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PubMedDate not supplied

Elevated parainfluenza virus type 1 antibody in patients with subacute sclerosing panencephalitis.

Parainfluenza virus hemagglutination inhibition (HI) antibodies were determined 3 times in the sera of 9 patients with subacute sclerosiing panencephalitis (SSPE) and 20 healthy controls matched for age and place of residence. Serum antibody against parainfluenza virus type 1 was significantly elevated in SSPE patients as compared with controls, whereas antibodies against type 2 and 3 were found to be in normal ranges. Higher titres of parainfluenza virus type 1 antibody might depend on: (1) dual viral infection, (2) cross-reaction between antigens of SSPE virus and parainfluenza virus type 1, and (3) non-specific activation of latent virus type 1 genome. The latter explanation seems to be particularly interesting since the parainfluenza type 1 antibody titres remained constant despite the clinical progression. This finding is comparable to the elevated titres against Epstein-Barr virus of adenovirus which have been found occasionally in this disease.

Adolescent↗
PubMed1994

Infection and immunoregulation of T lymphocytes by parainfluenza virus type 3.

Human parainfluenza virus type 3 (HPIV3) is a major cause of disease in newborns and infants. It also has a striking potential to reinfect individuals throughout their lives, suggesting that HPIV3 does not induce lifelong immunity; however, the operative mechanism for the failure to prevent reinfection is not known. We have assessed the potential of the virus to infect nontransformed human T lymphocytes and have found that T cells are readily infected by the virus. Productive infection requires activation of the T cells and results in a marked inhibition of proliferation. Furthermore, our results indicate that exposure to the virus, even without overt expression of viral proteins as detected by immunohistology, profoundly alters the functional capacity of the T cells. The capacity of the virus to regulate T-lymphocyte function may play an important role in the failure of the virus to induce lifelong immunity.

Adult↗
PubMed1991

The effect of some physical and serological treatments on haemofusing activity of bovine parainfluenza virus type 3.

Bovine parainfluenza virus type 3 irrespective of the time of its harvesting from Madin-Darby bovine kidney cells, expressed little or no haemofusing activity. Treatment of the virus by freezing and thawing, sonication or antibody and complement enhanced this activity. Moreover haemofusing activity did not correlate with the viral capacity for fusion of susceptible cells in monolayer cultures.

Animals↗
PubMed1979

Characterization of bovine parainfluenza virus type 3.

Bovine parainfluenza virus type 3 (PIV-3) has a buoyant density of 1.197. The RNA of PIV-3, like that of Sendai virus, is a single continuous chain which lacks polyadenylic acid sequences and tends to self-anneal to a marked extent. It has a sedimentation coefficient of 42S and a molecular weight of 4.5 X 10(6), being slightly smaller than Sendai virus RNA (47S, 5.3 X 10(6)). PIV-3 has 5 main structural proteins, of which 2 are glycoproteins. The molecular weights of protein 1, protein 2, protein 3, glycoprotein 1, and glycoprotein 2 were estimated to be 79,000, 68,000, 35,000, 69,000, and 55,000, respectively. Protein 2 was suggested to be nucleocapsid protein.

Animals↗
PubMed1995

Molecular evolution of the F glycoprotein of human parainfluenza virus type 1.

Human parainfluenza virus type 1 (hPIV1) is a major cause of upper and lower respiratory tract infections among children. Immunity is mediated at least in part by antibody to the fusion (F) surface glycoprotein. Thus, genetic variation in the F gene could influence host range, virulence, and immunity. To examine the genetic diversity among hPIV1 isolates, the F genes of hPIV1 isolates from a single geographic location were sequenced and compared with the F gene of a strain isolated in 1957. Genetic variation was 2.2%-3.4%, averaging 0.8 amino acid changes per year. Changes were progressive over time, and virus evolution was dominated by a single lineage. Three of 7 isolates tested did not induce syncytium formation in tissue culture. This phenotype could not be ascribed to a single unique mutation in the F gene, but these 3 isolates had mutations in the transmembrane region of the HN gene. It is unlikely that the limited genetic evolution of the F gene will be an obstacle to vaccine development.

Amino Acid Sequence↗
PubMed1971

Observations on clinical and immunofluorescent diagnosis of parainfluenza virus infections.

Immunofluorescent techniques have been applied to nasopharyngeal secretions for the rapid diagnosis of parainfluenza virus types 1, 2, and 3 infections. Seventy-five infections were found by isolation techniques; 55 of these had nasopharyngeal secretions taken and 53 were positive by direct examination. A comparison of the results of 60 neutralization tests with immunofluorescence applied to monkey kidney isolations showed complete agreement. Immunofluorescence appeared to be a satisfactory method for differentiating the various haemadsorption viruses. The importance of parainfluenza viruses and respiratory syncytial virus in croup was noted and the association of the parainfluenza viruses with acute respiratory virus infection was confirmed. The clinical relationship between respiratory syncytial virus and parainfluenza virus type 3 is discussed.

Carcinoma↗
PubMed1996

Specific interaction in vitro and in vivo of glyceraldehyde-3-phosphate dehydrogenase and LA protein with cis-acting RNAs of human parainfluenza virus type 3.

Human parainfluenza virus type 3 (HPIV3) genome RNA is transcribed and replicated by the virus-encoded RNA-dependent RNA polymerase, and specific cellular proteins play a regulatory role in these processes. To search for cellular proteins potentially interacting with HPIV3 cis-acting regulatory RNAs, a gel mobility shift assay was used. Two cellular proteins specifically interacted with the viral cis-acting RNAs containing the genomic 3'-noncoding region and the plus-sense leader sequence region. Surprisingly, by biochemical and immunological analyses, one of the cellular proteins was identified as the key glycolytic enzyme, glyceraldehyde-3-phosphate dehydrogenase (GAPDH). The other protein was characterized as the autoantigen, LA protein. Both GAPDH and LA protein also interacted with the same cis-acting RNA sequences in vivo and were found to be associated with the HPIV3 ribonucleoprotein complex in the infected cells. By double immunofluorescent labeling, GAPDH was found to be co-localized with viral ribonucleoprotein in the perinuclear region. These observations strongly suggest that cellular GAPDH and LA Protein participate in the regulation of HPIV3 gene expression.

Autoantigens↗
PubMed1982

Evidence of interferon production in the hamster lung after primary or secondary exposure to parainfluenza virus type 3.

Experimental infection of the hamster respiratory tract with parainfluenza virus type 3 has been used to study the pathogenesis of viral pneumonia and the host response to infection. In this study, hamsters inoculated intranasally with parainfluenza virus type 3 produced local interferon, which was detected in lung washes obtained by in situ lavage. Interferon activity was present as early as 2 days after infection, and titers correlated directly with the quantity of virus recovered in lung washes. Parainfluenza virus type 3 was sensitive to the antiviral state induced in vitro by the lung wash interferon. Infectious virus induced interferon in cultures of immune and nonimmune lung wash cells, primarily alveolar macrophages. A secondary response of immune, mixed cultures of lymphocytes and alveolar macrophages, stimulated with inactivated virus, produced low concentrations of interferon, perhaps type II. Lymphocyte-alveolar macrophage cultures produced a pH and temperature-sensitive interferon in response to mitogen induction, characteristics of type II or immune interferons in the human and murine systems. Interferon may be an early defense involved in recovery from primary infection with parainfluenza virus type 3, and may contribute to resistance to reinfection.

Animals↗
PubMed2006

Human parainfluenza virus type 1 but not Sendai virus replicates in human respiratory cells despite IFN treatment.

Sendai virus (SeV) and human parainfluenza virus type I (hPIV1) are highly homologous but have distinct host ranges, murine versus human. To identify the factors that affect the host specificity of parainfluenza viruses, we determined the infectivity and anti-IFN activities of SeV and hPIV1 in human and murine culture cells. SeV infected normal human lung MRC-5 and murine lung MM14.Lu or MLg2908 cells efficiently. Infection with SeV induced the release of IFN-beta into culture medium in MRC-5 cells at similar levels with that of cells infected with hPIV1. SeV or hPIV1 infections, as well as expression of SeV or hPIV1 C proteins, inhibited the nuclear localization of STAT1 induced by IFN-beta, suggesting that both SeV and hPIV1 C proteins block the IFN Jak/STAT pathway in MRC-5 cells. Pretreatment of MRC-5 cells with IFN suppressed replication of SeV and hPIV1 at an early stage of infection. However, hPIV1 overcame this suppression while SeV did not. SeV replication was restored in IFN-beta pretreated murine MM14.Lu cells, suggesting SeV anti-IFN activity is species specific. These results suggest that SeV is less effective than hPIV1 in overcoming antiviral activity in human cells, which could be one of the factors that restrict the host range of SeV.

Animals↗
PubMed2002

[Parainfluenza virus type 4 infections].

OBJECTIVE: To describe the clinical and epidemiological characteristics of parainfluenza virus type 4 infections in pediatric patients. METHODS: Inpatients and outpatients with lower respiratory tract infections were studied. Recorded data were age, sex, clinical diagnosis, temperature, oxygen saturation, chest radiograph and length of hospital stay. Nasopharyngeal aspirates were studied through indirect immunofluorescence, tissue culture and a new multiplex reverse-transcriptase polymerase chain reaction (RT-PCR) able to identify the four types of human parainfluenza virus in the same reaction. RESULTS: Two hundred thirty specimens from 191 patients were analyzed. Parainfluenza viruses were diagnosed in 35.1 %: 37.3 % type 1, 10.4 % type 2, 38.9 % type 3 and 13.4 % type 4. RNA from parainfluenza virus type 4 was amplified in 10 aspirates from nine patients. Of these, all except one were aged less than two years (range: 26 days to 23 months). The clinical diagnosis was bronchiolitis or wheezing associated with lower respiratory tract infection. Six patients required admission, with a mean oxygen saturation of 89.5 % and a mean length of hospital stay of 7.6 days. DISCUSSION: This is the first description of the characteristics of parainfluenza virus type 4 in Spain. Infections associated with this virus are not as mild as previously thought. Application of a multiplex RT-PCR allows identification of respiratory infections due to parainfluenza virus type 4 that would otherwise be underdiagnosed.

Child↗
PubMed1998

Outbreak of parainfluenza virus type 3 in an intermediate care neonatal nursery.

BACKGROUND: Of the four serotypes of human parainfluenza virus, parainfluenza type 3 causes the majority of infections in young children and infants. Parainfluenza type 3 can occur in newborns, although most are born with neutralizing antibodies. There have been only infrequent reports of parainfluenza type 3 causing nosocomial respiratory infection in the newborn nursery setting. We report an outbreak occurring in the intermediate care nursery (IMCN) at St. Boniface Hospital, Winnipeg, Canada. METHOD: On August 6, 1996, nursing staff of IMCN notified Infection Control that six infants had developed respiratory tract symptoms including nasal discharge and cough. Three more cases were recognized by August 8, 1996. Infection control precautions including cohorting of infant cases and ill staff, gowning and reinforcement of hand washing practices and visitor regulations were instituted. When two further cases occurred on August 9, 1996, the unit was closed to all admissions and remained closed until August 30, 1996. The last infant case occurred on August 10, 1996. RESULTS: The attack rate among infants was 63% (12 of 19). No mortality was associated with this outbreak and morbidity was minimal (no ventilator support was required), although one-half of the infants developed radiologic pulmonary infiltrates and one-half required supplemental oxygen therapy. Parainfluenza type 3 was isolated from nasopharyngeal secretions in 6 of 12 infant cases. There was a significant difference (P = 0.02) in age between the ill and non-ill infants; ill infants were a mean age of 42 days compared with a mean age of 11 days for non-ill infants at the midpoint of the outbreak. Sixteen of 65 (25%) IMCN nursing/medical staff reported an upper respiratory tract illness between July 10 and August 18, 1996. None of the staff was cultured. CONCLUSIONS: High patient census, limited numbers of full time staff, inadequate cohorting attempts because of staffing constraints and crowding in the IMCN were thought to be contributors to this outbreak. Institution of basic barrier precautions and temporary closure of the unit were effective in preventing further spread of the outbreak.

Canada↗
PubMed2006

Human trachea primary epithelial cells express both sialyl(alpha2-3)Gal receptor for human parainfluenza virus type 1 and avian influenza viruses, and sialyl(alpha2-6)Gal receptor for human influenza viruses.

We reported previously that the dominant receptors of influenza A and B viruses, and human and murine respiroviruses, were sialylglycoproteins and gangliosides containing monosialo-lactosamine type I-and II-residues, such as sialic acid-alpha2-3(6)-Galbeta1-3(4)-GlcNAcbeta1-. In addition, the Siaalpha2-3Gal linkage was predominantly recognized by avian and horse influenza viruses, and human parainfluenza virus type 1 (hPIV-1), whereas the Siaalpha2-6Gal linkage was mainly recognized by human influenza viruses (Paulson JC in "The Receptors'' [Conn M Ed] 2, 131-219 (1985); Suzuki Y, Prog Lipid Res 33, 429-57 (1994); Ito T, J Virol 73, 6743-51 (2000); Suzuki Y, J Virol 74, 11825-31 (2000); Suzuki T, J. Virol 75, 4604-4613 (2001); Suzuki Y, Biol. Pharm. Bull. 28, 399-408 (2005)). To clarify the distribution of influenza virus receptors on the human bronchial epithelium cell surface, we investigated a primary culture of normal human bronchial epithelial (NHBE) cells using two types of lectin (MAA and SNA), which recognize sialyl linkages (alpha2-3 and alpha2-6), using fluorescence-activated cell-sorting analysis. The results showed that both alpha2-3- and alpha2-6-linked Sias were expressed on the surface of primary human bronchial epithelial cells. The cells infected by hPIV-1 bound to MAA, confirming that cells targeted by hPIV-1 have alpha2-3-linked oligosaccharides. We also compared the ability of hPIV-1 and human influenza A virus to infect primary human bronchial epithelial cells pre-treated with Siaalpha2-3Gal-specific sialidase from Salmonella typhimurium. No difference was observed in the number of sialidase pre-treated and non-treated cells infected with human influenza A virus, which binds to Siaalpha2-6Gal-linked oligosaccharides. By contrast, the number of cells infected with hPIV-1 decreased significantly upon sialidase treatment. Thus, cultured NHBE cells showed both alpha2-3-linked Sias recognized by hPIV-1 and avian influenza virus receptors, and alpha2-6-linked Sias recognized by human influenza virus receptors.

Animals↗
PubMed2003

Parainfluenza virus infection in adult lung transplant recipients: an emergent clinical syndrome with implications on allograft function.

Parainfluenza virus is a common cause of seasonal upper respiratory tract infections in children and adults. Studies indicate that parainfluenza virus may play an important role in the etiology of respiratory tract infections in lung transplant recipients with an estimated incidence of 5.3 per 100 patients. Parainfluenza virus type 3 is the most frequent serotype in lung transplant patients. The rate of lower respiratory tract infections with parainfluenza virus among lung transplant recipients is between 10 and 66% of cases. In addition, trans-bronchial biopsy at the time of parainfluenza infection shows signs of acute allograft rejection. Subsequently, 32% of patients have been found to have active bronchiolitis obliterans at a median time of 6 months (range 1-14) postviral infection. These findings indicate that parainfluenza virus infections may have long-term implications for lung transplant recipients. Further studies are required to identify the mechanisms of immunomodulation of parainfluenza virus among these patients. In addition, controlled studies are needed to evaluate the efficacy of aerosolized ribavarin in the treatment of parainfluenza virus infection and to determine whether vaccines may be effective in these high-risk patients.

Administration, Inhalation↗
PubMed1981

Persistent parainfluenza virus shedding during isolation at the South Pole.

Persistent parainfluenza virus shedding in healthy young adults occurred throughout the 8 1/2-month winter isolation period at Amundsen-Scott South Pole Station during 1978. Two episodes of respiratory illness were observed after 10 and 29 weeks of complete social isolation. Throat swabs collected both routinely, and during each outbreak of respiratory illness, were directly inoculated into cell cultures. Parainfluenza virus types 1 and 3 were recovered from both symptomatic and asymptomatic subjects throughout the winter. No other viruses were obtained by these efforts. The presence of parainfluenza virus in these subjects long after the accepted incubation period for viral upper respiratory illness, and when the introduction of new virus to this community was impossible, suggests its persistence in man.

Animals↗
PubMed1983

Survival of human parainfluenza viruses in the South Polar environment.

The survival of human parainfluenza virus types 1, 2, and 3 was measured in both indoor and outdoor environments at South Pole Station, Antarctica, in an effort to determine the long-term survival of these viruses in this environment and to identify the possible source of respiratory tract illnesses which occurred in this isolated population in 1978 after 10 and 27 weeks of total social isolation. Viruses were applied to plastic petri plate surfaces which were then stored in indoor (21.4 degrees C; water vapor density, 1.50 g of water per m3) and outdoor environments (-22.4 to -33.2 degrees C; water vapor density, 0.706 and 0.247 g of water per m3). Parainfluenza virus type 1 at an initial titer of 3.75 log10 50% tissue culture infective doses per ml was inactivated after 4 days at room temperature and after 7 days outside. Parainfluenza virus type 2 and 3 at initial titers of 5.58 and 5.38 log10 50% tissue culture infective doses per ml were inactivated after 7 and 12 days, respectively, at room temperature and after 17 days of storage outside. Results indicate that the long-term survival of parainfluenza virus in either environment for up to 10 weeks is unlikely and probably did not provide the source of infectious virus responsible for the midisolation outbreaks of parainfluenza virus-related respiratory tract illnesses observed in this population during the 1978 winter season.

Antarctic Regions↗
PubMed2004

Adenovirus-mediated gene therapy enhances parainfluenza virus 3 infection in neonatal lambs.

Parainfluenza viruses are a common cause of seasonal respiratory disease, but in high-risk individuals (e.g., young children) these viruses can cause severe clinical manifestations that require hospitalization. Beta-defensins are a subclass of antimicrobial peptides with antiviral activity. Use of adenovirus-mediated beta-defensin gene expression has been proposed as therapy for chronic bacterial infections commonly seen in cystic fibrosis patients; however, its use during parainfluenza virus 3 (PIV3) infection has not been evaluated. The hypothesis in this experiment was that adenovirus expression of human beta-defensin 6 (HBD6) would diminish concurrent PIV3 infection in neonatal lambs. The group infected with adenovirus HBD6 and PIV3 had increased levels of pulmonary neutrophil recruitment compared to those for the group infected with PIV3 or PIV3 and adenovirus, with an increased respiration rate and body temperature late in the course of the PIV3-adenovirus HBD6 infection. Interestingly, the adenovirus-treated groups had higher levels of immunohistochemical staining for PIV3 and syncytial cell formation than the group infected with PIV3, suggesting that treatment with the adenovirus vector, regardless of whether it was carrying a target gene, exacerbated the PIV3 infection. The levels of expression of mRNA for antimicrobial surfactant proteins A and D and sheep beta-defensin 1 were increased by PIV3 and adenovirus treatment, and the increased levels of expression roughly corresponded to the degree of inflammation. While pulmonary administration of a high-dose adenovirus vector has been associated with undesirable inflammation, this is the first study to show that it can exacerbate concurrent viral infection, a concern that needs to be addressed for future studies of adenovirus in the lung. Additionally, this study showed that adenovirus-mediated HBD6 expression increases neutrophil recruitment, a recently described attribute of beta-defensins, with mild accentuation of PIV3 activity and inflammation.

Adenoviruses, Human↗
PubMed1981

Comparative inhibition of influenza and parainfluenza virus replication by ribavirin in MDCK cells.

Actinomycin D inhibited the yield of influenza virus hemagglutinin from MDCK cells infected at high multiplicity, but had little effect on the yield of parainfluenza virus hemagglutinin. In similar hemagglutinin yield experiments, ribavirin was only slightly more active (threefold) against influenza virus than against parainfluenza virus replication. In plaque inhibition experiments, ribavirin depressed influenza virus plaque formation by 50% at a concentration of approximately 3 micrograms/ml, whereas the corresponding figure for parainfluenza viruses was threefold higher. The concentration of ribavirin demonstrating anti-influenza activity was indistinguishable for that inhibiting host cell growth. It is concluded that, unlike actinomycin D, ribavirin is unlikely to have a major effect on the provision of host cell 5-germinal methylated cap structures and the subsequent priming of influenza messenger ribonucleic acid synthesis.

Animals↗
PubMed1996

Rescue of Sendai virus cDNA templates with cDNA clones expressing parainfluenza virus type 3 N, P and L proteins.

Several years ago, we reported that a Sendai virus (SeV) defective genome (DIH4UV) could be rescued in vivo with human parainfluenza virus type 1 (hPIV1) and bovine PIV3 but not by measles virus or vesicular stomatitis virus. It was concluded that the cis-acting RNA sequences were conserved within the SeV/PIV1/PIV3 group but that interactions between the polymerase complex (P-L) and the template protein N were unique for each virus. We have re-examined these conclusions using proteins expressed from cloned N, P and L genes for SeV and PIV3. The results demonstrate the specificity of the protein-protein interactions between polymerase and template, and confirm the prediction of the earlier work that PIV3 N, P and L proteins are capable of assembling and replicating SeV mini-genomes also expressed from a cDNA clone.

Animals↗