Respirovirus Infections
High-temperature effects on antibody response to viral antigen in mice. (1/462)
To determine the effects of high-temperature exposure on antibody response to viral antigen in mice, male BALB/c mice were placed for 13 days in animal chambers at 23 degrees C, 32 degrees C, and 35.5 degrees C. Rectal temperature rose from 37 degrees C to 39 degrees C on day 1 in a 35.5 degrees C environment. The rectal temperature was kept constant throughout the exposure period. The IgG-antibody to Sendai virus (SV) antigen was inhibited to about 50% of the control value (23 degrees C). The serum corticosterone concentration indicating thermal stress increased steadily, peaking on day 1 and then gradually decreased and recovered to the normal level on day 13. Body weight decreased to about 72% of the controls on day 13. Thymus and spleen weight decreased to 31.7% and 61.5% respectively. At 32 degrees C, these effects were less than at 35.5 degrees C. Effects of high-temperature exposure at 35.5 degrees C appeared to noticeably decrease thymus and spleen weight. It is clear that IgG-antibody response to SV antigen is suppressed by high-temperature exposure. (+info)IkappaB-mediated inhibition of virus-induced beta interferon transcription. (2/462)
We have examined the consequences of overexpression of the IkappaBalpha and IkappaBbeta inhibitory proteins on the regulation of NF-kappaB-dependent beta interferon (IFN-beta) gene transcription in human cells after Sendai virus infection. In transient coexpression studies or in cell lines engineered to express different forms of IkappaB under tetracycline-inducible control, the IFN-beta promoter (-281 to +19) linked to the chloramphenicol acetyltransferase reporter gene was differentially inhibited in response to virus infection. IkappaBalpha exhibited a strong inhibitory effect on virus-induced IFN-beta expression, whereas IkappaBbeta exerted an inhibitory effect only at a high concentration. Despite activation of the IkappaB kinase complex by Sendai virus infection, overexpression of the double-point-mutated (S32A/S36A) dominant repressors of IkappaBalpha (TD-IkappaBalpha) completely blocked IFN-beta gene activation by Sendai virus. Endogenous IFN-beta RNA production was also inhibited in Tet-inducible TD-IkappaBalpha-expressing cells. Inhibition of IFN-beta expression directly correlated with a reduction in the binding of NF-kappaB (p50-RelA) complex to PRDII after Sendai virus infection in IkappaBalpha-expressing cells, whereas IFN-beta expression and NF-kappaB binding were only slightly reduced in IkappaBbeta-expressing cells. These experiments demonstrate a major role for IkappaBalpha in the regulation of NF-kappaB-induced IFN-beta gene activation and a minor role for IkappaBbeta in the activation process. (+info)Sendai virus and simian virus 5 block activation of interferon-responsive genes: importance for virus pathogenesis. (3/462)
Sendai virus (SeV) is highly pathogenic for mice. In contrast, mice (including SCID mice) infected with simian virus 5 (SV5) showed no overt signs of disease. Evidence is presented that a major factor which prevented SV5 from productively infecting mice was its inability to circumvent the interferon (IFN) response in mice. Thus, in murine cells that produce and respond to IFN, SV5 protein synthesis was rapidly switched off. In marked contrast, once SeV protein synthesis began, it continued, even if the culture medium was supplemented with alpha/beta IFN (IFN-alpha/beta). However, in human cells, IFN-alpha/beta did not inhibit the replication of either SV5 or SeV once virus protein synthesis was established. To begin to address the molecular basis for these observations, the effects of SeV and SV5 infections on the activation of an IFN-alpha/beta-responsive promoter and on that of the IFN-beta promoter were examined in transient transfection experiments. The results demonstrated that (i) SeV, but not SV5, inhibited an IFN-alpha/beta-responsive promoter in murine cells; (ii) both SV5 and SeV inhibited the activation of an IFN-alpha/beta-responsive promoter in human cells; and (iii) in both human and murine cells, SeV was a strong inducer of the IFN-beta promoter, whereas SV5 was a poor inducer. The ability of SeV and SV5 to inhibit the activation of IFN-responsive genes in human cells was confirmed by RNase protection experiments. The importance of these results in terms of paramyxovirus pathogenesis is discussed. (+info)Enumeration of antigen-presenting cells in mice infected with Sendai virus. (4/462)
Substantial progress has been made in understanding Ag presentation to T cells; however, relatively little is known about the location and frequency of cells presenting viral Ags during a viral infection. Here, we took advantage of a highly sensitive system using lacZ-inducible T cell hybridomas to enumerate APCs during the course of respiratory Sendai virus infection in mice. Using lacZ-inducible T cell hybridomas specific for the immunodominant hemagglutinin-neuraminidase HN421-436/I-Ab and nucleoprotein NP324-332/Kb epitopes, we detected APCs in draining mediastinal lymph nodes (MLNs), in cervical lymph nodes, and also in the spleen. HN421-436/I-Ab- and NP324-332/Kb-presenting cells were readily detectable between days 3 and 9 postinfection, with more APCs present in the MLN than in the cervical lymph nodes. Interestingly, no infectious virus was detected in lymphoid tissue beyond day 6, suggesting that a depot of noninfectious viral Ag survives, in some form, for 2-3 days after viral clearance. Fractionation of the MLN demonstrated that APC frequency was enriched in dendritic cells and macrophages but depleted in the B cell population, suggesting that B cells do not form a large population of APCs during the primary response to this virus. (+info)Isotype- and subclass-specific responses to infection and reinfection with parainfluenza-3 virus: comparison of the diagnostic potential of ELISAs detecting seroconversion and specific IgM and IgA. (5/462)
Isotype- and subclass-specific indirect enzyme-linked immunosorbent assays were developed to detect parainfluenza-3 virus-specific IgG1, IgG2, IgM, and IgA responses. Sera were treated with protein G-agarose prior to testing for specific IgM and IgA to eliminate the possibility of false-positive results due to IgM-rheumatoid factor and to remove interisotypic competition due to specific IgG. IgM and IgA absorbance values were expressed as a percentage of the absorbance values of positive reference sera included on each plate (S/P%), and respective positive/negative threshold values of 15.0% and 28.0% were determined. The mean interval between experimental infection of 3 calves and initial detection of specific IgG1 and IgG2 responses was 8.0 and 9.3 days respectively, rising rapidly to an initial plateau 13.7 and 11.0 days postinfection (dpi). Reinfection of these calves at 30 dpi resulted in further rapid increases, with higher plateau values reached 13.0 (IgG1) and 13.7 (IgG2) days later. The mean interval between infection and the first positive IgM and IgA responses was 6.7 and 12.3 days, respectively. IgM S/P% values peaked at 13.0 dpi, with all 3 calves showing a secondary anamnestic response to reinfection, peaking 4.7 days later. The IgA response to initial infection was weak, with only 2 calves showing an obvious peak response at 15.0 dpi. A strong anamnestic IgA response to reinfection occurred in 2 calves, with a peak response 9.5 days later. Apparent biphasic and triphasic IgM and IgA responses were evident in some calves. Acute and convalescent serum samples from 80 calves involved in 17 outbreaks of respiratory disease were tested for specific IgM and IgA. Positive IgM results were detected in 15 outbreaks, with 71 sera from 44 calves testing positive. Although IgA-positive results were detected in the same 15 outbreaks, only 42 sera from 31 calves were positive. In a previous study, seroconversion was detected in 21 of these calves from 10 outbreaks. Thus the diagnostic potential of the assays was in the order IgM > IgA > seroconversion. The correlations between IgM and IgA, IgM and seroconversion, and IgA and seroconversion results for each calf were 73.8%, 58.8% and 62.5%, respectively. (+info)Outbreak of Hendra-like virus--Malaysia and Singapore, 1998-1999. (6/462)
During September 29, 1998-April 4, 1999, 229 cases of febrile encephalitis (111 [48%] fatal) were reported to the Malaysian Ministry of Health (MOH). During March 13-19, 1999, nine cases of similar encephalitic illnesses (one fatal) and two cases of respiratory illness occurred among abattoir workers in Singapore. Tissue culture isolation identified a previously unknown infectious agent from ill patients. This report summarizes the preliminary epidemiologic and laboratory investigations of these cases, which indicate that a previously unrecognized paramyxovirus related to, but distinct from, the Australian Hendra virus is associated with this outbreak. (+info)Comparison of the immunogenicity and efficacy of a replication-defective vaccinia virus expressing antigens of human parainfluenza virus type 3 (HPIV3) with those of a live attenuated HPIV3 vaccine candidate in rhesus monkeys passively immunized with PIV3 antibodies. (7/462)
Two parainfluenza virus type 3 (PIV3) vaccine candidates-cp45, a live attenuated derivative of the JS wild type (wt), and a replication-defective vaccinia virus recombinant expressing the hemagglutinin-neuraminidase or fusion glycoprotein of human PIV3 (modified vaccinia virus Ankara [MVA]/PIV3 recombinants)-were evaluated in rhesus monkeys to determine whether successful immunization could be achieved in the presence of passively transferred PIV3 antibodies. The cp45 virus, administered intranasally (in) and intratracheally (it) in the presence of high levels of PIV3 antibodies, replicated efficiently in the nasopharynx and protected against challenge with wt human PIV3. The MVA recombinants, administered in, it, and intramuscularly in the absence of passive antibody, conferred protection against replication of PIV3 wt challenge virus, but this was largely abrogated when immunization occurred in the presence of passive antibodies. Because immunization for the prevention of HPIV3 disease must occur in early infancy when maternal antibodies are present, the live attenuated cp45 virus continues to be a promising vaccine candidate for this age group. (+info)Update: outbreak of Nipah virus--Malaysia and Singapore, 1999. (8/462)
During March 1999, health officials in Malaysia and Singapore, in collaboration with Australian researchers and CDC, investigated reports of febrile encephalitic and respiratory illnesses among workers who had exposure to pigs. A previously unrecognized paramyxovirus (formerly known as Hendra-like virus), now called Nipah virus, was implicated by laboratory testing in many of these cases. Febrile encephalitis continues to be reported in Malaysia but has decreased coincident with mass culling of pigs in outbreak areas. No new cases of febrile illness associated with Nipah virus infection have been identified in Singapore since March 19, 1999, when abattoirs were closed. This report summarizes interim findings from ongoing epidemiologic and laboratory investigations in Malaysia and Singapore. (+info)Respiroviruses are a genus of viruses in the family *Paramyxoviridae* that includes several important human pathogens, such as parainfluenza virus (PIV) types 1, 2, and 3, and human respiratory syncytial virus (HRSV). These viruses are primarily transmitted through respiratory droplets and direct contact with infected individuals.
Respirovirus infections mainly affect the respiratory tract and can cause a range of symptoms, from mild upper respiratory tract illness to severe lower respiratory tract infections. The severity of the disease depends on various factors, including the age and overall health status of the infected individual.
Parainfluenza viruses are a common cause of acute respiratory infections in children, particularly in those under five years old. They can lead to croup, bronchitis, pneumonia, and other respiratory tract complications. In adults, PIV infections are usually less severe but can still cause upper respiratory symptoms, such as the common cold.
Human respiratory syncytial virus is another important respirovirus that primarily affects young children, causing bronchiolitis and pneumonia. Reinfection with HRSV can occur throughout life, although subsequent infections are typically less severe than the initial infection. In older adults and individuals with compromised immune systems, HRSV infections can lead to serious complications, including pneumonia and exacerbation of chronic lung diseases.
Prevention strategies for respirovirus infections include good personal hygiene practices, such as frequent handwashing and covering the mouth and nose when coughing or sneezing. Vaccines are not available for most respiroviruses; however, research is ongoing to develop effective vaccines against these viruses, particularly HRSV.
Respirovirus is not typically used as a formal medical term in modern taxonomy. However, historically, it was used to refer to a genus of viruses within the family Paramyxoviridae, order Mononegavirales. This genus included several important human and animal pathogens that cause respiratory infections.
Human respiroviruses include:
1. Human parainfluenza virus (HPIV) types 1, 2, and 3: These viruses are a common cause of upper and lower respiratory tract infections, such as croup, bronchitis, and pneumonia, particularly in young children.
2. Sendai virus (also known as murine respirovirus): This virus primarily infects rodents but can occasionally cause mild respiratory illness in humans, especially those who work closely with these animals.
The term "respirovirus" is not officially recognized by the International Committee on Taxonomy of Viruses (ICTV) anymore, and these viruses are now classified under different genera within the subfamily Pneumovirinae: Human parainfluenza viruses 1 and 3 belong to the genus Orthorubulavirus, while Human parainfluenza virus 2 is placed in the genus Metapneumovirus.
Murine respirovirus
Respirovirus
Reverse zoonosis
List of MeSH codes (C02)
Human parainfluenza viruses
Oncolytic virus
Paramyxoviridae
Bat mumps orthorubulavirus
Murine respirovirus - Wikipedia
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Viruses6
- Sendai virus is used as a backbone for vaccine development against Mycobacterium tuberculosis that causes tuberculosis, against HIV-1 that causes AIDS and against other viruses, including those that cause severe respiratory infections in children. (wikipedia.org)
- Human parainfluenza viruses (HPIVs) (family Paramyxoviridae ) are major causes of lower respiratory tract infections in infants and elderly persons. (cdc.gov)
- Several viruses may cause more or less severe acute respiratory infections in man, some of which are followed by systemic infection. (eur.nl)
- BACKGROUND: To investigate the impact of the coronavirus disease 2019 (COVID-19) outbreak on the prevalence of respiratory viruses among pediatric patients with acute respiratory infections in Xuzhou from 2015-2021. (bvsalud.org)
- Infections with viruses of the genus AVULAVIRUS , family PARAMYXOVIRIDAE . (nih.gov)
- A connection between cancer regression and viruses has long been theorised, and case reports of regression noted in cervical cancer , Burkitt lymphoma , and Hodgkin lymphoma , after immunisation or infection with an unrelated virus appeared at the beginning of the 20th century. (privacytools.io)
Acute respiratory tract infe3
- They are responsible for 30%-40% of all acute respiratory tract infections in infants and children. (medscape.com)
- Methods: Acute respiratory tract infections were collected from 13 hospitals in Shanghai from 2015 to 2021. (bvsalud.org)
- These three viral pathogens cause acute respiratory tract infections with substantial disease burden in the young, the elderly, and the immune-compromised. (bvsalud.org)
Parainfluenza Virus2
- Murine respirovirus, formerly Sendai virus (SeV) and previously also known as murine parainfluenza virus type 1 or hemagglutinating virus of Japan (HVJ), is an enveloped, 150-200 nm-diameter, negative sense, single-stranded RNA virus of the family Paramyxoviridae. (wikipedia.org)
- Objective: To study the infection status and epidemiological characteristics of parainfluenza virus (PIV) in acute respiratory tract infection adult cases in Shanghai from 2015 to 2021, and to provide a scientific basis for preventing and controlling PIV. (bvsalud.org)
Complications2
- Reinfection with HPIV can occur throughout life, with elderly and immunocompromised persons being at a greater risk for serious complications of infections. (medscape.com)
- This, together with traces of cellular lysis caused by viral infection, predispose to secondary complications with Mannheimia ( Pasteurella ) haemolytica and Pasteurella multocida . (ivami.com)
Genus2
- It typically infects rodents and it is not pathogenic for humans or domestic animals Sendai virus (SeV) is a member of the genus Respirovirus. (wikipedia.org)
- Among the 4 serotypes, HPIV3 (genus Respirovirus ) causes particularly severe disease, including bronchiolitis and pneumonia ( 1 - 3 ). (cdc.gov)
Lower respiratory trac1
- HPIVs primarily affect young children, in whom the pathogenic spectrum includes upper and lower respiratory tract infections. (medscape.com)
Predispose to secondary1
- The virus is immunosuppressive and may predispose to secondary bacterial infections. (wikipedia.org)
Paramyxoviridae1
- Bovine Parainfluenza type 3 (PI3) (presently Bovine Respirovirus 3) (-ssRNA, Paramyxoviridae, Respirovirus): Molecular diagnosis (RT-PCR). (ivami.com)
HPIV33
- Our findings suggest that wild nonhuman primates are susceptible to HPIV3 infection. (cdc.gov)
- HPIV3 infection also causes severe illness leading to death (35%-75% death rate) in patients receiving hematopoietic stem cell transplants ( 4 , 5 ). (cdc.gov)
- Thereafter, we investigated HPIV3 infection in wild nonhuman primates by using molecular and serologic methods. (cdc.gov)
Sendai3
- Inbred and outbred mouse and rat strains have very different susceptibility to Sendai virus infection. (wikipedia.org)
- It was shown that resistance to the lethal effects of Sendai virus in mice is genetically controlled and expressed through control of viral replication within the first 72 hours of infection. (wikipedia.org)
- Chimpanzees, macaques, squirrels, owls, and rhesus monkeys have been asymptomatically infected with HPIV-3 or HPIV-4, and only marmosets have developed symptomatic upper respiratory tract infections (URTIs) with HPIV-3 and Sendai virus. (medscape.com)
Infants2
Severe acute2
- The positive rate of PIV was 2.61% (133/5 104), compared with 2.32% (55/2 369) and 2.85% (78/2 735) in influenza-like cases (ILI) and severe acute respiratory infection (SARI) cases, respectively. (bvsalud.org)
- METHODS: Severe acute respiratory infection (SARI) cases in hospitalized children were collected from 2015-2021 in Xuzhou, China. (bvsalud.org)
Virus14
- The virus is responsible for a highly transmissible respiratory tract infection in mice, hamsters, guinea pigs, rats, and occasionally marmosets, with infection passing through both air and direct contact routes. (wikipedia.org)
- Epizootic infections of mice are usually associated with a high mortality rate, while enzootic disease patterns suggest that the virus is latent and can be cleared over the course of a year. (wikipedia.org)
- NO donor or NOS2 overexpression provides protection from virus infection in CF, suggesting that NO is sufficient for antiviral host defense in the human airway and is one strategy for antiviral therapy in CF children. (nih.gov)
- Recently, other researchers reported infections with human respiratory syncytial virus and human metapneumovirus in wild nonhuman primates in Africa ( 6 , 7 ). (cdc.gov)
- Respiratory epithelium appears to be the major site of virus binding and subsequent infection. (medscape.com)
- RePub, Erasmus University Repository: Vaccination against acute respiratory virus infections and measles in man. (eur.nl)
- Vaccination against acute respiratory virus infections and measles in man. (eur.nl)
- Many of the problems that have been encountered in the development of measles vaccines, proved to be similar in the development of vaccines against other paramyxoviruses causing acute respiratory infections in man, including respiratory syncytial virus. (eur.nl)
- This virus produces bovine infections, in which it causes a highly contagious disease called bovine parainfluenza 3 (BPI3). (ivami.com)
- Infection by the virus causes a mild respiratory disease that involves nasal and ocular secretions, moderate fever, cough, expectoration and increased respiratory rate. (ivami.com)
- Prevention of nosocomial respiratory syncytial virus infection. (ox.ac.uk)
- Pandemic influenza virus A(H1N1)pdm09 infection occurred in healthy children and young adults, but asthmatic patients presented more rapid progression of respiratory distress and plastic bronchitis. (bvsalud.org)
- The ability of a pathogenic virus to lie dormant within a cell (latent infection). (lookformedical.com)
- [15] Efforts to treat cancer through immunisation or virotherapy (deliberate infection with a virus), began in the mid-20th century. (privacytools.io)
Subsequent1
- If a mouse survives a SeV infection, it develops a lifelong immunity to subsequent viral infections. (wikipedia.org)
Nonhuman2
- Therefore, as a first step in determining the pervasiveness of infection in African wild nonhuman primates, we screened these animals for paramyxovirus in Zambia. (cdc.gov)
- There have been reports of human infections by some of the other nonhuman PIVs, but these have not been well established. (medscape.com)
Pathogens1
- They are considered opportunistic pathogens following STRESS, PHYSIOLOGICAL and/or a viral infection. (curehunter.com)
Mice1
- Treatment of both strains with exogenous IFN before and during viral infection led to an increase in survival time in C57BL/6 mice, but all animals of both strains ultimately succumb to SeV caused disease. (wikipedia.org)
Occur1
- Outbreaks of HPIV-3 infections occur yearly, mainly in spring and summer, and last longer than outbreaks of HPIV-1 and HPIV-2. (medscape.com)
Macrophage1
- Discussion: In conclusion, our study demonstrated that HAdV infection induced macrophage pyroptosis by triggering noncanonical inflammasome activation via a NF-kB-dependent manner, which may explore new perspectives on the pathogenesis of HAdV-induced inflammatory damage. (bvsalud.org)
Vitro2
- An in vitro cell model was employed to investigate the roles of noncanonical inflammasomes in macrophages in response to HAdV infection. (bvsalud.org)
- In vitro experiments revealed that HAdV infection promoted caspase-4/5 expression, activation and pyroptosis in differentiated THP-1 (dTHP-1) human macrophages via NF-κB, rather than STING signaling pathway. (bvsalud.org)
Hamsters1
- Asymptomatic infection can be induced in hamsters, guinea pigs, and adult ferrets by all 5 serotypes of HPIV (HPIV-1, HPIV-2, HPIV-3, HPIV-4a, and HPIV-4b). (medscape.com)
PIVs1
- Human PIVs (HPIVs) are currently divided into 5 serotypes-HPIV-1, HPIV-2, HPIV-3, HPIV-4a, and HPIV-4b-in 2 different genera: Respirovirus (HPIV-1 and HPIV-3) and Rubulavirus (HPIV-2 and HPIV-4). (medscape.com)
Experimental1
- Sporadic detection of natural cases in animals alongside successful experimental infections of pets, such as cats, ferrets and dogs, raises questions about the susceptibility of animals under natural conditions of pet ownership. (lstmed.ac.uk)
Adults1
- HPIVs are also a cause of community-acquired respiratory tract infections of variable severity in adults. (medscape.com)
Survival1
- In vivo, we demonstrated that IL18-hUCMSC infusion could reduce the body weight loss caused by a viral infection and significantly improve the survival rate. (bvsalud.org)
Animals2
- Visualization of SeV infection in live animals demonstrates this difference. (wikipedia.org)
- Here, we report a large-scale study to assess SARS-CoV-2 infection in 919 companion animals living in northern Italy, sampled at a time of frequent human infection. (lstmed.ac.uk)
Common1
- Parainfluenza 3 infection is common in many countries. (ivami.com)
Study1
- This study aims to explore the broad roles of noncanonical inflammasomes during HAdV infection to investigate the regulatory mechanism of HAdV-induced pulmonary inflammatory damage. (bvsalud.org)
Natural1
- Natural infection occurs by way of the respiratory tract. (wikipedia.org)