Infections with viruses of the genus RUBULAVIRUS, family PARAMYXOVIRIDAE.
A genus of the family PARAMYXOVIRIDAE (subfamily PARAMYXOVIRINAE) where all the species have hemagglutinin and neuraminidase activities but lack a C protein. MUMPS VIRUS is the type species.
A species of RUBULAVIRUS associated particularly with acute laryngotracheitis (CROUP) in children aged 6 months to 3 years.

Development of a blocking ELISA for screening antibodies to porcine rubulavirus, La Piedad Michoacan Virus. (1/34)

A blocking enzyme-linked immunosorbent assay (ELISA) was developed to detect antibodies to porcine rubulavirus (La Piedad Michoacan Virus [LPMV]) in serum samples from pigs. The test, based on a monoclonal antibody against the LPMV hemagglutinin-neuraminidase glycoprotein, had a sensitivity of 99% and a specificity of 97%. The results of this test were in agreement with those obtained by an indirect ELISA and hemagglutination inhibition, indirect immunofluorescence, and virus neutralization tests. The blocking ELISA is considered the most suitable test for routine screening for antibodies against LPMV.  (+info)

Detection and identification of human parainfluenza viruses 1, 2, 3, and 4 in clinical samples of pediatric patients by multiplex reverse transcription-PCR. (2/34)

We describe a multiplex reverse transcription-PCR (m-RT-PCR) assay that is able to detect and differentiate all known human parainfluenza viruses (HPIVs). Serial dilution experiments with reference strains that compared cell culture isolation and m-RT-PCR showed sensitivities ranging from 0.0004 50% tissue culture infective dose (TCID(50)) for HPIV type 4B (HPIV-4B) to 32 TCID(50)s for HPIV-3. As few as 10 plasmids containing HPIV PCR products could be detected in all cases. When 201 nasopharyngeal aspirate specimens from pediatric patients hospitalized for lower respiratory illness were tested, m-RT-PCR assay detected 64 HPIVs (24 HPIV-3, 23 HPIV-1, 10 HPIV-4, and 7 HPIV-2), while only 42 of them (21 HPIV-1, 14 HPIV-3, 6 HPIV-2, and 1 HPIV-4 isolates) grew in cell culture. Our m-RT-PCR assay was more sensitive than either cell culture isolation or indirect immunofluorescence with monoclonal antibodies for the detection of HPIV infections. Also, HPIV-4 was more frequently detected than HPIV-2 in this study, suggesting that it may have been underestimated as a lower respiratory tract pathogen because of the insensitivity of cell culture.  (+info)

The V protein of human parainfluenza virus 2 antagonizes type I interferon responses by destabilizing signal transducer and activator of transcription 2. (3/34)

Type I interferon (IFN) induces antiviral responses through the activation of the ISGF3 transcription factor complex that contains the subunit proteins STAT1, STAT2, and p48/ISGF3 gamma/IRF9. The ability of some human paramyxoviruses to overcome IFN actions by specific proteolysis of STAT proteins has been examined. Infection of cells with type 2, but not type 1 or type 3 human parainfluenza virus (HPIV) leads to a loss of cellular STAT2 protein. Expression of a single HPIV2 protein derived from the V open reading frame blocks IFN-dependent transcriptional responses in the absence of other viral proteins. The loss of IFN response is due to V-protein-induced proteolytic degradation of STAT2. Expression of HPIV2 V causes the normally stable STAT2 protein to be rapidly degraded, and this proteolytic activity can be partially alleviated by proteasome inhibition. No V-protein-specific effects on STAT2 mRNA levels were observed. The results indicate that the V protein of HPIV2 is sufficient to recognize and target a specific cellular transcription factor for destruction by cellular machinery.  (+info)

High resistance of human parainfluenza type 2 virus protein-expressing cells to the antiviral and anti-cell proliferative activities of alpha/beta interferons: cysteine-rich V-specific domain is required for high resistance to the interferons. (4/34)

Human parainfluenza type 2 virus (hPIV-2)-infected HeLa (HeLa-CA) cells and hPIV-2 V-expressing HeLa (HeLa-V) cells show high resistance to alpha/beta interferons (IFN-alpha/beta) irrespective of whether vesicular stomatitis virus or Sindbis virus is used as a challenge virus. When Sindbis virus is used, these cells show high susceptibility to human IFN-gamma. Furthermore, the multiplication of HeLa-V cells is not inhibited by IFN-alpha/beta. HeLa cells expressing the N-terminally truncated V protein show resistance to IFN-alpha/beta, showing that the IFN resistance determinant maps to the cysteine-rich V-specific domain. A complete defect of Stat2 is found in HeLa-CA and HeLa-V cells, whereas the levels of Stat1 expression are not significantly different among HeLa, HeLa-CA, HeLa-P, and HeLa-V cells, indicating that IFN-alpha/beta resistance of HeLa-CA and HeLa-V cells is due to a defect of Stat2. HeLa-SV41V cells show high resistance to all IFNs, and no expression of Stat1 can be detected. Stat2 mRNA is fully detected in HeLa-V cells. Stat2 was scarcely pulse-labeled in the HeLa-V cells, indicating that synthesis of Stat2 is suppressed or Stat2 is very rapidly degraded in HeLa-V cells. The V protein suppresses the in vitro translation of Stat2 mRNA more extensively than that of Stat1 mRNA. An extremely small amount of Stat2 can be detected in HeLa-V cells treated with proteasome inhibitors. The half-life of Stat2 is approximately 3.5 and 2 h in uninfected and hPIV-2-infected HeLa cells, respectively. This study shows that synthesis of Stat2 may be suppressed and Stat2 degradation is also enhanced in hPIV-2-infected HeLa and HeLa-V cells.  (+info)

Rapid and sensitive method using multiplex real-time PCR for diagnosis of infections by influenza a and influenza B viruses, respiratory syncytial virus, and parainfluenza viruses 1, 2, 3, and 4. (5/34)

Laboratory diagnosis of viral respiratory infections is generally performed by virus isolation in cell culture and immunofluorescent assays. Reverse transcriptase PCR is now recognized as a sensitive and specific alternative for detection of respiratory RNA viruses. A rapid real-time multiplex PCR assay was developed for the detection of influenza A and influenza B viruses, human respiratory syncytial virus (RSV), parainfluenza virus 1 (PIV1), PIV2, PIV3, and PIV4 in a two-tube multiplex reaction which used molecular beacons to discriminate the pathogens. A total of 358 respiratory samples taken over a 1-year period were analyzed by the multiplex assay. The incidence of respiratory viruses detected in these samples was 67 of 358 (19%) and 87 of 358 (24%) by culture and real-time PCR, respectively. Culture detected 3 influenza A virus, 2 influenza B virus, 57 RSV, 2 PIV1, and 2 PIV3 infections. All of these culture-positive samples and an additional 5 influenza A virus, 6 RSV, 2 PIV1, 1 PIV2, 1 PIV3, and 3 PIV4 infections were detected by the multiplex real-time PCR. The application of real-time PCR to clinical samples increases the sensitivity for respiratory viral diagnosis. In addition, results can be obtained within 6 h, which increases clinical relevance. Therefore, use of this real-time PCR assay would improve patient management and infection control.  (+info)

Exaggerated IL-8 and IL-6 responses to TNF-alpha by parainfluenza virus type 4-infected NCI-H292 cells. (6/34)

Respiratory viruses induce and potentiate airway inflammation, which is related to the induction of proinflammatory mediators such as interleukin (IL)-8 and IL-6. Here we report on mechanisms implicated in IL-8 and IL-6 production by airway epithelium-like NCI-H292 cells exposed to parainfluenza virus type 4a (PIV-4). PIV-4 readily infected NCI-H292 cells as reflected by intracellular PIV-4 antigen expression. PIV-4 infection triggered a biphasic IL-8 and IL-6 mRNA response. Transient transfection with truncated and mutated promoter constructs identified NF-kappaB and activator protein (AP)-1, and CCAAT-enhancer binding protein (C/EBP) as the relevant transcription factors for PIV-4-induced IL-8 and IL-6 gene transcription, respectively. An increase of DNA-binding activities for NF-kappaB and C/EBP paralleled the induction of the first and second IL-8 and IL-6 mRNA peaks, whereas the onset of AP-1 paralleled the first IL-8 mRNA peak only. The second mRNA peak, apparently dependent on viral replication, coincided also with a marked reduction of IL-8 and IL-6 mRNA degradation. Importantly, cells at the time of the reduced mRNA degradation displayed an exaggerated IL-8 and IL-6 protein production to a secondary stimulus, as exemplified by steeper dose-response curves to TNF-alpha. Thus PIV-4 infection enhances epithelial IL-8 and IL-6 production by transcriptional and posttranscriptional mechanisms. The previously unrecognized phase of reduced IL-8 and IL-6 mRNA degradation and the concurrent amplified epithelial IL-8 and IL-6 responses may play an important role in virus-induced potentiation of airway inflammation.  (+info)

Altered function in CD8+ T cells following paramyxovirus infection of the respiratory tract. (7/34)

For many respiratory pathogens, CD8+ T cells have been shown to play a critical role in clearance. However, there are still many unanswered questions with regard to the factors that promote the most efficacious immune response and the potential for immunoregulation of effector cells at the local site of infection. We have used infection of the respiratory tract with the model paramyxovirus simian virus 5 (SV5) to study CD8+ T-cell responses in the lung. For the present study, we report that over time a population of nonresponsive, virus-specific CD8+ T cells emerged in the lung, culminating in a lack of function in approximately 85% of cells specific for the immunodominant epitope from the viral matrix (M) protein by day 40 postinfection. Concurrent with the induction of nonresponsiveness, virus-specific cells that retained function at later times postinfection exhibited an increased requirement for CD8 engagement. This change was coupled with a nearly complete loss of functional phosphoprotein-specific cells, a response previously shown to be almost exclusively CD8 independent. These studies add to the growing evidence for immune dysregulation following viral infection of the respiratory tract.  (+info)

Abortive versus productive viral infection of dendritic cells with a paramyxovirus results in differential upregulation of select costimulatory molecules. (8/34)

Dendritic cells are the most potent antigen-presenting cell for priming naive T cells. Optimal activation of T cells requires that dendritic cells undergo a process of maturation resulting in the increased expression of costimulatory molecules, such as CD40, CD86, and CD80, and the production of cytokines. In this study we analyzed the effect of infection of dendritic cells obtained from two strains of mice, BALB/c and C57BL/6, with the paramyxovirus simian virus 5 (SV5). Our results show that C57BL/6 bone marrow-derived dendritic cells (BMDC) are much more permissive to infection with SV5 at a multiplicity of infection (MOI) of 10 PFU/cell compared to BALB/c BMDC, as determined by the production of viral proteins and progeny. However, infection of BALB/c BMDC with a higher MOI of 50 PFU/cell resulted in a productive infection with the production of significant amounts of viral proteins and progeny. Regardless of the permissivity to infection, both BALB/c and C57BL/6 BMDC efficiently upregulated CD40 and CD86. However, CD80 upregulation correlated with the level of expression of viral proteins and the production of viral progeny. While secreted alpha/beta interferon was required for increased expression of all three molecules, optimal CD80 expression was dependent on an additional signal provided by a productive viral infection. These findings provide evidence that the signals controlling the expression of costimulatory molecules following viral infection are distinct. Further, they suggest that the amount of virus encountered and/or the permissivity of a dendritic cell to infection can alter the resulting maturation phenotype and functional capacity of the infected dendritic cell.  (+info)

Rubulavirus infections refer to a group of viral illnesses caused by members of the Rubulavirus genus, which is part of the Paramyxoviridae family. The most well-known rubulavirus is the mumps virus, which causes mumps, a contagious disease characterized by swelling of the salivary glands, fever, and pain while chewing or swallowing. Other rubulaviruses include parainfluenza viruses 1 and 3, which can cause respiratory illnesses such as bronchitis and pneumonia. Rubulavirus infections are typically spread through respiratory droplets or direct contact with infected individuals. Vaccination is available for some rubulavirus infections, such as mumps.

Rubulavirus is a genus in the family Paramyxoviridae, order Mononegavirales. It includes several viruses that primarily cause respiratory infections in humans and animals. The most well-known rubulaviruses affecting humans are the human parainfluenza viruses (HPIV) 2 and 4, which can cause croup and bronchitis, and mumps virus, which causes mumps. These viruses are typically spread through respiratory droplets and direct contact with infected individuals. They have enveloped, non-segmented, negative-sense RNA genomes.

Parainfluenza Virus 2, Human (HPIV-2) is a type of respiratory virus that belongs to the family Paramyxoviridae and genus Respirovirus. It is one of the four serotypes of human parainfluenza viruses (HPIVs), which also include HPIV-1, HPIV-3, and HPIV-4.

HPIV-2 primarily infects the upper respiratory tract and causes mild to moderate symptoms similar to those caused by other respiratory viruses. The infection can lead to inflammation of the nose, throat, and voice box (larynx), resulting in a runny nose, sore throat, cough, and hoarseness. In some cases, HPIV-2 can also cause croup, a condition characterized by a barking cough and stridor (high-pitched breathing sounds) due to inflammation of the upper airways.

HPIV-2 is highly contagious and spreads through respiratory droplets produced when an infected person talks, coughs, or sneezes. The virus can also be transmitted by touching contaminated surfaces and then touching the mouth, nose, or eyes. HPIV-2 infections are most common in infants and young children, but people of all ages can become infected.

There is no specific treatment for HPIV-2 infections, and management typically involves supportive care to alleviate symptoms. Preventive measures include good hygiene practices, such as frequent handwashing, covering the mouth and nose when coughing or sneezing, and avoiding close contact with sick individuals. Vaccines are not available for HPIV-2 infections, but research is ongoing to develop effective vaccines against these viruses.

The rubulavirus genus can then be divided into two main groups, based on the type of pathogen. Rubulavirus genus contains human ... In other words, the vaccine for human mumps appears to reduce the risk of infection from the bat mumps virus. Tropism in bats ... Bat Mumps Rubulavirus (BMV), and Menangle (MenPV). Bat mumps rubulavirus (BMV) is a spherical shaped negative sense single ... "Rubulavirus ~ ViralZone page". viralzone.expasy.org. Retrieved 2019-12-04. EST, Jessica Wapner On 02/09/17 at 10:29 AM (2017-02 ...
... www.thepigsite.com/pighealth/article/444/blue-eye-disease-be Porcine Rubulavirus infection, http://www.cfsph.iastate.edu/ ... "La Piedad Michoacán Paramyxovirus Infection". Blue eye disease is a viral disease that is commonly identified by encephalitis, ... associated with a paramyxovirus infection". Veterinary Record. 122 (1): 6-10. doi:10.1136/vr.122.1.6. PMID 3363809. S2CID ... piglets High mortality in piglets Swollen testicles Loss of libido Blue eye disease is caused by the porcine rubulavirus, which ...
... respiratory syncytial virus infections MeSH C02.782.580.600.680 - rubulavirus infections MeSH C02.782.580.600.680.500 - mumps ... cardiovirus infections MeSH C02.782.687.207 - common cold MeSH C02.782.687.359 - enterovirus infections MeSH C02.782.687.359. ... deltaretrovirus infections MeSH C02.782.815.200.260 - enzootic bovine leukosis MeSH C02.782.815.200.470 - htlv-i infections ... avulavirus infections MeSH C02.782.580.600.080.600 - newcastle disease MeSH C02.782.580.600.400 - henipavirus infections MeSH ...
In 2018, Mumps rubulavirus was renamed to Mumps orthorubulavirus to accompany Rubulavirus being abolished and replaced with the ... Infection leads to fever, muscle pain, and painful swelling of the parotid glands, two salivary glands situated on the sides of ... Infection may also involve many other tissues and organs, resulting in a variety of inflammatory reactions such as encephalitis ... Within a few years after isolation, vaccines protecting against MuV infection had been developed. MuV was first recognized as a ...
HPIV-1, HPIV-2 and HPIV-3 have been linked with up to a third of these infections. Upper respiratory infections (URI) are also ... These include: HPIVs belong to two genera: Respirovirus (HPIV-1 & HPIV-3) and Rubulavirus (HPIV-2 & HPIV-4). HPIVs are ... However, infections have been induced in other animals (both under natural and experimental situations), although these were ... It is estimated that there are 5 million children with lower respiratory infections (LRI) each year in the United States alone ...
Diseases associated with this family include measles, mumps, and respiratory tract infections. The family has four subfamilies ... The respirovirus-henipavirus-morbillivirus clade may be basal to the avulavirus-rubulavirus clade. Animal virology Virology " ... of the single promoter model by having its genes arranged in relative order of protein needed for successful infection. For ...

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