Incorporation of tritiated uridine into KB cells infected with parainfluenza 3 virus.
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A total of 814 newborns were examined using a highly sensitive method of indication of viral antigens. A high incidence of congenital viral infection was revealed: 450 per 1000 live-born children. Enteroviral infections (mainly Coxsackie) ranked first in prevalence. These infections in the newborns are mainly caused by the vertical transmission of enteroviruses from mothers with persistent forms of infections. Virtually all the other viruses (influenza viruses, cytomegalovirus, herpes simplex virus, parainfluenza, measles, and rubella viruses) are detected in the newborns included in the group at a high risk of vertical transmissions of enteroviral infections. In the majority of cases the said viruses were detected in association with enteroviruses.
We examined serum amyloid protein A (SAA) and C-reactive protein (CRP) as inflammatory markers of viral and bacterial infections. Both acute-phase reactants increased in the acute stage and thereafter decreased in the convalescent stage. In viral infections, the mean serum concentrations of SAA during the acute stage were 141 mg/L in infections with adenovirus, 77 mg/L with measles virus, 63 mg/L with influenza virus, 55 mg/L with parainfluenza virus, 31 mg/L with respiratory syncytial virus, and 31 mg/L in aseptic meningitis. The mean serum concentration of CRP was 19 mg/L for adenovirus infection and < 7 mg/L in all other viral infections. The SAA concentrations were 5- to 11-fold greater than the CRP concentrations. Both the SAA and the CRP concentrations were higher in bacterial infections than in viral infections. Changes in the concentrations of serum SAA paralleled those in serum CRP in bacterial infection; during the course of viral infection, however, serum SAA tended to disappear more quickly than CRP did. SAA appears to be a clinically useful marker of inflammation in acute viral infections, with or without significant changes in the CRP concentration.
Disease is a potential threat to many endangered populations and may originate from sympatric domestic species. This paper describes a cross-sectional serological survey of canine pathogens carried out in domestic (n = 70) and wild dogs (Lycoan pictus) (n = 6), in Tsumkwe District, northeastern Namibia. Evidence of past exposure to canine distemper virus, canine adenovirus and parainfluenza virus was evident in both wild and domestic dogs with this, the first, documented exposure of free-living wild dogs to canine distemper. Domestic dogs were also exposed to rabies virus, canine parvovirus and coronavirus. There was no pathogen to which wild dogs, but not domestic dogs, were exposed. With wild dogs known to be susceptible to rabies and canine distemper, these may be the greatest threat to this population of wild dogs, although some wild dogs can clearly survive infection with canine distemper.
Gianotti-Crosti syndrome (GCS), a self-limiting papulovesicular acrodermatitis often associated with underlying viral infection, is mainly described in children. Nine children with GCS were evaluated with dermatologic examination and serologic tests for viral infections. Therapy was modified according to the subjective symptoms of patients, which included characteristic acrolocated papulovesicles, generalized skin eruption, and mild to severe pruritus. Results of serologic investigations revealed Epstein-Barr virus, Coxsackie A virus, parvovirus B19, and parainfluenza virus 1/2. In three children no underlying viral infection was found. Therapeutic interventions included topical clioquinol lotion 1 percent, topical application of corticosteroids, systemic antihistaminic therapy, and systemic methylprednisolone. Skin lesions resolved after 2 to 4 weeks in treated as well as in nontreated children. Although GCS in children often lacks close association with a causative viral infection, such severe infections as hepatitis B and human immunodeficiency virus must be considered. Whole-body involvement seems to correlate with severe pruritus and additional general symptoms requiring more intensive therapy.
Infections with influenza virus, A/Beijing 353/89 (H3N2) strain, to which there were associated parainfluenza virus type 3, 739-2D strain, adenovirus type 3, and respiratory syncytial virus Long strain, were experimentally induced in white mice. The experimental models were set up so as to permit the obtaining of an associated infection with three viruses, in which the influenza virus should be inoculated the first, the participation of the others being variable, according to their presence by alternation. The infections were detected by means of the presence of homologous serum antibodies, of positive immunofluorescence reactions in the pulmonary tissue, of the histological, histochemical and histoenzymatic lesions at the level of the respiratory system, as well as of pathomorphological changes in other organs. The severity of lesions varied from one to another infection produced by a viral association. At the level of the pulmonary parenchyma, the inflammatory lesion had a frequency of 100%. The severest pathomorphological picture characterized the diffuse interstitial lymphohistio-macrophagocytic bronchopneumonia. The bronchopulmonary block was marked by cytoinfiltrative processes, with a prevalence of lymphocytes in the infection with influenza virus + adenovirus + respiratory syncytial virus, but with a proportionality between lymphocytes and histiocytes in the other infections. The lesion of the highest incidence was the thickening of interalveolar septa, as a consequence of stasis hyperemia, oedema and lymphohistio-macrophagocytic cytoinfiltrate, sometimes associated with hyalinosis of tunica media of the blood vessels and of the Reisseisen's muscle. In other organs, particularly in the liver and kidney, vascular lesions, stasis hyperemia, inflammatory and dystrophico-inflammatory lesions were present; in the spleen, megakaryocyte hyperplasia was recorded at a significant rate in associated infections in which the adenovirus was present.
Biologically speaking, Sendai virus (SeV), the murine parainfluenza virus type 1, is perceived as a common respiratory pathogen that is endemic in many rodent colonies throughout the world. Currently it is believed that SeV is the leading cause of pneumonia in mice and together with the mouse hepatitis viruses, is the most prevalent and important of the naturally occurring infections of mice. The scientific community also considers SeV as the archetype organism of the Paramyxoviridae family because most of the basic biochemical, molecular and biologic properties of the whole family were derived from its own characteristics. Recently, scientific interest for this old pathogen has re-emerged, this time because of its potential value as a vector for gene transfer. This review aimed at drawing an exhaustive picture of this multifaceted pathogen.
Both virus-mediated damage to airway tissues and induction of pro-inflammatory cytokines such as interleukin-8 (IL-8) could contribute to symptom severity during viral respiratory infections in children. To test the hypothesis that IL-8 contributes to the pathogenesis of respiratory symptoms during naturally acquired respiratory viral infections in children, nasal wash samples collected from infants with acute viral infections (n = 198) or from healthy uninfected infants (n = 31) were analysed for IL-8. Nasal wash IL-8 was positively related to age in uninfected children (rs = 0.36, p < 0.05). Respiratory syncytial virus (RSV) infection caused more severe respiratory symptoms compared to infections with influenza A, parainfluenza viruses, or rhinoviruses. In addition, RSV, parainfluenza and rhinovirus infections increased levels of IL-8 in nasal lavage fluid, and there were some differences in the ability of the viruses to induce IL-8 production (RSV>influenza, p < 0.05). Finally, there were significant correlations between nasal wash IL-8 levels and symptom scores during infections with rhinovirus (rs = 0.56, p < 0.001) or influenza A (rs = 0.45, p < 0.05), but not with parainfluenza virus or RSV. These findings provide evidence of a close relationship between the generation of IL-8 and symptoms during acute community-acquired infections with rhinovirus or influenza A. In contrast, for RSV and parainfluenza infections, factors in addition to IL-8 production appear to contribute to the generation of clinical symptoms.
The hemagglutinin-neuraminidase (HN) gene of human type 3 parainfluenza virus has been inserted into a baculovirus expression vector under the control of the polyhedrin promoter. HN protein produced in insect cells by the recombinant baculovirus appeared to be glycosylated, was transported to the cell surface, and was biologically active. All of the HN epitopes previously mapped functionally to a region(s) involved in neuraminidase and/or hemagglutination activities were conformationally unaltered on the recombinant protein. The HN produced in this system also induced a protective immune response in immunized cotton rats. From these studies we conclude that the HN expressed in insect cells represents a source of authentic HN glycoprotein suitable for structural analysis and immunization.
cDNAs encoding the G glycoprotein of respiratory syncytial virus and the hemagglutinin-neuraminidase (HN) glycoprotein of parainfluenza virus type 3 were modified by site-specific mutagenesis and restriction fragment replacement to encode chimeric proteins consisting of the cytoplasmic and transmembrane domains of one protein fused to the ectodomain of the other. In the case of the HN ectodomain attached to the G transmembrane and cytoplasmic domains, cell surface expression of the chimera was reduced. Otherwise, the presence of the heterologous transmembrane and cytoplasmic domains had little effect on the processing of the HN or G ectodomain, as assayed by the acquisition of N-linked and O-linked carbohydrates, transport to the cell surface and, in the case of HN, folding, oligomerization, and hemadsorption activity. These results showed that the synthesis and processing of each ectodomain did not require the homologous transmembrane and cytoplasmic domains. In particular, O glycosylation of the G protein was specified fully by its ectodomain, even though this domain is highly divergent among the respiratory syncytial virus antigenic subgroups. In addition, whereas the cytoplasmic and transmembrane domains of the G protein were relatively highly conserved, they were nonetheless fully replaceable without significantly affecting processing.
Feeder calves were vaccinated with modified live virus (MLV) bovine parainfluenza-3 (PI-3) vaccines by the nasal and parenteral routes. Thirty days later they were challenged with the SF-4 strain of virus. Serum hemagglutination-inhibition (HI) antibodies and neutralizing antibodies in nasal secretions were compared with unvaccinated control calves. Both vaccines produced satisfactory circulating antibodies, but intranasal vaccination produced higher levels of antibodies in nasal secretions. After challenge PI-3 virus was not isolated from the vaccinated calves or two contact control unvaccinated calves but was isolated from all unvaccinated control calves isolated from vaccinated calves.
Only rarely do GUG (or CUG or ACG) codons which precede the 5'-proximal AUG function as initiators of protein synthesis, even when they are within a context that contains a purine at position -3 and a G at +4. For example, the upstream GUG of the human parainfluenza virus type 1 (hPIV1) P gene is initiated by ribosomes at high frequency, whereas a seemingly similar GUG codon in the hPIV3 P gene is not used at all. We have examined the reasons for this by expressing chimeric hPIV3/hPIV1 mRNAs, both in vivo and in vitro. A major determinant for efficient GUG utilization was located downstream of the GUG, but this did not appear to be involved in the formation of secondary structure. Rather, the sequence immediately downstream was found to be critical; this determinant was mapped to positions +5 and +6. GUG could be used efficiently for ribosomal initiation when the second codon was GAU but not when it was GUA. Similar results were found when other non-AUG start sites, the Sendai virus P gene ACG and the c-myc-1 CUG, were examined. These results suggest that positions +5 and +6 are important determinants for initiation at non-AUG start sites, and that they are recognized independently of the overall secondary structure of the mRNA.
A hospital virology laboratory in Hong Kong tested 10,852 sera by complement fixation (CF) for antibodies against agents of respiratory disease between 1 July 1986 and 31 December 1991. Ten commercially supplied antigens were used: influenza virus types A and B, parainfluenza virus types 1, 2 and 3, adenovirus, respiratory syncytial virus (RSV), Mycoplasma pneumoniae, Chlamydia species and Coxiella burnetii. Single sera comprised 69% of the total, including sera from 7488 patients investigated for LRTI with paired acute and convalescent samples. A total of 167 pairs (21.6%) showed rising CF titres, 82 of them against M. pneumoniae. Of the 809 patients, 365 were children under 11 years of age: 115 (31.5%) showed rising titres, including 51 with antibodies against M. pneumoniae, 21 against RSV, 17 against adenovirus and 10 against parainfluenza type 3. Viral antigen detection by immunofluorescence and virus isolation were also used: these methods yielded more positive findings than did CF test serology for the corresponding agents. The cost of the tests performed is discussed in relation to their contribution to the aetiological diagnosis of LRTI, and changes in the service to be offered are outlined.
Thiosemicarbazones of N-alkyl-2-chloroindole-3-carboxaldehydes were synthesized and investigated for antiviral activity against RNA virus (parainfluenza type 3, HA-I/CR-8 stock) and DNA virus (vaccinia virus, HID stock). The effect of lipophilicity on the activity against vaccinia virus was considered. Relative lipophilicities were measured by a reversed phase thin-layer chromatographic technique. The most active compound N-isopropyl-2-chloroindole-3-carboxaldehyde thiosemicarbazone appeared comparable for its activity to methisazone.