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PubMed1981

Parainfluenza virus infections in the Cirencester Survey: seasonal and other characteristics.

Parainfluenza viruses were isolated 165 times during 14 years surveillance of the illnesses of a general practice population of around 3700. Type 1 isolations numbered 57, type 2 isolations 22 and type 3 isolations 86, representing annual rates of 33, 13 and 50 infections respectively per 10000 of population. Type 4 parainfluenza virus was not isolated. Three major classes of illness gave the following rates: sore throats (Throats) nine, acute febrile respiratory diseases (FRD) 23, acute non-febrile respiratory diseases (non-FRD) 71. The illnesses caused by the three types isolated were similar. Type 1 infections were most abundant in November and type 2 infections in December, and only 11.4% of these types were isolated in the warm semester April through September. Type 3 infections were seasonally bi-modal, with a winter peak in January and an even greater prevalence (66% of the total) in the warm semester. Type 3 infections in the warmer months and in the later years of the Survey were usually more severe. Type 3 virus may therefore be heterogeneous, one subtype possessing and the other lacking the genetic mechanism of "cold-season' prevalence. Geographical discontinuity between summer and winter isolation strengthens the case for the existence of the two subtypes of type 3 parainfluenza virus. Type 3 infections caused the majority of the infections in very young infants. Type 2 infections were widely distributed at all ages. Females were attacked more often than males: type 1, 68.4%; type 2, 63.6%; type 3, 53.5%. Type 3 infections in males outnumbered those in females up to 60 years of age, whereas female predominance became apparent in types 1 and 2 before 10 years of age. All types were widely and sparsely distributed, areas of prevalence changing from year to year. Recurrences occurred only twice, both with type 3 infections. Six persons suffered both a type 1 and a type 3 infection, and one person suffered both a type 2 and a type 3 infection.

Adolescent↗
PubMed1966

Antibody response of guinea pigs to trivalent parainfluenza virus vaccine prepared from embryonated eggs.

A trivalent parainfluenza virus vaccine has been tested in guinea pigs. The parainfluenza 2 virus vaccine component was superior in the magnitude of antibody titers, and in the ability to convert animals serologically after two doses of an undiluted or a 10-fold diluted vaccine. The parainfluenza 1 virus vaccine gave a higher percentage of conversion than parainfluenza 3 virus vaccine after administration of two doses of either undiluted or 10-fold diluted vaccine.

Animals↗
PubMed1993

Meningitis due to parainfluenza virus type 3: report of two cases and review.

We report the cases of two infants with meningitis due to parainfluenza virus type 3. This is the first time that documented clinical and laboratory details have been reported for a 1-month-old infant with meningitis due to parainfluenza virus type 3 (our second case). We reviewed the literature and determined that CNS involvement by parainfluenza virus type 3 appears rare. Clinicians should be aware that parainfluenza virus type 3, one of the most common causes of viral respiratory infection in infancy, can also produce infection of the CNS and that hemadsorption testing of CSF specimens submitted for viral culture is necessary for detecting these paramyxoviruses.

Cerebrospinal Fluid↗
PubMed1984

Serological diagnosis of parainfluenza virus infections by enzyme immunoassay with special emphasis on purity of viral antigens.

Enzyme immunoassay (EIA) for parainfluenza virus type 1, 2, and 3 antibodies was compared with the complement fixation test (CF) as a diagnostic method in 180 patients with respiratory symptoms. The CF test detected rises in parainfluenza virus antibodies in 30 cases, whereas EIA detected 47 rises. Patients with antibody rises in parainfluenza or mumps virus antibodies were studied for cross-reactions by CF, hemagglutination inhibition (HAI), and EIA using purified viral envelope glycoprotein and nucleocapsid preparations. All methods showed marked cross-reactivity between parainfluenza virus type 1 and 3 antibodies. Mumps virus infection often raised heterologous antibodies even against purified viral antigens. Rabbit antisera produced against viral envelope glycoproteins showed heterologous antibody responses between parainfluenza 1 and 3 antibodies and between parainfluenza 1 and mumps antibodies by HAI, EIA, and immunoprecipitation. The cross-reactive antibodies were usually directed against both of the envelope glycoproteins, HN and F proteins, of the viruses.

Antibodies, Viral↗
PubMed1995

Differences in the role of the cytoplasmic domain of human parainfluenza virus fusion proteins.

We have investigated the roles of the cytoplasmic domains of the human parainfluenza virus type 2 (PI2) and type 3 (PI3) fusion (F) proteins in protein transport and cell fusion activity. By using the vaccinia virus-T7 transient expression system, a series of F protein cytoplasmic tail truncation mutants was studied with respect to intracellular and surface expression and the ability to induce cell fusion when coexpressed with the corresponding hemagglutinin-neuraminidase (HN) proteins. All of the cytoplasmic tail truncation mutants of PI2F were expressed at high levels intracellularly or on cell surfaces as measured by immunoprecipitation and cell surface biotinylation assays. In addition, when coexpressed with PI2HN, these truncation mutants of PI2F were all found to be essentially unimpaired in the ability to induce cell fusion as measured by a quantitative cell fusion assay. In contrast, surface expression and cell fusion activity were found to be eliminated by a mutant of PI3F in which the entire cytoplasmic tail was deleted, and the mutant protein appeared to be unable to assemble into a high-molecular-weight oligomeric structure. To further investigate whether there is a specific sequence requirement in the cytoplasmic tail of PI3F, a chimeric protein consisting of the PI3F extracellular and transmembrane domains and the PI2F cytoplasmic tail was constructed. This chimeric protein was detected on the surface, and it was capable of inducing cell fusion when expressed together with PI3HN, although the fusogenic activity was reduced compared with that of wild-type PI3F. These results demonstrate that although PI2 and PI3 viruses belong to the same parainfluenza virus genus, these viruses show marked differences with respect to functional requirements for the cytoplasmic tail of the F glycoprotein.

Amino Acid Sequence↗
PubMed2001

Chimeric bovine respiratory syncytial virus with attachment and fusion glycoproteins replaced by bovine parainfluenza virus type 3 hemagglutinin-neuraminidase and fusion proteins.

Chimeric bovine respiratory syncytial viruses (BRSV) expressing glycoproteins of bovine parainfluenza virus type 3 (BPIV-3) instead of BRSV glycoproteins were generated from cDNA. In the BRSV antigenome cDNA, the open reading frames of the major BRSV glycoproteins, attachment protein G and fusion protein F, were replaced individually or together by those of the BPIV-3 hemagglutinin-neuraminidase (HN) and/or fusion (F) glycoproteins. Recombinant virus could not be recovered from cDNA when the BRSV F open reading frame was replaced by the BPIV-3 F open reading frame. However, cDNA recovery of the chimeric virus rBRSV-HNF, with both glycoproteins replaced simultaneously, and of the chimeric virus rBRSV-HN, with the BRSV G protein replaced by BPIV-3 HN, was successful. The replication rates of both chimeras were similar to that of standard rBRSV. Moreover, rBRSV-HNF was neutralized by antibodies specific for BPIV-3, but not by antibodies specific to BRSV, demonstrating that the BRSV glycoproteins can be functionally replaced by BPIV-3 glycoproteins. In contrast, rBRSV-HN was neutralized by BRSV-specific antisera, but not by BPIV-3 specific sera, showing that infection of rBRSV-HN is mediated by BRSV F. Hemadsorption of cells infected with rBRSV-HNF and rBRSV-HN proved that BPIV-3 HN protein expressed by rBRSV is functional. Colocalization of the BPIV-3 glycoproteins with BRSV M protein was demonstrated by confocal laser scan microscopy. Moreover, protein analysis revealed that the BPIV-3 glycoproteins were present in chimeric virions. Taken together, these data indicate that the heterologous glycoproteins were not only expressed but were incorporated into the envelope of recombinant BRSV. Thus, the envelope glycoproteins derived from a member of the Respirovirus genus can together functionally replace their homologs in a Pneumovirus background.

Animals↗
PubMed1979

Establishment of persistent infection by parainfluenza virus type 3: role of a syncytium inhibitor.

A strain of parainfluenza virus type 3 (para 3) that had undergone a series of undiluted passages failed to produce syncytia when inoculated on to Vero cells at a high m.o.i. The strain repeatedly produced stable persistent infections. Persistently infected cells were resistant to superinfection by homologous virus, showed the presence of virus-specific antigen and shed low quantities of infectious virus into the supernatant fluid. The undiluted passage parainfluenza virus type 3 strain produced a substance that inhibited syncytium formation by homologous virus and by measles virus but appeared to have no effect on virus replication. This inhibitor had no demonstrable effect on unrelated viruses, including some that produced syncytia. It had a mol. wt. between 3500 and 14000, was acid- and heat-labile, and was inactivated by anti-para 3 serum.

Animals↗
PubMed2000

African green monkeys provide a useful nonhuman primate model for the study of human parainfluenza virus types-1, -2, and -3 infection.

Human parainfluenza virus (HPIV) types-1, -2, and -3 are significant causes of both upper and lower respiratory tract disease in infants and children. Although there are two live attenuated vaccines for the prevention of HPIV-3 disease in phase 1 clinical trials, vaccines are not currently available for prevention of HPIV-1 or -2 disease. Our laboratory is developing candidate vaccines for the prevention of HPIV-1, -2, and -3 disease, and a suitable nonhuman primate model is needed for evaluation of these vaccine candidates prior to administration to humans. We evaluated the replication of HPIV-1 and -2 in six different species of nonhuman primates and found both viruses to replicate most efficiently in African green monkeys and chimpanzees. We then compared the replication of HPIV-3 in African green monkeys to that in rhesus macaques, which we have used previously, and found that HPIV-3 replicated to higher titer in African green monkeys. In summary, African green monkeys provide a very useful nonhuman primate for the evaluation of HPIV-1, -2, and -3 vaccine candidates, especially for the evaluation of various combinations of these PIV vaccines and for vaccine strategies that employ sequential immunization.

Animals↗
PubMedDate not supplied

Isolation of parainfluenza virus type 3 from an infant with meningoencephalitis.

A parainfluenza virus type 3 strain was isolated from the cerebrospinal fluid of an infant with a clinical diagnosis of meningoencephalitis. Specific HAI antibodies to parainfluenza virus type 3, ranging in titer from 1/80 to 1/160 could be detected in the infant's serum. A 2-fold rise in the level of complement fixing serum antibodies-from 1/16 at the first to 1/32 at the second collection-was recorded.

Antibodies, Viral↗
PubMed1988

Comparison between parainfluenza virus type 2 and simian virus 5: monoclonal antibodies reveal major antigenic differences.

Marked differences in the apparent Mrs of the HN, NP and F proteins of simian virus 5 (SV5) and parainfluenza virus type 2 (PF-2) were revealed by SDS-PAGE. To examine the antigenic relationships between SV5, PF-2 and other paramyxoviruses, monoclonal antibodies (MAbs) specific to PF-2 were isolated. These antibodies had specificities for the HN, NP and P proteins and together with 54 MAbs to SV5 were tested for their ability to react with SV5, PF-2, PF-3, mumps and measles virus proteins. Most of these MAbs (55 out of 60) reacted with homologous virus only. However, five reacted with both SV5 and PF-2. These antibodies had reactivities to the NP, M and P proteins. Furthermore, one of the antibodies with reactivity to the P protein also reacted with mumps virus. Although none of the 21 MAbs with specificities for the HN protein of either SV5 or PF-2 cross-reacted with heterologous virus, some antigenic similarities between the HN protein of SV5 and PF-2 could be detected. This was demonstrated by raising a series of polyclonal antisera to purified preparations of SV5 or PF-2 HN proteins in BALB/c mice, and testing for their ability to neutralize both SV5 and PF-2 and also to immunoprecipitate the HN proteins of these viruses. Surprisingly, while low levels of cross-neutralizing antibody could be detected in some sera (e.g. neutralization of SV5 1:1600 and of PF-2 1:80), other sera with similar neutralization titres against homologous virus failed to neutralize heterologous virus. Furthermore, only a minority of the anti-HN antisera showed any immune-precipitating activity against the heterologous HN protein.

Animals↗
PubMed1997

Parainfluenza virus type 4 infections in pediatric patients.

BACKGROUND: The purpose of this study was to describe the clinical characteristics and epidemiology of parainfluenza virus type 4 infections in pediatric patients. METHODS: Hospital records of 13 patients from whom parainfluenza virus type 4 was isolated were retrospectively reviewed. RESULTS: Parainfluenza virus type 4 infection was associated with upper respiratory tract disease, severe lower respiratory tract disease requiring hospitalization in 10 of 13 patients and aseptic meningitis. Nine of the 10 hospitalized patients were < 24 months old (mean age, 8.3 months) and required hospitalization for 4 to 25 days (mean, 5.5 days). CONCLUSIONS: Serious illnesses associated with parainfluenza virus type 4 infections are more common than previously recognized.

Child↗
PubMed1995

Parainfluenza virus type 2 meningitis and parotitis in an 11-year-old child.

We describe the case of an 11-year-old Bolivian boy with parotitis and aseptic meningitis to demonstrate that parainfluenza virus type 2 can cause disseminated infection in a normal child. Parainfluenza virus type 2 was isolated from nasopharyngeal and CSF specimens from the patient and was confirmed to be parainfluenza virus type 2 by hemadsorption inhibition and by complement fixation. Parainfluenza virus type 2 may cause aseptic meningitis and parotitis.

Child↗
PubMed2002

The long noncoding region of the human parainfluenza virus type 1 f gene contributes to the read-through transcription at the m-f gene junction.

Sendai virus (SV) and human parainfluenza virus type 1 (hPIV1) have genomes consisting of nonsegmented negative-sense RNA in which the six genes are separated by well-conserved intergenic (IG) sequences and transcriptional start (S) and end signals. In hPIV1-infected cells, transcriptional termination at the M-F gene junction is ineffective; a large number of M-F read-through transcripts are produced (T. Bousse, T. Takimoto, K. G. Murti, and A. Portner, Virology 232:44-52, 1997). In contrast, few M-F read-through transcripts are detected in SV-infected cells. Sequence analysis indicated that the hPIV1 IG and S sequences in the M-F junction differ from those of SV. Furthermore, the hPIV1 F gene contains an unusually long noncoding sequence. To identify the cis-acting elements that prevent transcriptional termination at the M-F junction, we rescued recombinant SV (rSVhMFjCG) in which its M-F gene junction was replaced by that of hPIV1. Cells infected with rSVhMFjCG produced an abundance of M-F read-through transcripts; this result indicated that the hPIV1 M-F junction is responsible for inefficient termination. When one or both of the IG and S sites in rSVhMFjCG were replaced by those of SV, the efficiency of transcriptional termination increased but not to the level observed in wild-type SV-infected cells. Deletion of most of the long noncoding region of the hPIV1 F gene in rSVhMFjCG in addition to the mutations in IG and S signals resulted in efficient termination that was equivalent to the level observed in wild-type virus-infected cells. Therefore, the long noncoding sequence of the hPIV1 F gene contains cis-acting element(s) that affects transcriptional termination. Our evaluation of the effect of inefficient transcriptional termination on viral replication in culture revealed that cells infected with rSVhMFjCG produced less F protein than cells infected with wild-type SV and that assembly of the recombinant SV in culture was less efficient. These phenotypes seem to be responsible for the extended survival of mice infected with rSVhMFjCG.

Animals↗
PubMed1994

Cell-to-cell contact not soluble factors mediate suppression of lymphocyte proliferation by bovine parainfluenza virus type 3.

We have previously characterized the ability of parainfluenza virus type 3-infected (PIV-3) and noninfected bovine alveolar macrophages (BAM) to support lymphocyte proliferation. While uninfected macrophages support proliferation of lymphocytes stimulated with concanavalin A (Con A), ovalbumin, and interleukin 2 (IL-2), lymphocyte [3H]thymidine incorporation was suppressed in the presence of PIV-3-infected BAM. Since viral infection of macrophages has been shown to alter arachidonic acid metabolism and cytokine secretion, we have determined if arachidonate metabolism or the lack of IL-1 and IL-2 mediated the suppression of lymphocyte proliferation by PIV-3. Inhibition of arachidonic acid metabolism failed to reverse the suppressive effect of viral infection as did supplementation of cultures with bovine recombinant IL-1 beta, IL-2, or lymphocyte-conditioned medium. Further, lymphocytes proliferated normally when physically separated from virus infected BAM by a semipermeable membrane. Stimulation of lymphocytes in contact with infected BAM resulted in marked suppression of lymphocyte [3H]thymidine incorporation. Interactions between stimulated lymphocytes and PIV-3-infected BAM resulted in PIV-3 infection of lymphocytes. Virus infection of lymphocytes was confirmed ultrastructurally by the presence of characteristic parainfluenza virus inclusions and virus budding from lymphocyte plasma membranes. It was concluded that suppression of lymphocyte proliferation by PIV-3 is mediated in part by infection of stimulated lymphocytes during cell-to-cell contact with BAM.

Animals↗
PubMed1990

Characterization of an in vitro system for the synthesis of mRNA from human parainfluenza virus type 3.

A cell extract derived from human parainfluenza virus type 3-infected human lung carcinoma (HLC) cells synthesized mRNA in vitro. Under optimal conditions, the extract was able to support transcription of all virus-encoded genes as determined by hybridization analyses. The RNA products contained full-length poly(A)-containing mRNA species similar to those observed in acutely infected cells. Further purification of the viral nucleocapsids from the infected HLC cell extract resulted in total loss of the capacity of the extract to synthesize mRNA in vitro. However, the addition of cytoplasmic extracts from uninfected HLC cells to the nucleocapsid preparations restored transcription to levels observed in the infected cell lysates, indicating requirement of a host factor(s) in the human parainfluenza virus type 3 transcription process. In distinction to the abundant transcription observed in the cell extract from HLC cells, cell extract prepared from CV-1 cells failed to support transcription in vitro. High levels of RNase activity in the cell extract from CV-1 cells appears to be the principal reason for this difference.

Animals↗
PubMed1993

The complete nucleotide sequence of two cold-adapted, temperature-sensitive attenuated mutant vaccine viruses (cp12 and cp45) derived from the JS strain of human parainfluenza virus type 3 (PIV3).

Two cold-passaged mutant vaccine viruses (cp12 and cp45) derived from the JS wild-type (wt) strain of human parainfluenza virus type 3 (PIV3) have been sequenced. These mutant viruses display the cold-adapted (ca), temperature-sensitive (ts), and attenuation (att) phenotypes. Sequence data indicate that both cp12 and cp45 sustained nucleotide substitutions during cold passage and subsequent cloning. Fifteen nucleotide changes were present in cp12 and 18 in cp45. Of these changes, some were present in the sequence of the prototype wt strain (Wash/47885/57) or were non-coding changes present in the open reading frames (ORFs). These were considered unlikely to be of significance in contributing to phenotypic differences between the mutants and the JS wt. There were nine remaining changes in cp12 and eight in cp45 that would most likely contribute to their phenotypes. For cp12, two were non-coding changes in regulatory regions, one in the 3' genome leader and one in the NP gene transcription start signal. The remaining seven changes resulted in amino acid substitutions in NP, F, HN, and L. For cp45, two mutations were in a non-coding regulatory region, the 3' genome leader. The remaining six changes resulted in amino acid substitutions in F, HN, and L. Only one amino acid substitution was conserved between cp12 and cp45 (a valine to alanine change at position 384 of the HN gene). These results should prove useful in the future in understanding the genetic basis of attenuation of the cold-passaged PIV3 candidate vaccine viruses.

Adaptation, Physiological↗
PubMed1988

Current approaches to the development of vaccines effective against parainfluenza viruses.

Infection of infants and children with parainfluenza viruses can lead to serious lower respiratory tract disease. In order to review new information on the genetic organization, epidemiology, and immunobiology of these viruses and of respiratory syncytial virus, WHO, in conjunction with the National Institute of Allergy and Infectious Diseases, held a workshop in Bethesda, MD, USA, 4-5 May 1987. New data on the immunobiology and epidemiology of human parainfluenza 3 virus were presented that should facilitate the development of a vaccine against this pathogen.

Child↗