plan.
The symptoms of PAN can vary depending on the location and severity of the inflammation, but may include:
* Fever
* Headache
* Joint pain and swelling
* Skin rash or lesions
* Abdominal pain
* Weight loss
* Fatigue
* Numbness or weakness in the limbs
The exact cause of PAN is not known, but it is believed to be an autoimmune disorder, meaning that the body's immune system mistakenly attacks healthy tissues. It can occur at any age, but is more common in adults between the ages of 40 and 60.
There is no cure for PAN, but treatment options include:
* Corticosteroids to reduce inflammation
* Immunosuppressive drugs to suppress the immune system
* Plasmapheresis to remove harmful antibodies from the blood
* Biologics to target specific proteins involved in the disease process
The prognosis for PAN varies depending on the severity and location of the inflammation, as well as the promptness and effectiveness of treatment. In general, the condition can be challenging to diagnose and treat, and the long-term outcome is often uncertain.
1. Common cold: A viral infection that affects the upper respiratory tract and causes symptoms such as sneezing, running nose, coughing, and mild fever.
2. Influenza (flu): A viral infection that can cause severe respiratory illness, including pneumonia, bronchitis, and sinus and ear infections.
3. Measles: A highly contagious viral infection that causes fever, rashes, coughing, and redness of the eyes.
4. Rubella (German measles): A mild viral infection that can cause fever, rashes, headache, and swollen lymph nodes.
5. Chickenpox: A highly contagious viral infection that causes fever, itching, and a characteristic rash of small blisters on the skin.
6. Herpes simplex virus (HSV): A viral infection that can cause genital herpes, cold sores, or other skin lesions.
7. Human immunodeficiency virus (HIV): A viral infection that attacks the immune system and can lead to acquired immunodeficiency syndrome (AIDS).
8. Hepatitis B: A viral infection that affects the liver, causing inflammation and damage to liver cells.
9. Hepatitis C: Another viral infection that affects the liver, often leading to chronic liver disease and liver cancer.
10. Ebola: A deadly viral infection that causes fever, vomiting, diarrhea, and internal bleeding.
11. SARS (severe acute respiratory syndrome): A viral infection that can cause severe respiratory illness, including pneumonia and respiratory failure.
12. West Nile virus: A viral infection that can cause fever, headache, and muscle pain, as well as more severe symptoms such as meningitis or encephalitis.
Viral infections can be spread through contact with an infected person or contaminated surfaces, objects, or insects such as mosquitoes. Prevention strategies include:
1. Practicing good hygiene, such as washing hands frequently and thoroughly.
2. Avoiding close contact with people who are sick.
3. Covering the mouth and nose when coughing or sneezing.
4. Avoiding sharing personal items such as towels or utensils.
5. Using condoms or other barrier methods during sexual activity.
6. Getting vaccinated against certain viral infections, such as HPV and hepatitis B.
7. Using insect repellents to prevent mosquito bites.
8. Screening blood products and organs for certain viruses before transfusion or transplantation.
Treatment for viral infections depends on the specific virus and the severity of the illness. Antiviral medications may be used to reduce the replication of the virus and alleviate symptoms. In severe cases, hospitalization may be necessary to provide supportive care such as intravenous fluids, oxygen therapy, or mechanical ventilation.
Prevention is key in avoiding viral infections, so taking the necessary precautions and practicing good hygiene can go a long way in protecting oneself and others from these common and potentially debilitating illnesses.
Types of Aortic Arch Syndromes:
1. Turner Syndrome: A genetic disorder that affects females and is caused by a missing X chromosome. This condition can result in short stature, infertility, and heart defects, including aortic arch syndrome.
2. Down Syndrome: A genetic disorder that occurs when there is an extra copy of chromosome 21. This condition can cause a range of symptoms, including heart defects such as aortic arch syndrome.
3. Williams Syndrome: A rare genetic disorder caused by a deletion of genetic material from chromosome 7. This condition is characterized by cardiovascular problems, including aortic arch syndrome.
4. Marfan Syndrome: An inherited disorder that affects the body's connective tissue, including the heart and blood vessels. This condition can cause aortic arch syndrome and other cardiovascular problems.
5. Ehlers-Danlos Syndrome: A group of inherited disorders that affect the body's connective tissue, including the heart and blood vessels. This condition can cause aortic arch syndrome and other cardiovascular problems.
Symptoms of Aortic Arch Syndromes:
1. Chest pain or pressure
2. Shortness of breath
3. Dizziness or fainting
4. Pulse deficiency in the arms or legs
5. Blue discoloration of the skin (cyanosis)
6. Heart murmurs
7. Abnormal heart rhythms
Diagnosis of Aortic Arch Syndromes:
1. Physical examination and medical history
2. Electrocardiogram (ECG)
3. Echocardiography
4. Cardiac catheterization
5. Magnetic resonance imaging (MRI) or computed tomography (CT) scans
Treatment of Aortic Arch Syndromes:
1. Medications to control symptoms such as high blood pressure, heart failure, or abnormal heart rhythms
2. Surgery to repair or replace the aortic arch, including open-heart surgery or minimally invasive procedures
3. Monitoring and follow-up care to manage the condition and prevent complications.
Prognosis for Aortic Arch Syndromes:
The prognosis for aortic arch syndromes varies depending on the underlying cause of the condition, the severity of the symptoms, and the effectiveness of treatment. In general, early diagnosis and appropriate treatment can improve the outlook for individuals with these conditions. However, without proper care, the condition can be life-threatening.
Equine arteritis virus leader TRS hairpin (LTH)
Equine viral arteritis
SND1
Betaarterivirus suid 1
Veterinary virology
Arteriviridae
Ionophore
EAV
ATCvet code QI05
List of MeSH codes (B04)
History of virology
List of MeSH codes (C02)
Equine arteritis virus, complete genome - Nucleotide - NCBI
Development of an antigen-capture ELISA for the quantitation of equine arteritis virus in culture supernatant. | Arch Virol...
Changed and Deleted MeSH Headings-2019. NLM Technical Bulletin. 2018 Nov-Dec
Replication of lactate dehydrogenase-elevating virus in macrophages. 2. Mechanism of persistent infection in mice and cell...
Novel Arterivirus Associated with Outbreak of Fatal Encephalitis in European Hedgehogs, England, 2019 - Volume 27, Number 2...
ArboCat Virus: Epizootic Hemorrhagic Disease of Deer (EHDV)
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Rob Mackay » College of Veterinary Medicine » University of Florida
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Strategies for Vaccinating Mares, Foals, and Weanlings | IVIS
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Equine Archives - Texas A&M Veterinary Medical Diagnostic Laboratory
Westside Animal Hospital - Veterinarian in Cincinnati, OH
Rethinking Equine Vaccinations - Part 1 | IVC Journal
CDV Healthcare Sentence Highlighting - PMC Open Access
Recombinant2
- 6. Recombinant equine arteritis virus as an expression vector. (nih.gov)
- The cloning treatment used an anti-equine Compact disc3 mAb (38,39) and human being recombinant IL-2 (rhuIL-2), which stimulates equine lymphocytes (15,19,22,40), in a way that autologous APC and particular antigen weren't required during enlargement in tradition. (biopaqc.com)
Horses5
- Initial findings of the virus' virulence and potential for transmission between equids and artiodactyls were alarming and provided the impetus for experimental studies, which showed that disease could be induced in members of an additional 8 mammalian taxa: dogs, cats, horses, mice, hamsters, pigs, goats, and marmosets ( 4 - 6 ). (cdc.gov)
- Horses have traditionally been immunized with killed vaccines, although MLV equine vaccines have more recently become available. (ivcjournal.com)
- Intro Cytotoxic T lymphocytes get excited about the control of a number of important intracellular pathogens of horses, including equine herpes disease-1 (1-7), equine arteritis disease (8), and (9,10). (biopaqc.com)
- In horses contaminated with equine infectious anemia disease (EIAV), a lentivirus having a world-wide distribution, CTL are essential in the control of viral replication and medical disease (11-22). (biopaqc.com)
- Prior to the efforts of epitope specificity, MHC course I presentation, practical avidity, and TCR affinity to CTL-mediated safety against intracellular pathogens of horses could be rigorously dissected, a trusted solution to clone epitope-specific equine CTL is necessary. (biopaqc.com)
Infectious anemia1
- Classical examples of this latter situation occur with retroviral infection such as human AIDS or the animal equivalents (e.g. equine infectious anemia). (ivcjournal.com)
Antigenic2
Infections2
Closely related1
- By neutralization tests, Ibaraki virus was more closely related to EHD virus, serotype 2 (Alberta strain). (cdc.gov)
Identical1
- Cloned CTL will be beneficial for identical research in the equine similarly, but solutions to clone equine CTL never have been described. (biopaqc.com)
Polymerase3
- 14. Efficient expression of small RNA polymerase III genes from a novel simian virus 40 vector and their effect on viral gene expression. (nih.gov)
- Postmortem examination showed nonsuppurative meningoencephalitis with neuronal and glial intranuclear inclusion bodies ( Figure 1 , panel A ). PCR targeting of conserved regions of herpesvirus DNA polymerase genes identified a virus in the brain with 98% homology to EHV-1 in a 165-bp segment of DNA ( 2 , 7 ). (cdc.gov)
- Subsequently, 2 other PCRs targeting an additional 742 bp of the DNA polymerase gene (sense primer 5′-GCATYWTCCCCCCGTTKATRAC-3′ and antisense primer 5′-ATAGYSAARRCCACGCCTTY-3′) and 1,181 bp of the glycoprotein B (gB) gene (sense primer 5′-CTTGTGAGATCTAACCGCAC-3′ and antisense primer 5′-GGGTATAGAGCTTTCATGGGG-3′) identified the virus as EHV-9 and enabled more precise strain determination ( 2 ). (cdc.gov)
Cells6
- 1. Regulation of viral transcription in cells infected with iododeoxyuridine-substituted simian virus 40 as a model for the activation by iododeoxyuridine of latent viral genomes. (nih.gov)
- 4. DNA sequences outside the simian virus 40 early region cause downregulation of T-antigen production in permissive simian cells. (nih.gov)
- 9. Host range analysis of simian virus 40, BK virus and chimaeric SV40/BKV: relative expression of large T-antigen and Vp1 in infected and transformed cells. (nih.gov)
- 12. [Localization of virus sequences in heavy nuclear RNA of mouse cells transformed by SV40]. (nih.gov)
- The mechanism of arterivirus cell entry has not been fully elucidated, although these viruses are thought to enter cells through receptor-mediated endocytosis. (nih.gov)
- Cells had been tagged indirectly with anti-equine Compact disc3 mAb F6G (IgG1) (38,39) (from Dr. Jeffery Stott, College or university of California, Davis) and anti-equine Compact disc8 mAb ETC91A (IgG3) (42). (biopaqc.com)
Concern2
- The potential vulnerability of diverse species to EHV-9 has raised concern about the virus as an anthropozoonotic pathogen ( 2 - 6 ). (cdc.gov)
- The residual virulence (infectivity) and environmental contamination resulting from the shedding of vaccine virus is of concern not only for domestic animal populations but also for wildlife. (ivcjournal.com)
Study2
- To study cell entry and infectivity of arteriviruses, high quality virus stocks are necessary. (nih.gov)
- In a study evaluating the growth of equine arteritis virus (EAV) and porcine reproductive and respiratory syndrome virus (PRRSV), we compared the robotic plating technique with the standard manual plating technique in the MA-104 cell line and evaluated the consistency of the robot performance over 2 months in the MARC-145 cell line. (nih.gov)
Thought1
- We thought we would clone CTL particular for the conserved EIAV Rev-QW11 epitope, which can be identified by high avidity CTL (20), and it is shown from the equine leukocyte antigen (ELA)-A1 haplotype-associated MHC course I substances 7-6 and Vanoxerine 2HCl Vanoxerine 2HCl 141 (17,25). (biopaqc.com)
Human1
- 17. Defective and wild-type human T-cell leukemia virus type I proviruses: characterization of gene products and trans-interactions between proviruses. (nih.gov)
Entry1
- Click on the PDF icon to the left to view a copy of this virus entry in PDF format. (cdc.gov)
Found1
- The virus was also found in an aborted Persian onager. (cdc.gov)
Influenza virus2
- Nemoto M , Yamanaka T , Bannai H , Tsujimura K , Kondo T , Matsumura T . Development and evaluation of a reverse transcription loop-mediated isothermal amplification assay for H3N8 equine influenza virus. (cdc.gov)
- Reverse transcription loop-mediated isothermal amplification was used to detect equine influenza virus in the nasal swab samples ( 7 ). (cdc.gov)
Polymerase chain re2
- Comparison of two real-time reverse transcription polymerase chain reaction assays for the detection of Equine arteritis virus nucleic acid in equine semen and tissue culture fluid. (nih.gov)
- Rapid, single-step differentiation of equid herpesviruses 1 and 4 from clinical material using the polymerase chain reaction and virus-specific primers. (cdc.gov)
Bucyrus1
- The isolated virus was propagated in cell cultures and confirmed as EAV by indirect immunofluorescence and virus neutralisation, using a serum specific for the reference Bucyrus strain of EAV. (nih.gov)
Porcine2
- Tajima S , Kotaki A , Yagasaki K , Taniwaki T , Moi ML , Nakayama E , Identification and amplification of Japanese encephalitis virus and Getah virus propagated from a single porcine serum sample: a case of coinfection. (cdc.gov)
- In a study evaluating the growth of equine arteritis virus (EAV) and porcine reproductive and respiratory syndrome virus (PRRSV), we compared the robotic plating technique with the standard manual plating technique in the MA-104 cell line and evaluated the consistency of the robot performance over 2 months in the MARC-145 cell line. (nih.gov)
Isolation5
- This paper describes the first isolation of equine arteritis virus (EAV) in Argentina. (nih.gov)
- The virus was isolated from the semen of an imported seropositive stallion held in isolation at a breeding farm in Tandil in the Buenos Aires Province. (nih.gov)
- Yago K , Hagiwara S , Kawamura H , Narita M . A fatal case in newborn piglets with Getah virus infection: isolation of the virus. (cdc.gov)
- Li XD , Qiu FX , Yang H , Rao YN , Calisher CH . Isolation of Getah virus from mosquitos collected on Hainan Island, China, and results of a serosurvey. (cdc.gov)
- Kamada M , Ando Y , Fukunaga Y , Kumanomido T , Imagawa H , Wada R , Equine Getah virus infection: isolation of the virus from racehorses during an enzootic in Japan. (cdc.gov)
Detection1
- Detection of equine arteritis virus by real-time TaqMan reverse transcription-PCR assay. (cdc.gov)
Horses6
- The equine industry is very important for Argentina and international movement of horses is very intensive. (nih.gov)
- Getah virus infection of Indian horses. (cdc.gov)
- Imagawa H , Ando Y , Kamada M , Sugiura T , Kumanomido T , Fukunaga Y , Sero-epizootiological survey on Getah virus infection in light horses in Japan. (cdc.gov)
- Of 49 febrile horses tested by reverse transcription PCR, 25 were positive for Getah virus. (cdc.gov)
- Outbreaks of Getah virus infection have occurred among horses in 1978, 1979, and 1983 in Japan ( 2 ) and in 1990 in India ( 6 ). (cdc.gov)
- we identified Getah virus infection among these horses. (cdc.gov)
Getah Virus Infection3
- An outbreak of Getah virus infection occurred among racehorses in Japan during September and October 2014. (cdc.gov)
- An inactivated whole-virus vaccine (Nisseiken Co., Ltd, Tokyo, Japan) is available to prevent Getah virus infection and is mainly administered to thoroughbred racehorses registered by the Japan Racing Association. (cdc.gov)
- The outbreak of Getah virus infection in 1978 occurred at this facility. (cdc.gov)
Newborn piglets1
- the virus is also pathogenic to pig fetuses and newborn piglets ( 3 , 4 ) and can cause fever in humans ( 5 ). (cdc.gov)
Genus2
- The type species of the genus ARTERIVIRUS and the etiologic agent of an important equine respiratory disease causing abortion, pneumonia, or other infections. (nih.gov)
- Getah virus (genus Alphavirus , family Togaviridae ) is a mosquito-borne virus that was first isolated in Malaysia in 1955 from Culex spp. (cdc.gov)
Infection3
- Izumida A , Takuma H , Inagaki S , Kubota M , Hirahara T , Kodama K , Experimental infection of Getah virus in swine. (cdc.gov)
- Herpes simplex virus (HSV) meningitis is associated with primary genital HSV infection and HIV infection. (medscape.com)
- Exposure to rodents suggests infection with lymphocytic choriomeningitis virus (LCM) virus and Leptospira infection. (medscape.com)
Reverse transcription1
- Reverse transcription PCR (RT-PCR) was conducted using a primer pair targeting nonstructural protein 1 (NSP1) of Getah virus (OneStep RT-PCR Kit, QIAGEN, Hilden, Germany) by using the RNA extracted from the blood samples ( 8 ). (cdc.gov)
Neutralization2
- By neutralization tests, Ibaraki virus was more closely related to EHD virus, serotype 2 (Alberta strain). (cdc.gov)
- A virus neutralization test for Getah virus was conducted on Vero cells using the MI-110 strain, which was isolated in 1978 ( 11 ) and is the current vaccine strain, as described previously ( 12 ) with slight modification. (cdc.gov)
Suggests1
- Serologic evidence suggests that Getah virus is widespread from Eurasia to Australasia ( 1 , 2 ). (cdc.gov)
Study1
- To study cell entry and infectivity of arteriviruses, high quality virus stocks are necessary. (nih.gov)
Fever1
- Patients with meningitis caused by the mumps virus usually present with the triad of fever, vomiting, and headache. (medscape.com)
Japan2
- Phylogenetic analyses of the nucleotide sequences of the (A) nonstructural protein 1 (NSP1) gene (nt 218-598) and (B) capsid gene (nt 7645-8196) of Getah virus isolated in Japan, 2014. (cdc.gov)
- Viruses detected in 2014 were phylogenetically different from the virus isolated in Japan in 1978. (cdc.gov)