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PubMed1990

Molecular cloning and sequence analysis of human parainfluenza type 4A virus HN gene: its irregularities on structure and activities.

We cloned the cDNA of human parainfluenza type 4A virus (PIV-4A) HN gene by reverse-transcription of virus-specific mRNAs and genomic RNA, and determined the complete nucleotide sequence of the HN gene. The predicted HN protein sequence of PIV-4A showed significant relatedness with those of other paramyxoviruses, SV5, NDV, MuV, PIV-3, BPIV-3, indicating a common ancestor. The homologies between the viruses suggested that PIV-4A is more closely related to NDV, SV5, and MuV than to the parainfluenza viruses, PIV-3, bovine parainfluenza type 3 virus (BPIV-3), and Sendai virus (SV). Sixty amino acids were commonly conserved among the viruses, other than PIV-4A. Two of these amino acids were substituted in PIV-4A HN and are predicted to be located near the active site of the neuraminidase. The analysis of neuraminidase of PIV-4 revealed that the activity is hardly detectable, suggesting the significant effect of the substituted amino acid sites on neuraminidase activity.

Amino Acid Sequence↗
PubMed1995

Evaluation of the antiviral activity of N-(phosphonoacetyl)-L-aspartate against paramyxoviruses in tissue culture and against respiratory syncytial virus in cotton rats.

N-(phosphonoacetyl)-L-aspartate (PALA), a potent inhibitor of L-aspartic acid transcarbamoylase, was evaluated for cytotoxicity and antiviral activity against three different paramyxoviruses in tissue culture, and for antiviral efficacy and toxicity in vivo using a cotton rat-respiratory syncytial virus (RSV) model. Significant in vitro cytotoxicity was observed in proliferating cultures of HEp-2 (IC50 = 250 micrograms/ml) and Vero cells (IC50 = 32 micrograms/ml), but was less evident in cultures containing confluent monolayers (i.e., stationary cells) of these cells, or in cultures of Madin Darby canine kidney (MDCK) cells (these IC50 values were all > or = 750 micrograms/ml, with 1000 micrograms/ml being the maximum concentration tested). Mean selective indices (ratio of the median cytotoxic dose: median efficacious dose) of 1, 72 and 146 were obtained against parainfluenza virus type 3, RSV and measles virus, respectively, when PALA was tested against these viruses using confluent HEp-2 and Vero cell monolayers. In cotton rats, significant reductions in pulmonary titers (0.8-1.4 log10/g lung) compared to pulmonary viral titers in placebo-treated control animals, were consistently seen in cotton rats given > or = 10 mg of PALA/kg/day (b.i.d.) intraperitoneally on days 1-3 postinfection with either subtype A or B RSV. No toxic effects were noted even in animals given 100 mg of PALA/kg/day for 7 consecutive days.

Animals↗
PubMed1985

Immunoglobulin G subclass antibody responses in influenza A and parainfluenza type 1 virus infections.

Antibody responses in immunoglobulin G1, G2, G3, G4, A (IgA1) and M isotypes were studied in 10 patients with an acute influenza A and in another 10 patients with a parainfluenza type 1 virus infection using radioimmunoassay with standardized monoclonal anti-immunoglobulins. A four-fold or greater increase of antibody in patients have an acute influenza A virus infection, were found in IgG1 (all 10 cases), IgG3 (seven cases), IgG4 (eight cases) and in IgA1 (six cases) whereas IgG2 and IgM responses were observed only in one and three cases, respectively. The antibody titre values were converted to immunoglobulin units by multiplying the titre by a pre-determined correction coefficient compensating for the varying affinity of the individual monoclonal anti-immunoglobulins. These units were then used to calculate the actual proportions of each isotype. In the convalescent phase, 78% of total anti-influenza A antibodies were estimated to be of IgG1 isotype and other immunoglobulin isotypes varied from 3 to 7% of total. Similar results in parainfluenza virus antibodies were obtained with serum pairs from patients with an acute parainfluenza virus infection.

Antibodies, Viral↗
PubMedDate not supplied

Clinical observations on mechanical ventilation for respiratory failure in bronchiolitis.

An unusually large number of infants (82) were admitted to Stanford University Hospital from November 1, 1983, through May 31, 1985, with a diagnosis of bronchiolitis requiring oxygen therapy. A larger percentage of these infants (17/82 = 21%) than generally expected required mechanical ventilation for respiratory failure. Fourteen infants had respiratory syncytial virus (RSV) infections, and three had parainfluenza virus infections. Ten patients had respiratory difficulties as neonates. The mechanical ventilation of the children requiring respiratory assistance was characterized by high minute ventilation with high tidal volumes (15 to 20 ml/kg) and slow respiratory rates (16 to 22 breaths/min). Peak inspiratory pressure averaged (mean +/- SD) 35 +/- 6 cm H2O in the RSV group and 34 +/- 6 cm H2O in the parainfluenza group. The mean number of days on the ventilator was 9.7 +/- 3.1 for the RSV group and 8.3 +/- 2.9 for the parainfluenza group. All were extubated within 17 days of presentation and discharged within 28 days. The complications encountered included pneumothorax and acute pulmonary hypertension.

Bronchiolitis, Viral↗
PubMed2000

Comparison of identical temperature-sensitive mutations in the L polymerase proteins of sendai and parainfluenza3 viruses.

The L subunit of the RNA-dependent RNA polymerase of negative strand RNA viruses is believed to possess all the enzymatic activities necessary for viral transcription and replication. Mutations in the L proteins of human parainfluenza virus type 3 (PIV3) and vesicular stomatitis virus (VSV) have been shown to confer temperature sensitivity to the viruses; however, their specific defects have not been determined. Mutant PIV3 L proteins expressed from plasmids were tested for temperature sensitivity in transcription and replication in a minigenome reporter system in cells and for in vitro transcription from purified PIV3 template. The single L mutants, Y942H and L992F, were temperature sensitive (ts) in both assays, although viral RNA synthesis was not completely abolished at the nonpermissive temperature. Surprisingly, the T1558I L mutant was not ts, although its cognate virus was ts. Thus the ts defect in this virus may be due to the abrogation of an essential interaction of the mutant polymerase with a host cell component, which is not measured by the RNA synthesis assays. Most of the combinations of the PIV3 L mutations were not additive and did not show temperature sensitivity in in vitro transcription. Since they were ts in the minigenome assay in vivo, replication appears to be specifically defective. The ts mutations in PIV3 and VSV L proteins were also substituted into the Sendai L protein to compare the defects in related systems. Only Sendai Y942H L was ts in both transcription and replication. One Sendai L mutant, L992F, gave much better replication than transcription. Several other mutants could transcribe but not replicate in vitro, while replication in vivo was normal.

Amino Acid Sequence↗
PubMed1991

Effects of 4-ipomeanol on bovine parainfluenza type 3 virus-induced pneumonia in calves.

Previous research has demonstrated that 4-ipomeanol toxicosis can enhance the severity of para-influenza virus-induced pneumonia in mice. The objectives of this study were to determine whether calves are susceptible to 4-ipomeanol-induced enhancement of parainfluenza type 3 viral pneumonia and to determine whether 4-ipomeanol alters pulmonary replication of parainfluenza virus. Male Holstein calves were injected with either 4-ipomeanol (3 mg/kg) or vehicle (polyethylene glycol) 3 days prior to intratracheal inoculation with either parainfluenza virus or sham inoculum of culture medium. Calves in the four treatment groups (ipomeanol-parainfluenza, ipomeanol-medium, vehicle-parainfluenza, and vehicle-medium) were necropsied at 5 days after inoculation with parainfluenza virus or medium. The lungs were studied by correlated methods of light and electron microscopy, digitizing morphometry and pulmonary lavage to quantitate the severity of pneumonia. Pulmonary viral titers were determined, and viral antigen was identified in the lung by immunoperoxidase technique. The calves in the ipomeanol-virus treatment group had over a 9-fold higher (P less than 0.05) volume density of virus-induced interstitial pneumonia than did the calves in the other three treatment groups. This 4-ipomeanol-enhanced viral pneumonia was associated with significantly greater (P less than 0.05) numbers of pulmonary macrophages and neutrophils in the lavage fluid and higher (P less than 0.05) pulmonary titers of pulmonary infectious parainfluenza virus. Four-ipomeanol-enhanced viral pneumonia was characterized in part by extensive hyperplasia of type II alveolar epithelial cells and by dense aggregates of macrophages and neutrophils in alveolar spaces and interalveolar septa. The results indicate that 4-ipomeanol exacerbates interstitial pneumonia in calves induced by bovine parainfluenza type 3 virus.

Animals↗
PubMed2005

Contamination of a specific-pathogen-free rat breeding colony with Human parainfluenzavirus type 3.

Routine antibody surveillance for Sendai virus in a breeding colony suggested viral invasion into laboratory rats. A more specific haemagglutination-inhibition test implied that the agent was related closely to Human parainfluenza virus type 3 (hPIV3), rather than Sendai virus. To isolate this virus, Vero cells were inoculated with lung homogenates of 30 young animals from the colony. One of the cultures became positive at the second passage by RT-PCR directed to the hPIV3 NP and L genes. Cytopathic effect with cell fusion was observed at the third passage. The HN gene of this virus (KK24) had >93 % similarity to those of other hPIV3 isolates, suggesting a human origin of KK24. Experimental intranasal inoculation of KK24 into SD rats showed virus replication in the lungs at 3-5 days post-infection (p.i.). Pathological examination of the lungs at day 5 p.i. indicated a moderate detachment, degradation and apoptosis of bronchial epitheliocytes with peribronchial mononuclear infiltrations. At day 7 p.i., these changes became less prominent, and no lesions were apparent at day 10 p.i. or later. The infected rats seroconverted at day 7 p.i. On the contrary, none of the 30 experimentally infected ICR mice showed any pathological lesions in their lungs, despite seroconversion at 7 days p.i. These results suggest that hPIV3 can invade rat colonies and has a moderate and transient pathogenicity in rats. This is the first report of non-experimental hPIV3 infection in laboratory rats, unexpectedly detected by antibody screening for Sendai virus.

Animals↗
PubMedDate not supplied

[The antiviral activity of deitiforin in experimental para-influenza infection].

Deitiforin in HEp-2 cell culture was shown to inhibit replication of the reference PIV-3 strain when administered 1 hour before virus inoculation. The most marked effect of the drug was observed in the first 4 days of observation. In experimental newborn mice infected with parainfluenza virus 3 deitiforin protected the animals from developing the infection. In humans given deitiforin reaction to vaccination was found to develop 5-6 times more rarely than in the control group, PIV-3 could be isolated twice as rarely, and a diagnostically significant rise of specific antibody levels was observed less frequently.

Adult↗
PubMed1986

Complete sequence of the major nucleocapsid protein gene of human parainfluenza type 3 virus: comparison with other negative strand viruses.

The sequence of the major nucleocapsid protein (NP) mRNA and its encoded protein were deduced by sequencing a cDNA clone representing the complete mRNA. The cDNA sequence was confirmed by dideoxynucleotide sequencing of purified viral genomic RNA by primer extension using synthetic oligonucleotides. The NP mRNA contains 1,641 nucleotides exclusive of poly(A) and encodes an NP protein of 515 amino acids. Alignment of the human parainfluenza type 3 virus (PF3) NP protein sequence with that of Sendai virus showed that the two proteins shared considerable sequence identity (58.8%). Additional comparisons provided highly significant statistical evidence that the PF3 NP protein sequence is related to those of measles and canine distemper viruses, but there was no evidence of relatedness with the nucleocapsid proteins of respiratory syncytial virus, influenza B virus, or vesicular stomatitis virus.

Amino Acid Sequence↗
PubMed1974

Molecular weight determination of Sendai and Newcastle disease virus RNA.

The molecular weights of Sendai and Newcastle disease virus RNA were estimated by sedimentation in sucrose gradients and by length measurements in the electron microscope under both denaturing and nondenaturing conditions. Sedimentation analyses under denaturing conditions yielded molecular weight estimates of 2.3 x 10(6) to 2.6 x 10(6), whereas length measurements yielded estimates of 5.2 x 10(6) to 5.6 x 10(6) for both denatured and nondenatured viral RNA. It would appear that the conditions of denaturation used (99% dimethyl sulfoxide at 26 C, and reaction with 1.1 M formaldehyde for 10 min at 60 C) do not equally denature parainfluenza virus RNA and other RNAs, such as cellular rRNA, 45S rRNA precursor, and R17 RNA.

Animals↗
PubMed1992

Diagnosis and management of parotitis.

Of all the salivary glands, the parotid gland is most commonly affected by an inflammatory process. Infections of the parotid gland range from acute to severe. Assessment of the disease process should differentiate local primary parotid infection from systemic infection when this gland is also involved as part of a generalized inflammatory condition. Viral parotitis can be caused by paramyxovirus (mumps), Epstein-Barr virus, coxsackievirus, and influenza A and parainfluenza viruses. Acute suppurative parotitis is generally caused by Staphylococcus aureus, Streptococcus species, and rarely, gram-negative bacteria. Anaerobic bacteria, mostly Peptostreptococcus species and Bacteroides species, and pigmented Porphyromonas species and Prevotella species have been recently recognized as an important cause of this infection. beta-Lactamase-producing organisms can be isolated in almost three fourths of the patients. Predisposing factors to suppurative infections are dehydration, malnutrition, oral neoplasms, immunosuppuration, sialolithiasis, and medications that diminish salivation. Pus, aspirated from a suppurative parotic abscess, should be plated on media that are supportive for the growth of aerobic and anaerobic bacteria, mycobacteria, and fungi. Early and proper antimicrobial therapy may prevent suppuration. Initial empiric therapy that is directed against both aerobic and anaerobic bacteria may be required until a specific causal diagnosis is available. Surgical drainage may be indicated when pus has formed. This may prevent complications and facilitate recovery.

Diagnosis, Differential↗
PubMed1985

Etiology of community-acquired pneumonia in patients requiring hospitalization.

The etiology of community-acquired pneumonia was studied in 127 patients with roentgenologically verified pneumonia who needed hospitalization. Etiology was determined on the basis of a positive blood culture and/or a significant antibody titer increase. Streptococcus pneumoniae was the probable etiological agent in 69 patients, nontypeable Haemophilus influenzae in five patients, Streptococcus pyogenes in two patients, and Legionella pneumophila and Staphylococcus aureus in one patient each. Evidence of Mycoplasma pneumoniae infection was found in 18 patients and of Chlamydia psittaci infection in three patients. Influenza virus type A was the cause of infection in 15 patients. One patient had infection with influenza virus type B, one patient with parainfluenza virus type 1, and three patients with respiratory syncytial virus. In 20 patients there was evidence of infection with more than one microorganism. No etiological agent was found in 27 patients. Since Streptococcus pneumoniae was the predominant etiological agent penicillin should be drug of first choice in patients with pneumonia who need treatment in hospital. In young adults, however, the high frequency of Mycoplasma pneumoniae infection would justify the use of erythromycin or doxycycline as drug of first choice.

Adolescent↗
PubMed2005

Investigation into the causes of canine infectious respiratory disease: antibody responses to canine respiratory coronavirus and canine herpesvirus in two kennelled dog populations.

Two training centres for working dogs were monitored for one year to determine the presence of viruses and viral antibodies and their association with canine infectious respiratory disease (CIRD). Tonsillar swabs and serum were obtained from dogs on entry into the kennels and in regular intervals thereafter. Additional samples were collected during outbreaks of CIRD. The swabs were examined by virus culture and PCR for canine parainfluenza virus, canine adenovirus, canine herpesvirus (CHV) and canine respiratory coronavirus (CRCoV). Furthermore the prevalence of antibodies to CHV and CRCoV was determined. During this study CIRD was reported mainly in one of the two kennels investigated. In that kennel antibody responses to CRCoV indicated a seasonal occurrence of the virus, which coincided with two outbreaks of respiratory disease. CHV antibody responses were detected throughout the year. In the other kennel, which reported few cases of CIRD a high prevalence of antibodies to CRCoV was detected on entry but only sporadic seroconversions to CRCoV or CHV. By PCR three dogs were found positive for CRCoV in one kennel whereas all PCR tests for other viruses were negative for both kennels. Virus culture failed to detect any viruses in either kennel.

Animals↗
PubMed2005

TNF-alpha and IFN-alpha enhance influenza-A-virus-induced chemokine gene expression in human A549 lung epithelial cells.

Lung epithelial cells are the primary cellular targets for respiratory virus pathogens such as influenza and parainfluenza viruses. Here, we have analyzed influenza A, influenza B and Sendai virus-induced chemokine response in human A549 lung epithelial cells. Influenza virus infection resulted in low CCL2/MCP-1, CCL5/RANTES, CXCL8/IL-8 and CXCL10/IP-10 production at late times of infection. However, when cells were pretreated with TNF-alpha or IFN-alpha, influenza-A-virus-induced chemokine production was greatly enhanced. Cytokine pretreatment resulted in enhanced expression of RIG-I, IKKepsilon, interferon regulatory factor (IRF)1, IRF7 and p50 proteins. Most importantly, influenza-A-virus-induced DNA binding of IRF1, IRF3, IRF7 and NF-kappaB onto CXCL10 ISRE and NF-kappaB elements, respectively, was markedly enhanced in cytokine-pretreated cells. Our results suggest that IFN-alpha and TNF-alpha have a significant role in priming epithelial cells for higher cytokine and chemokine production in influenza A virus infection.

Blotting, Northern↗
PubMed2004

Control of nonsegmented negative-strand RNA virus replication by siRNA.

Our laboratory provided the first proof-of-concept that double-stranded short interfering RNA (ds-siRNA) can act as potent and specific antiviral agents. Designed against specific mRNAs of nonsegmented negative-stranded RNA (NNR) viruses, siRNAs abrogated expression of the corresponding viral proteins, and generated the predicted viral phenotypes. Knockdown was demonstrated across different genera: respiratory syncytial virus (RSV), a pneumovirus; vesicular stomatitis virus (VSV), a rhabdovirus; and human parainfluenza virus (HPIV), a paramyxovirus. The targeted genes could have a wide range of functions, thus documenting the versatility of the technique. Interestingly, antisense single-stranded siRNA (ss-siRNA) was also effective, albeit at a higher concentration. NNR viral genomic and antigenomic RNA, which are encapsidated by nucleocapsid protein and serve as templates for viral RNA-dependent RNA polymerase, were resistant to siRNA. Together, siRNAs offer complementary advantages over traditional mutational analyses that are difficult to perform in NNR viruses, and are also an important new tool to dissect host-virus interactive pathways.

Gene Expression Regulation, Viral↗
PubMed2003

Role of respiratory viruses in children with acute otitis media.

OBJECTIVE: The role of viral infection in acute otitis media (AOM) has not been fully elucidated. We determined the presence of various respiratory viruses in middle ear fluid (MEF) specimens from children with AOM in order to determine whether viral infection or combined effects of viral and bacterial infection enhance or prolong the inflammation in the middle ear, thus worsening clinical outcome. METHODS: Multiplex nested reverse transcription-polymerase chain reactions was carried out to detect influenza A and B viruses, respiratory syncytial virus (RSV) types A and B, parainfluenza virus types 1, 2, and 3; rhinovirus; and adenovirus in 93 MEF specimens from 79 children with AOM. And we examined whether viral infection with or without an identifiable bacterial infection affect clinical outcomes in AOM. We considered persistent MEF (fluid accumulation in the middle ear persisting up to 1 month after treatment), early recurrence of AOM (within 1 month after initial improvement), and recurrent AOM (more than three recurrences during 6 months of follow up) as indicators for evaluating clinical outcomes. RESULTS: One or more respiratory viruses were detected in 39 specimens (42%); a total of 42 viral infections identified (three specimens were infected by two viruses). Of the 42 infections, RSV type A was detected in 29, adenovirus in eight, rhinovirus in three, and influenza virus in two. RSV accounted for 73% of viral detections. In children younger than 2 years, RSV infection combined with Streptococcus pneumoniae or Hemophilus influenzae infection carried a higher risk for persistent middle ear effusion than infection with RSV infection alone or those bacterial infection alone. CONCLUSIONS: Accordingly, vaccination of young children against RSV as well as S. pneumoniae and H. influenzae is important in improving the prognosis in AOM.

Acute Disease↗
PubMed2003

The antiviral activity of naturally occurring proteins and their peptide fragments after chemical modification.

Chemical modification of the proteins bovine serum albumin, alpha-lactalbumin, beta-lactoglobulin and chicken lysozyme by 3-hydroxyphthalic anhydride (3-HP) yielded compounds which exerted antiviral activity in vitro as compared with the native unmodified proteins. Of the three enveloped viruses tested, human herpes simplex virus type 1 (HSV-1), bovine parainfluenza virus type 3 and porcine respiratory corona virus, only HSV-1 proved sensitive to the 3-HP-proteins. All of the chemically modified proteins presented antiviral activity against HSV-1 when assayed before, during or after infection. However, to achieve HSV-1 inhibition, significantly higher concentrations of the modified proteins were required if present before infection as compared to during or after infection. Our results suggest that multiple mechanisms are involved in the inhibition of HSV-1 infection. Proteolytical digestion of albumin, alpha-lactalbumin, beta-lactoglobulin and lysozyme by trypsin, chymotrypsin and pepsin yielded several peptide fragments with antiherpetic activity. Chemical modification of these peptide fragments by 3-HP generated peptides with antiviral activity, however, this was almost always combined with a cytotoxic effect on the Vero cells. Overall, our results suggest that targeted chemical modification of some natural products might provide compounds effective against HSV-1 infection.

Albumins↗