Cardiovirus
Mengovirus
Encephalomyocarditis virus
Picornaviridae
Theilovirus
Theiler's viruses with mutations in loop I of VP1 lead to altered tropism and pathogenesis. (1/262)
Theiler's murine encephalomyelitis viruses are picornaviruses that can infect the central nervous system. The DA strain produces an acute polioencephalomyelitis followed by a chronic demyelinating disease in its natural host, the mouse. The ability of DA virus to induce a demyelinating disease renders this virus infection a model for human demyelinating diseases such as multiple sclerosis. Here we describe the generation and characterization of DA virus mutants that contain specific mutations in the viral capsid protein VP1 at sites believed to be important contact regions for the cellular receptor(s). A mutant virus with a threonine-to-aspartate (T81D) substitution in VP1 loop I adjacent to the putative virus receptor binding site exhibited a large-plaque phenotype but had a slower replication cycle in vitro. When this mutant virus was injected into susceptible mice, an altered tropism was seen during the acute stage of the disease and the chronic demyelinating disease was not produced. A virus with a threonine-to-valine substitution (T81V) did not cause any changes in the pattern or extent of disease seen in mice, whereas a virus with a tryptophan substitution at this position (T81W) produced a similar acute disease but was attenuated for the development of the chronic disease. A change in amino acids in a hydrophobic patch located in the wall of the pit, VP1 position 91, to a hydrophilic threonine (V91T) resulted in a profound attenuation of the acute and chronic disease without persistence of virus. This report illustrates the importance of the loop I of VP1 and a site in the wall of the pit in pathogenesis and that amino acid substitutions at these sites result in altered virus-host interactions. (+info)Differentiation of M1 myeloid precursor cells into macrophages results in binding and infection by Theiler's murine encephalomyelitis virus and apoptosis. (2/262)
Infection of susceptible mouse strains with BeAn, a less virulent strain of Theiler's murine encephalomyelitis virus (TMEV), results in immune system-mediated demyelinating lesions in the central nervous system (CNS) similar to those in multiple sclerosis. Since macrophages appear to carry the major detectable antigen burden in vivo, and purification of sufficient cell numbers from the CNS for detailed analysis is difficult, macrophage-like cell lines provide an accessible system with which to study virus-macrophage interactions. The myeloid precursor cell line M1 differentiates in response to cytokines and expresses many characteristics of tissue macrophages. Incubation of TMEV with undifferentiated M1 cells produced neither infection nor apoptosis, whereas differentiated M1 (M1-D) cells developed a restricted virus infection and changes indicative of apoptosis. Virus binding and RNA replication as well as cellular production of alpha/beta interferons increased with differentiation. Although the amount of infectious virus was highly restricted, BeAn-infected M1-D cells synthesized and appropriately processed virus capsid proteins at levels comparable to those for permissive BHK-21 cells. Analysis of Bcl-2 protein family expression in undifferentiated and differentiated cells suggests that susceptibility of M1-D cells to apoptosis may be controlled, in part, by expression of the proapoptotic alpha isoform of Bax and Bak. These data suggest that macrophage differentiation plays a role in susceptibility to TMEV infection and apoptosis. (+info)Pimobendan inhibits the production of proinflammatory cytokines and gene expression of inducible nitric oxide synthase in a murine model of viral myocarditis. (3/262)
OBJECTIVES: This study was designed to examine the effects of pimobendan in a murine model of viral myocarditis in relation to proinflammatory cytokine production and nitric oxide (NO) synthesis by inducible NO synthase (iNOS) in the heart. BACKGROUND: Pimobendan has been recently confirmed to improve both acute and chronic heart failure. Since the modulation of myocardial necrosis and contractile dysfunction by various proinflammatory cytokines may be partially mediated by the production of nitric oxide, the effects of pimobendan on the production ofproinflammatory cytokines and NO were investigated in an animal model of viral myocarditis involving heart failure. METHODS: DBA/2 mice were inoculated with the encephalomyocarditis virus. To observe its effect on survival up to 14 days, pimobendan (0.1 mg/kg or 1 mg/kg) or vehicles were given from the day of virus inoculation (day 0) orally once daily. The effects of pimobendan on histological changes, cytokine production, NO production and iNOS gene expression in the heart were studied in mice treated either with pimobendan, 1 mg/kg or with vehicles only, and sacrificed seven days after virus inoculation. RESULTS: The survival of mice improved in a dose-dependent fashion such that a significant difference (p < 0.02) was found between the higher-dose pimobendan group (20 of 30 [66.7%]) and the control group (11 of 30 [36.7%]). Histological scores for cellular infiltration (1.1+/-0.1 vs. 2.0+/-0.0, p < 0.001), intracardiac tumor necrosis factor (TNF)-alpha (18.2+/-1.8 vs. 35.8+/-4.2 pg/mg heart, p < 0.001) and interleukin (IL)-1beta (9.3 +/-1.2 vs. 26.6+/-7.1 pg/mg heart, p < 0.01) were significantly lower in the mice given pimobendan versus those of the control mice. Interleukin-6 levels (7.1+/-0.8 vs. 9.2+/-1.9 pg/mg heart) were also lower in the mice treated with pimobendan. Furthermore, intracardiac NO production was significantly (p < 0.001) less in the pimobendan group (0.165+/-0.004 nmol/mg heart) than in the control group (0.291+/-0.051 nmol/mg heart), and intracardiac iNOS gene expression in the mice given pimobendan was 74% lower than it was in the control animals (p < 0.01). CONCLUSIONS: These findings suggest that the beneficial effects of pimobendan in viral myocarditis are partially mediated by the inhibition of both proinflammatory cytokine production and NO synthesis by iNOS. (+info)Targeted overexpression of elafin protects mice against cardiac dysfunction and mortality following viral myocarditis. (4/262)
Serine elastases degrade elastin, stimulate vascular smooth muscle cell migration and proliferation, and are associated with myocardial damage. To evaluate the impact of elastase inhibition on cardiovascular development and disease, transgenic mice were created in which the mouse preproendothelin-1 promoter was used to target elafin overexpression to the cardiovascular system. To distinguish the transgene from endogenous elafin, constructs were made incorporating a FLAG sequence; the COOH-terminus FLAG-tagged elafin construct produced a stable, functionally active gene product and was used to create transgenic mice. Consistent with endothelin expression, abundant elafin mRNA was observed in transgenic F1 embryos (embryonic day 13.5) and in adult transgenic mice heart, trachea, aorta, kidney, lung, and skin, but not in liver, spleen, and intestine. Functional activity of the transgene was confirmed by heightened myocardial elastase inhibitory activity. No tissue abnormalities were detected by light microscopy or elastin content. However, injection of 10 plaque-forming units (PFU) of encephalomyocarditis virus resulted in death within 11 days in 10 out of 12 nontransgenic mice compared with one out of nine transgenic littermates. This reduced mortality was associated with better cardiac function and less myocardial inflammatory damage. Thus, elafin expression may confer a protective advantage in myocarditis and other inflammatory diseases. (+info)Encephalomyocarditis (EMC) virus infection in PC12 and C6 cells. (5/262)
PC12 cells derived rom rat pheochromocytoma and C6 cells derived from rat glioma were infected with 0.3 plaque forming units (PFU)/cell of the D variant of encephalomyocarditis virus (EMC-D), after pretreatment with or without nerve growth factor (NGF). The virus titres in medium and cells were investigated at 6, 12, 24, 48 and 72 h post infection (HPI), and histopathology and viral antigens in cells were examined at 24 and 48 HPI, respectively. As a result, neither viral replication nor light and electron microscopic changes were observed in PC12 cell cultures without NGF-pretreatment. On the contrary, in PC12 cell cultures with NGF-pretreatment, the virus titre prominently increased at 12 HPI, and peaked at 48 HPI. In addition, distinct histological and ultrastructural changes with viral antigens in cells were observed. C6 cells showed similar morphology and susceptibility to EMC-D-infection irrespective of NGF-pretreatment. Namely, the virus titres in C6 cell cultures increased slightly and viral antigens were found in a small number of C6 cells, but there were no evident histological and ultrastructural changes. These results suggest that PC12 cells pretreated with NGF and C6 cells are susceptible to EMC-D infection in vitro. (+info)Interstitial fibrin-fibronectin deposition with T cell infiltrates precedes fibrosis in murine viral myocarditis. (6/262)
This study was carried out to investigate interstitial fibrin and fibronectin deposition and subsequent myocardial connective tissue abnormalities in BALB/c-nu/+ (euthymic and normal T cell function) and BALB/c-nu/nu (athymic and T cell-deficient) mice. Both types of mice were inoculated with encephalomyocarditis virus and sacrificed periodically. Sections of the hearts were stained with haematoxylin-eosin, trichrome, lymphocyte subsets, silver impregnation, and fibrin or fibronectin. In addition, myocardial collagen concentration was measured. Interstitial fibrin and fibronectin appeared in parallel with inflammatory T lymphocytes and myocardial necrosis in the BALB/c-nu/+ mice. The changes increased until 14 days, subsequently decreasing with time. Interstitial fibrosis and abnormal reticulin fibres were absent until 7 days postinfection, and then increased with time until 60 days. In BALB/c-nu/nu mice, in contrast, although myocardial necrosis and fibrin-fibronectin deposition associated with immature T lymphocytes were evident on days 7 and 14, subsequent myocardial fibrosis and reticulin fibre abnormalities were minimal on days 30 and 60. In BALB/c-nu/+ mice, myocardial collagen concentration increased on day 30, but it did not in BALB/c-nu/nu mice. Thus, interstitial fibrin-fibronectin deposition resulting from virus-induced and T lymphocyte-mediated myocyte necrosis precedes the subsequent development of interstitial fibrosis and abnormal reticulin architectures in this model of murine myocarditis. (+info)Theiler's murine encephalomyelitis virus infection induces early expression of c-fos in astrocytes. (7/262)
We have determined whether Theiler's murine encephalomyelitis virus (TMEV), a picornavirus that produces demyelination in genetically susceptible strains of mice, induces c-fos in pure quiescent cultures of mouse brain astrocytes. As observed in Northern blots, the expression of this immediate early gene increases in a dose-dependent manner, with its expression peaking at a multiplicity of infection of 100. The expression of c-fos is transient, peaking after 30 min and disappearing 2 h after infection. The virus is quickly internalized at 37 degrees C upon binding to its specific receptor located at the cell surface and is actively replicated in the cytoplasm of the astrocytes, as demonstrated by FACS flow cytometry. Using the same technique, nuclear translation of c-fos mRNA is also shown. The specificity of viral induction is demonstrated by its neutralization with TMEV-specific antibodies and by the fact that only viral particles and not purified protein components VP1, VP2, and VP3 induced proto-oncogene expression. This rapid induction of c-fos in astrocytes could be the first stage in the infection of these central nervous system cell populations by TMEV. The biological relevance of these findings is assessed by the demonstration of c-fos activation after viral infection in vivo. (+info)Potential role of CD4+ T cell-mediated apoptosis of activated astrocytes in Theiler's virus-induced demyelination. (8/262)
Intracerebral inoculation of Theiler's murine encephalomyelitis virus (TMEV) into susceptible mouse strains results in a chronic, immune-mediated demyelinating disease similar to human multiple sclerosis. Here, we examined the role of astrocytes as an APC population in TMEV-induced demyelination and assessed the potential consequences of T cell activation following Ag presentation. IFN-gamma-pretreated astrocytes were able to process and present all the predominant T cell epitopes of TMEV to virus-specific T cell hybridomas, clones, as well as bulk T cells. Despite low levels of proliferation of T cells due to prostaglandins produced by astrocytes, such Ag presentation by activated astrocytes induced the production of IFN-gamma, a representative proinflammatory cytokine, in TMEV-specific Th cell clones derived from the CNS of virus-infected mice. Furthermore, these Th cell clones mediate lysis of the astrocytes in vitro in a Fas-dependent mechanism. TUNEL staining of CNS tissue demonstrates the presence of apoptotic GFAP+ cells in the white matter of TMEV-infected mice. These results strongly suggest that astrocytes could play an important role in the pathogenesis of TMEV-induced demyelination by activating T cells, subsequently leading to T cell-mediated apoptosis of astrocytes and thereby compromising the blood-brain barrier. (+info)Cardiovirus infections are a type of viral infection that affects the heart muscle, leading to cardiomyopathy and potentially heart failure. The most common cause of cardiovirus infections is the adenovirus, which is a common virus that can infect people of all ages.
Symptoms of Cardiovirus Infections:
The symptoms of cardiovirus infections can vary depending on the severity of the infection and the individual's overall health. Common symptoms include:
* Chest pain or discomfort
* Shortness of breath
* Fatigue
* Swelling of the legs, ankles, and feet
* Fast or irregular heartbeat
* Low blood pressure
Diagnosis of Cardiovirus Infections:
To diagnose a cardiovirus infection, a healthcare provider will typically perform a physical examination and ask about the individual's symptoms. They may also order one or more diagnostic tests, such as:
* Electrocardiogram (ECG) to measure the heart's electrical activity
* Echocardiogram to visualize the heart and its function
* Blood tests to look for signs of inflammation or cardiac damage
Treatment of Cardiovirus Infections:
There is no specific treatment for cardiovirus infections, but the following treatments may be recommended to manage symptoms and prevent complications:
* Rest and avoiding strenuous activities
* Medications to control heart rate and rhythm
* Diuretics to reduce fluid buildup in the body
* Oxygen therapy to improve oxygen levels in the blood
Prevention of Cardiovirus Infections:
Preventing cardiovirus infections is challenging, but taking steps to avoid exposure can help reduce the risk. These steps include:
* Practicing good hygiene, such as washing hands frequently and avoiding close contact with people who are sick
* Avoiding sharing food, drinks, or personal items with people who are sick
* Covering the mouth and nose when coughing or sneezing
* Staying home from work or school if experiencing symptoms
It is important to note that cardiovirus infections can be severe and potentially life-threatening, especially for certain populations such as older adults, young children, and people with underlying heart conditions. If you suspect you or someone else may have a cardiovirus infection, it is essential to seek medical attention right away.
Cardiovirus
Saffold virus
Theiler's encephalomyelitis virus
Cardiovirus A
Picornain 3C
List of MeSH codes (C02)
Picornavirus
Bat virome
Mengovirus
Erbovirus
Saffold Cardioviruses of 3 Lineages in Children with Respiratory Tract Infections, Beijing, China - Volume 16, Number 7-July...
DeCS
HuGE Navigator|Genopedia|PHGKB
DeCS 2008 - versión 17 de Marzo de 2008
Pesquisa | Portal Regional da BVS
Structural studies of human picornaviruses directed towards development of anti-viral compounds | CEITEC - výzkumné centrum
Enterovirus a human. Medical search. Definitions
MH DELETED MN ADDED MN
MH DELETED MN ADDED MN
MH DELETED MN ADDED MN
Saffold virus, a human Theiler's-like cardiovirus, is ubiquitous and causes infection early in life - PubMed
Saffold Cardioviruses of 3 Lineages in Children with Respiratory Tract Infections, Beijing, China - Volume 16, Number 7-July...
Picornavirus Infections: Background, Pathophysiology, Epidemiology
HuGE Navigator|Genopedia|PHGKB
MeSH Browser
MeSH Browser
DeCS
Picornavirus Infections: Background, Pathophysiology, Epidemiology
TERM
Descriptors in 2013 MeSH. Preferred term only. December 14, 2012
Metagenomics for the Discovery of Novel Human Viruses
TREE NUMBER DESCRIPTOR
I ntegrated
About Viral and Phage Genome Processing and Tools - The NCBI Handbook - NCBI Bookshelf
MH DELETED MN ADDED MN
MH DELETED MN ADDED MN
MH DELETED MN ADDED MN
c33c
Genera1
- We will use X-ray crystallography to determine virion structures of representative viruses from Parechovirus, Kobuvirus, Cardiovirus, and Cosavirus genera and Human Rhinovirus-C species. (ceitec.eu)
PICORNAVIRIDAE2
- Infecciones producidas por virus del género CARDIOVIRUS, familia PICORNAVIRIDAE. (bvsalud.org)
- Infections caused by viruses of the genus CARDIOVIRUS, family PICORNAVIRIDAE. (bvsalud.org)
Viral infection2
- During RNA viral infection, RIG-I-like receptors (RLRs) recognize the intracellular pathogenic RNA species derived from viral replication and activate antiviral innate immune response by stimulating type 1 interferon expression. (bvsalud.org)
- Inflammation of brain parenchymal tissue as a result of viral infection. (lookformedical.com)
Genome2
- Although IFN-ß mRNA was detected within infected cells, this response usually occurs during the middle stages of infection, after genome replication has taken place. (bvsalud.org)
- Furthermore, we will investigate how picornaviruses initiate infection by analyzing genome release from virions and its translocation across lipid membrane. (ceitec.eu)
Therapeutic1
- The key roles RLR signaling play in both anti-infection and immune disease conditions highlight the therapeutic potential in targeting this important molecular pathway. (bvsalud.org)
Occurs1
- Although serologic surveys have shown that SAFV-3 infection occurs early in life ( 7 ), the pathogenicity of SAFV is still unclear. (cdc.gov)
Respiratory2
- To clarify the potential for respiratory transmission of Saffold cardiovirus (SAFV) and characterize the pathogen, we analyzed respiratory specimens from 1,558 pediatric patients in Beijing. (cdc.gov)
- We identified and characterized 7 SAFV strains, which belonged to 3 distinct lineages, from respiratory samples of children with lower and upper respiratory tract infections (LRTIs and URTIs, respectively). (cdc.gov)
Virus3
- Mammalian cells have developed specialized receptors that detect RNA with unusual structures or of foreign origin - a hallmark of many virus infections. (bvsalud.org)
- Here, we show that this virus, which causes mild diarrhea, growth retardation, and damage of the villi of the small intestinal mucosa in piglets, induces an IFN response upon infection of PK-15 cells. (bvsalud.org)
- Vaccines with both inactivated and live attenuated virus have proven effective in immunizing against the infection. (lookformedical.com)
Disease2
- However, because 3 patients had co-infections, we could not definitively say SAFV caused disease. (cdc.gov)
- However, it is increasingly appreciated that these RNA sensors can also be activated in the absence of infection, and that this 'self-activation' can be pathogenic and promote disease. (bvsalud.org)
Early1
- Early detection of infection is a central and critical component of our innate immune system. (bvsalud.org)
Picornaviridae2
- Infections caused by viruses of the genus CARDIOVIRUS , family PICORNAVIRIDAE . (nih.gov)
- Género de la familia PICORNAVIRIDAE que causa encefalitis y miocarditis en roedores. (bvsalud.org)
SAFV11
- Saffold cardiovirus (SAFV) and characterize the pathogen, for the 5 untranslated region (UTR) ( 3 ). (cdc.gov)
- The 5 and co-infections, we could not defi nitively say SAFV caused 3 UTR sequences were determined by using the RACE disease. (cdc.gov)
- After being cloned into the Saffold cardiovirus (SAFV) is a new piconavirus, origi- pGEM-T Easy vector (Promega, Madison, WI, USA), all nally identifi ed from fecal samples of a female infant PCR products were verifi ed by sequencing. (cdc.gov)
- SAFV-3 infection occurs early in life ( 7 ), the pathogenicity tion test kit (SERODIA-MYCO II, Fujirebio, Japan). (cdc.gov)
- The virus is genetically related to Theiler's virus and classified as a new species in the genus Cardiovirus, which until the discovery of SAFV did not contain human viruses. (nih.gov)
- By analogy with the rodent cardioviruses, SAFV may be a relevant new human pathogen. (nih.gov)
- To clarify the potential for respiratory transmission of Saffold cardiovirus (SAFV) and characterize the pathogen, we analyzed respiratory specimens from 1,558 pediatric patients in Beijing. (cdc.gov)
- However, because 3 patients had co-infections, we could not definitively say SAFV caused disease. (cdc.gov)
- Saffold cardiovirus (SAFV) is a new piconavirus, originally identified from fecal samples of a female infant with fever of unknown origin ( 1 ). (cdc.gov)
- Although serologic surveys have shown that SAFV-3 infection occurs early in life ( 7 ), the pathogenicity of SAFV is still unclear. (cdc.gov)
- We identified and characterized 7 SAFV strains, which belonged to 3 distinct lineages, from respiratory samples of children with lower and upper respiratory tract infections (LRTIs and URTIs, respectively). (cdc.gov)
Genus1
- In addition, this family contains a number of viruses that infect animals, including members of the genus Cardiovirus such as Encephalomyocarditis virus (EMCV) and Theiler's murine encephalomyelits virus (TMEV). (nih.gov)
Encephalomyocarditis1
- Cardiovirus (type species, encephalomyocarditis virus) is a classic infection in mice, although it has been observed to cause disease in humans. (medscape.com)
Viruses1
- In diseases and samples where the concentration of viruses is high relative to other cells, such as respiratory secretions in acute respiratory infections or stool in acute gastroenteritis, the clinical sensitivity of the viral microarrays is comparable to that of specific PCR assays for the same viruses. (medscape.com)