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PubMed1999

A multiplex RT-PCR for the detection of parainfluenza viruses 1-3 in clinical samples.

Parainfluenza viruses (PIV) are an important cause of respiratory morbidity. Conventional diagnostic methods for detection of PIV are time consuming or lack sensitivity. A multiplex PCR that detects PIV 1-3 was developed using novel primers for PIV viruses 1 and 2 and primers for PIV 3 described previously. Following RNA extraction a single multiplex reverse transcription was undertaken using antisense primers specific for each virus type. This was followed by a 40-cycle multiplex PCR using primers directed towards the haemagglutinin-neuraminidase coding region of each virus type. Products were probed with type-specific fluorescein labelled internal probes and detected by chemiluminescence. Cultured PIV viruses were detectable to a sensitivity of 1 TCID50. The technique was applied to 57 nasal aspirates taken from children presenting with various acute respiratory conditions and analysed previously by culture, immunofluorescence and/or serology. It was possible to detect PIV 1, 2 or 3 in 13/13 samples found previously positive for PIV by tissue culture, 13/15 found previously positive by immunofluorescence and 6/10 that coincided with positive serology. None of the samples found previously positive for other viruses (26) or negative to virus detection (6) were found positive by RT-PCR. It is concluded that this method is as sensitive as combined immunofluorescence and tissue culture for the detection of the PIV viruses 1-3 and should be useful for rapid diagnosis of PIV 1-3 infections.

Animals↗
PubMed1993

Infections due to parainfluenza virus type 4 in children.

Parainfluenza viruses are a major cause of hospitalization for respiratory illness in children. The spectrum of clinical illness associated with infection due to parainfluenza type 4 virus has not been well defined. It is technically difficult to isolate the virus in tissue culture, and because illness is generally reported to be mild, in many cases, patients may not seek medical attention. We describe a series of 10 children with parainfluenza type 4 virus infection who were seen at the Montreal Children's Hospital between 1988 and 1992. There were five males and five females whose average age was 29.7 months. Infection was associated with symptoms of bronchiolitis or pneumonia in 5 children, paroxysmal coughing in 3 infants, apnea in 1 newborn, and aseptic meningitis in 1 child. Hospitalization was required for 8 of the 10 children. It appears that infection with parainfluenza type 4 virus may be more common than previously recognized, and it may be associated with more severe infections.

Apnea↗
PubMed1980

Secretory immunological response in infants and children to parainfluenza virus types 1 and 2.

The secretory immunological responses to natural infection with parainfluenza viruses ae not well defined. Nasopharyngeal secretion specimens from 20 infants and children naturally infected with parainfluenza virus type 1 or type 2 were examined for class-specific antibody and virus-neutralizing activity. There was a marked discordance in individual secretions between immunoglobulin A (IgA) antibody (as measured by indirect immunofluorescence) and neutralizing activity (as determined by either hemadsorption plaque or 50% tissue culture infective dose reduction) to the infecting parainfluenza virus type. Many secretions contained neutralizing activity in the absence of detectable IgA antibody; conversely, secretions with measureable IgA antibody frequently lacked neutralizing activity. Moreover, there was no relationship between neutralizing activity and the course of illness. All 11 patients with serial secretion specimens showed a fourfold or greater titer rise in IgA antibody to the homologous parainfluenza virus type. Antibody usually appeared 7 to 10 days after the onset of symptoms and peaked at about 2 weeks. This response did not appear to be related to age or to severity of illness. in general, the secretory responses resembled those seen in infants infected with respiratory syncytial virus.

Antibodies, Heterophile↗
PubMed2003

Effects of human metapneumovirus and respiratory syncytial virus antigen insertion in two 3' proximal genome positions of bovine/human parainfluenza virus type 3 on virus replication and immunogenicity.

A live attenuated bovine parainfluenza virus type 3 (PIV3), harboring the fusion (F) and hemagglutinin-neuraminidase (HN) genes of human PIV3, was used as a virus vector to express surface glycoproteins derived from two human pathogens, human metapneumovirus (hMPV) and respiratory syncytial virus (RSV). RSV and hMPV are both paramyxoviruses that cause respiratory disease in young children, the elderly, and immunocompromised individuals. RSV has been known for decades to cause acute lower respiratory tract infections in young children, which often result in hospitalization, while hMPV has only been recently identified as a novel human respiratory pathogen. In this study, the ability of bovine/human PIV3 to express three different foreign transmembrane surface glycoproteins and to induce a protective immune response was evaluated. The RNA-dependent RNA polymerase of paramyxoviruses binds to a single site at the 3' end of the viral RNA genome to initiate transcription of viral genes. The genome position of the viral gene determines its level of gene expression. The promoter-proximal gene is transcribed with the highest frequency, and each downstream gene is transcribed less often due to attenuation of transcription at each gene junction. This feature of paramyxoviruses was exploited using the PIV3 vector by inserting the foreign viral genes at the 3' terminus, at position 1 or 2, of the viral RNA genome. These locations were expected to yield high levels of foreign viral protein expression stimulating a protective immune response. The immunogenicity and protection results obtained with a hamster model showed that bovine/human PIV3 can be employed to generate bivalent PIV3/RSV or PIV3/hMPV vaccine candidates that will be further evaluated for safety and efficacy in primates.

Animals↗
PubMed1982

Rapid diagnosis of parainfluenza virus infection in children.

The indirect immunofluorescent-antibody (IFA) assay for detection of parainfluenza virus antigen was performed on samples of nasopharyngeal secretions obtained from infants and children with various respiratory illnesses to determine the usefulness of the IFA assay for rapid diagnosis of parainfluenza virus infection. Ninety-four samples of nasopharyngeal secretions were obtained from 78 children during a community outbreak of parainfluenza virus infection. Application of the IFA assay revealed the presence of parainfluenza antigen in 67 of the 94 samples. When these same specimens were inoculated into tissue culture, the presence of parainfluenza virus was confirmed in 62 (93%) of the 67 IFA-positive specimens by hemadsorption on tissue culture monolayers (31 cases), presence of parainfluenza hemagglutinin in infected tissue culture fluids (23 cases), or by other methods (8 cases). Only four IFA-negative specimens were subsequently shown to be positive for parainfluenza virus by tissue culture infectivity. The IFA assay provided a more rapid and more accurate method for diagnosis of parainfluenza infection in children than did routine tissue culture methods employed currently.

Adolescent↗
PubMed1993

Parainfluenza virus infection in adult bone marrow transplant recipients.

The clinical course of parainfluenza virus infection occurring in 8 of 265 (3%) adult bone marrow transplant recipients during 1991 was reviewed. Parainfluenza virus type 3 was isolated from all eight patients. The clinical course ranged from self-limited upper respiratory tract infections (2 patients) to severe lower respiratory tract disease (6 patients) associated with a 50% mortality. This study highlights the important role of community respiratory viruses such as parainfluenza virus in the etiology of pneumonia in immunocompromised adults.

Adult↗
PubMed1985

Experimental parainfluenza virus infection in mice: growth and spread of a highly pathogenic variant of parainfluenza 3 virus in the mouse brain.

We had previously showed that following intracerebral inoculation of newborn mice, the 910 N and M strains of bovine parainfluenza 3 virus induce a non-lethal hydrocephalus and a lethal disease with marked thymic and splenic atrophy, respectively. Moreover, only the M virus was lethal for 2-week-old mice. In the present study, we demonstrate that the M virus multiplies and spreads in the mouse brain invading the thalamus, hypothalamus and brain stem beyond the ependyma whereas the 910 N virus causes only slight ependymitis. This growth and spread of M virus was blocked by passive immunization 3 days after infection. Mouse embryo brain cell cultures were infected with M and 910 N viruses, about 50 per cent became antigen-positive for M whereas only a small proportion of cells were positive for the 910 N virus. However, the latter did produce higher yeilds of infectious virus than M.

Animals↗
PubMed1984

Evaluation of cold-adapted and temperature-sensitive mutants of parainfluenza virus type 3 in weanling hamsters.

Cold-adapted (ca) and temperature-sensitive (ts) mutants of parainfluenza virus 3 were produced by serially passaging wild type (wt) parainfluenza virus 3 at 20 degrees C 45 times. Previously, plaque-purified viruses (clones) were selected from the wt parent and from cold passage levels 7, 12, 18, and 45 and characterized in vitro. In the present study, we evaluated at least one mutant from each cold passage level for attenuation in hamsters. Four of the five mutants tested were ts and ca (one each from cold passage levels 7, 12, 18, and 45) and one was ca but not ts (from cold passage 18). Groups of hamsters were inoculated intranasally with either parent wt or mutant virus. Four or five hamsters from each group were sacrificed prior to inoculation and daily on the first, second, third, fourth, and sixth or seventh day postinoculation and the amount of virus in nasal turbinates and lungs was quantitated. The quantity of virus recovered from the hamsters and the parainfluenza virus 3 antibody titers were inversely related to the cold passage level. Two of the mutants did not replicate in hamsters. Cold adaptation of parainfluenza virus 3 resulted in progressive attenuation of the virus in weanling hamsters. These highly attenuated mutants are suitable for evaluation in children as live virus vaccines.

Animals↗
PubMed1976

Effect of passive antibody on parainfluenza virus type 3 pneumonia in hamsters.

Both parainfluenza virus type 3 and respiratory syncytial virus may produce life-threatening pneumonia or bronchiolitis in infants less than 6 months old. Almost all infants in this age group possess passively acquired maternal antibodies to both viruses. It has been suggested that maternal antibodies may actually participate in the pathogenesis of these diseases in early infancy. This investigation examined the effect of moderate levels of passive antibody on the development of pneumonia in hamsters infected intranasally with parainfluenza virus type 3. The pneumonitis produced in this model was not enhanced by the presence of moderate levels of serum antibody to this virus. Furthermore, reinfection after an initial "sensitizing" infection under the cover of passive antibody did not result in a more severe pneumonitis. These studies do not support either of the two hypotheses that have been advanced to explain the pathogenesis of infections with respiratory syncytial virus in early infancy.

Animals↗
PubMed1993

Isolation of parainfluenza virus type 3 from cerebrospinal fluid associated with aseptic meningitis.

Parainfluenza virus type 3 has been isolated from the cerebral spinal fluid (CSF) from six individuals--four children and two adults--over a 10-year period. All had fever, and four had signs of meningitis. All recovered uneventfully, including one child undergoing chemotherapy for medulloblastoma. The clinical presentation of this child who developed parainfluenza virus type 3 meningitis is described, and the cases of five other individuals with parainfluenza virus type 3 isolated from the CSF are briefly reviewed. The paramyxovirus parainfluenza type 3, in addition to mumps virus, may be considered capable of infecting the central nervous system.

Adult↗
PubMed1988

Immunization with vaccinia virus recombinants that express the surface glycoproteins of human parainfluenza virus type 3 (PIV3) protects patas monkeys against PIV3 infection.

Patas monkeys (Eryphrocebus patas) were immunized intradermally with two vaccinia virus recombinants that individually express the hemagglutinin-neuraminidase glycoprotein or the fusion glycoprotein of human parainfluenza virus type 3 (PIV3). These immunizations induced a high titer of PIV3 serum-neutralizing antibodies. At 1 month after immunization, monkeys were challenged intratracheally with PIV3. Subsequent virus replication was reduced in these monkeys by 3.2 log10 and 1.9 log10 (mean peak virus titers) in the upper and lower respiratory tracts, respectively, compared with control animals. The average duration of virus shedding was also reduced from 9.0 to 3.4 days in the upper respiratory tract and from 5.3 to 1.2 days in the lower respiratory tract. These findings demonstrate that a single intradermal dose of live recombinant vaccinia viruses can significantly restrict the replication of a virus which primarily infects the epithelial cells of the respiratory tract.

Animals↗
PubMed2025

Distinct Evolutionary Signatures of Human Parainfluenza Viruses 2 and 4 Reveal Host Antagonism Divergence and Phylogenetic Discordance.

Human parainfluenza virus 2 (HPIV-2) and human parainfluenza virus 4 (HPIV-4) are significant but underappreciated respiratory pathogens, particularly among high-risk populations including children, the elderly, and immunocompromised individuals. In this study, we sequenced 101 HPIV-2 and HPIV-4 genomes from respiratory samples collected in western Washington State and performed comprehensive evolutionary analyses using both new and publicly available sequences. Phylogenetic and phylodynamic analyses revealed that both HPIV-2 and HPIV-4 evolve at significantly faster rates compared to the mumps virus, a reference human orthorubulavirus. Notably, while HPIV-2 demonstrated the highest evolutionary rates in the surface glycoprotein HN, consistent with humoral immune-driven selection, the innate immune antagonist V/P gene evolved fastest in HPIV-4. We identified a hypervariable region within the HPIV-4V/P protein (residues 35 to 75), which structural modeling placed in a loop overlapping a known interferon antagonism domain in other paramyxovirus V proteins, though HPIV-4 is functionally incompetent in this activity. Expanded phylogenetic analysis across the Paramyxoviridae family uncovered a striking evolutionary discordance: while the HN glycoprotein and L polymerase of HPIV-4 and its 2 closest bat-derived viruses clustered within the Orthorubulavirus genus, their nucleoprotein (N), phosphoprotein (P), matrix (M), and fusion (F) proteins formed a distinct lineage outside the Rubulavirinae subfamily. Together, these findings highlight the distinct evolutionary trajectories of HPIV-2 and HPIV-4, raise hypotheses around complex Paramyxoviridae zoonotic events including recombination-like patterns, and demonstrate limitations of current L protein-based taxonomic classification schemes.

Humans↗
PubMedDate not supplied

Experimental infections with some pneumotropic viruses in the mouse. Note II. Virological and pathomorphological aspects of experimental associated infections with parainfluenza virus, adenovirus and respiratory syncytial virus in the mouse.

Associated infections with long-strain parainfluenza virus type 3, adenovirus type 3 and respiratory syncytial virus were experimentally induced in white mice. They were pointed out by the appearance of homologous serum antibodies, positive IF reactions in the pulmonary tissue, and histological, histochemical and histoenzymatic lesions, which were more severe than those of controls infected with single virus of those mentioned above, since they involved wider areas and had a high frequency. The pathomorphological changes made up an inflammatory, exudative, alternative and predominantly infiltrative lymphohistiocytic picture, mainly pulmonary (diffuse interstitial bronchopneumonia, sometimes with a peribronchovascular location, of a cuff-like aspect), hepatic, renal and cardiac, but dystrophic processes were also present--hyalinosis of tunica media in the lung, hepatocyte cytoplasm vacuolizations on areas of various sizes of lobuli--, especially in associated infections with parainfluenza virus type 3 and adenovirus type 3. Megakaryocytic hyperplasia in the spleen, present in all the experimental models, was also described. Generally, the modified structural aspects made up and pointed out a complex pathological process.

Adenoviridae Infections↗
PubMed1999

Generation of a parainfluenza virus type 1 vaccine candidate by replacing the HN and F glycoproteins of the live-attenuated PIV3 cp45 vaccine virus with their PIV1 counterparts.

Parainfluenza virus type 1 (PIV1) is a major cause of croup in infants and young children, and a vaccine is needed to prevent the serious disease caused by this virus. In the present study, a live attenuated PIV1 vaccine candidate was generated by modification of the extensively-studied PIV3 cold-passaged (cp) cp45 vaccine candidate using the techniques of reverse genetics. The HN and F glycoproteins of the PIV3 cp45 candidate vaccine virus were replaced with those of PIV1. This created a live attenuated PIV1 vaccine candidate, termed rPIV3-1 cp45, which contained the attenuated background of the PIV3 cp45 vaccine virus together with the HN and F protective antigens of PIV1. Three of the 15 mutations of cp45 lie within the HN and F genes, and those in the F gene are attenuating. Thus, some attenuation might be lost by the HN and F glycoprotein replacement. To address this issue we also constructed a derivative of PIV3 cp45, designated rPIV3 cp45 (F(wt)HN(wt)), that possessed wild type PIV3 HN and F glycoproteins but retained the 12 other cp45 mutations. rPIV3 cp45 (F(wt)HN(wt)) replicated in the respiratory tract of hamsters to a level three- to four-fold higher than rPIV3 cp45, indicating that loss of the two attenuating mutations in the cp45 F gene effected a slight reduction in the overall attenuation of cp45 for hamsters. However, the chimeric rPIV3-1 cp45 virus was about 5-fold more restricted in replication in hamsters than rPIV3 cp45 and about 15- to 20-fold more restricted than rPIV3 cp45 (F(wt)HN(wt)). This suggests that two components contribute to the attenuation of the new chimeric rPIV3-1 cp45 PIV1 vaccine candidate: one being the 12 cp45 mutations, which provide most of the observed attenuation, and the other resulting from the introduction of the heterologous PIV1 HN and F proteins into PIV3 (i.e., a chimerization effect). rPIV3-1 cp45 was observed to be immunogenic and protective against challenge with wild type PIV1 in hamsters. This virus shows sufficient promise that it should be evaluated further as a candidate live attenuated vaccine strain for preventing severe lower respiratory tract PIV1 disease in infants and young children.

Animals↗
PubMed1996

Identification of the sequences responsible for nuclear targeting of the V protein of human parainfluenza virus type 2.

In human parainfluenza virus type 2 (hPIV-2)-infected cells, anti-phosphoprotein (P)-specific monoclonal antibody (MAb) densely stained the perinuclear regions of infected cells throughout infection, indicating that the P protein was localized exclusively in the cell cytoplasm. By contrast, antigens recognized by MAbs directed against the P-V-common domain of hPIV-2 were located predominantly in the cytoplasm, but in some hPIV-2-infected cells they were also found in the nuclei, suggesting that a fraction of hPIV-2 V protein is localized there. hPIV-2 V protein expressed from a cDNA clone was localized in the nuclei of transfected cells. By using indirect immunofluorescence analyses, we examined the intracellular localization of various sequentially deleted V proteins, to determine the nuclear localization signals (NLS) of the V protein. Two noncontiguous regions in the V protein were required for nuclear localization and retention, since deletion of these regions [region I (aa 1-46) and region II (aa 175-196)] resulted in cytoplasmic localization. Both regions resulted in nuclear localization independently. A nucleoplasmin-like NLS was identified in region II but no consensus targeting sequence could be found in region I. When NP protein was co-expressed with V protein or the N-terminal fragment (aa 1-46) of V protein, a fraction of the NP protein was translocated into cell nuclei.

Amino Acid Sequence↗
PubMed2005

Entry of parainfluenza virus into cells as a target for interrupting childhood respiratory disease.

Human parainfluenza viruses cause several serious respiratory diseases in children for which there is no effective prevention or therapy. Parainfluenza viruses initiate infection by binding to cell surface receptors and then, via coordinated action of the 2 viral surface glycoproteins, fuse directly with the cell membrane to release the viral replication machinery into the host cell's cytoplasm. During this process, the receptor-binding molecule must trigger the viral fusion protein to mediate fusion and entry of the virus into a cell. This review explores the binding and entry into cells of parainfluenza virus type 3, focusing on how the receptor-binding molecule triggers the fusion process. There are several steps during the process of binding, triggering, and fusion that are now understood at the molecular level, and each of these steps represents potential targets for interrupting infection.

Antiviral Agents↗
PubMed1996

Host range restriction of parainfluenza virus growth occurs at the level of virus genome replication.

To illuminate the molecular basis for host range restriction of parainfluenza virus replication, we have examined the types of virus macromolecules produced during abortive infection of nonpermissive MDBK cells with human parainfluenza virus type 1 (hPIV1). While these cells do not support production of hPIV1 virus, they can be infected by hPIV1 as evidenced by accumulation of intracellular viral NP and HN proteins. HPIV1 is also able to drive transcription of a synthetic analog of Sendai virus (SV) genome RNA transfected into virus-infected MDBK cells. In contrast to transcription, hPIV1 genome replication does not occur in MDBK cells. Intracellular full-length genome RNA was detected only in trace amounts 2 days after infection, and was undetectable 4 days after infection. Full-length antigenome (+) sense RNA was not detectable. Nucleocapsid complexes failed to accumulate in the cytoplasm of nonpermissive cells, and no detectable nucleocapsids were released into the medium as virus particles. The data indicate that defective vRNA synthesis and/or nucleocapsid formation is responsible for the inability of hPIV1 to grow in MDBK cells. Our data also show that hPIV1 is capable of providing all helper functions for packaging SV synthetic genome analogs into infectious particles, but these SV-specific RNAs encapsidated with hPIV1 proteins are in turn not replicated by SV proteins. These results suggest that functional protein-protein interactions between parainfluenza virus strains have more stringent requirements than do protein-RNA interactions.

Animals↗