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PubMedDate not supplied

Detection of bovine viruses in fetal bovine serum used in cell culture.

This investigation employed a viral screening method detect endogenous bovine virus contaminants in commercially supplied fetal bovine serum. Fifty-one lots of fetal bovine serum from 14 suppliers were examined. Over 30% of the lots tested were found to contain bovine viruses; they included bovine virus diarrhea virus, parainfluenza type3-like virus, bovine herpesvirus-1, bovine enterovirus type 4, and an unidentified cytopathogenic agent. Of the 51 lots, 20 had been pretested by the suppliers and were considered to be free of known viral contaminants. Our viral screening methods revealed that five of these pretested lots, or 25%, contained endogenous bovine viruses.

Animals↗
PubMed1988

Sulfated polysaccharides are potent and selective inhibitors of various enveloped viruses, including herpes simplex virus, cytomegalovirus, vesicular stomatitis virus, and human immunodeficiency virus.

Several sulfated polysaccharides (dextran sulfate, pentosan polysulfate, fucoidan, and carrageenans) proved to be potent inhibitors for herpes simplex virus, human cytomegalovirus, vesicular stomatitis virus, Sindbis virus, and human immunodeficiency virus. They were moderately inhibitory to vaccinia virus but not inhibitory to adenovirus, coxsackievirus, poliovirus, parainfluenza virus, and reovirus. These results indicate that, with the exception of parainfluenza virus, enveloped viruses are specifically susceptible to the inhibitory activity of sulfated polysaccharides.

Carrageenan↗
PubMed2004

Recombinant Sendai virus expressing the G glycoprotein of respiratory syncytial virus (RSV) elicits immune protection against RSV.

Although RSV causes serious pediatric respiratory disease, an effective vaccine does not exist. To capture the strengths of a live virus vaccine, we have used the murine parainfluenza virus type 1 (Sendai virus [SV]) as a xenogeneic vector to deliver the G glycoprotein of RSV. It was previously shown (J. L. Hurwitz, K. F. Soike, M. Y. Sangster, A. Portner, R. E. Sealy, D. H. Dawson, and C. Coleclough, Vaccine 15:533-540, 1997) that intranasal SV protected African green monkeys from challenge with the related human parainfluenza virus type 1 (hPIV1), and SV has advanced to clinical trials as a vaccine for hPIV1 (K. S. Slobod, J. L. Shenep, J. Lujan-Zilbermann, K. Allison, B. Brown, R. A. Scroggs, A. Portner, C. Coleclough, and J. L. Hurwitz, Vaccine, in press). Recombinant SV expressing RSV G glycoprotein was prepared by using reverse genetics, and intranasal inoculation of cotton rats elicited RSV-specific antibody and elicited protection from RSV challenge. RSV G-recombinant SV is thus a promising live virus vaccine candidate for RSV.

Animals↗
PubMed2004

Evaluation of a quadrivalent inactivated vaccine for the protection of cattle against diseases due to common viral infections.

Efficacy of an inactivated quadrivalent vaccine containing infectious bovine rhinotracheitis (IBR) virus, parainfluenza type 3 (PI3) virus, bovine virus diarrhoea virus (BVDV) and bovine respiratory syncytial virus (BRSV) was assessed in naive bovine calves to evaluate short-term (4-18 weeks) and long-term (24-38 weeks) protection following the basic intramuscular vaccination regime of 2 inoculations a month apart. Vaccination was staggered between the long-term and the short-term groups by about 5 months so that both groups, along with a matched group of 6 unvaccinated (control) calves, could be challenged at the same time. Sequential challenges at intervals of 3-8 weeks were done in the order: IBR virus (intranasally, IN), PI3 virus (IN and intratracheally, IT), pestiviruses (IN) and BRSV (IN and IT). The IBR virus challenge produced febrile rhinotracheitis (FRT) in control calves but both the severity and the duration of FRT was significantly reduced in both vaccinated groups. The amount and the duration of IBR virus shed by the vaccinated groups was significantly reduced compared to the control group. Although PI3 virus, pooled pestivirus and BRSV challenges did not result in a noteworthy disease, challenge virus shedding (amount and duration) from the upper (all 3 viruses) and the lower (BRSV) respiratory tracts was significantly reduced in vaccinated groups. After pestivirus challenge, sera and leukocytes from all control calves were infectious for 6-9 days whereas virus was recovered only from leukocytes in vaccinated calves and only for 1.6-2.7 days. Thus a standard course of the quadrivalent vaccine afforded a significant protection against IBR virus, PI3 virus, BVDV and BRSV for at least 6 months.

Animals↗
PubMed1975

Meaning of circulating antibody titers in the infections of parainfluenza 3 virus and RS virus.

It is generally accepted that secretory antibodies play a very important role in the prevention of respiratory infections, but it is also considered that the circulating antibody level is a very significant indication of the establishment of infections. In parainfluenza 3 and RS virus infections, reinfections are very common but seem to depend more or less upon circulating antibody levels. There is a correlation between circulating antibody level and infection rate in parainfluenza 3 infection in some groups of school children in our observations of about one year. In the case of RS virus infection, observations were made in some nursery institutions and an experience in school children, in which also a circulating antibody level of some degree presents indications of infection rates.

Age Factors↗
PubMed2000

Bovine viral diarrhea viral infections in feeder calves with respiratory disease: interactions with Pasteurella spp., parainfluenza-3 virus, and bovine respiratory syncytial virus.

The prevalence of bovine viral diarrhea virus (BVDV) infections was determined in a group of stocker calves suffering from acute respiratory disease. The calves were assembled after purchase from Tennessee auctions and transported to western Texas. Of the 120 calves, 105 (87.5%) were treated for respiratory disease. Sixteen calves died during the study (13.3%). The calves received a modified live virus BHV-1 vaccine on day 0 of the study. During the study, approximately 5 wk in duration, sera from the cattle, collected at weekly intervals, were tested for BVDV by cell culture. Sera were also tested for neutralizing antibodies to BVDV types 1 and 2, bovine herpesvirus-1 (BHV-1), parainfluenza-3 virus (PI-3V), and bovine respiratory syncytial virus (BRSV). The lungs from the 16 calves that died during the study were collected and examined by histopathology, and lung homogenates were inoculated onto cell cultures for virus isolation. There were no calves persistently infected with BVDV detected in the study, as no animals were viremic on day 0, nor were any animals viremic at the 2 subsequent serum collections. There were, however, 4 animals with BVDV type 1 noncytopathic (NCP) strains in the sera from subsequent collections. Viruses were isolated from 9 lungs: 7 with PI-3V, 1 with NCP BVDV type 1, and 1 with both BVHV-1 and BVDV. The predominant bacterial species isolated from these lungs was Pasteurella haemolytica serotype 1. There was serologic evidence of infection with BVDV types 1 and 2, PI-3V, and BRSV, as noted by seroconversion (> or = 4-fold rise in antibody titer) in day 0 to day 34 samples collected from the 104 survivors: 40/104 (38.5%) to BVDV type 1; 29/104 (27.9%) to BVDV type 2; 71/104 (68.3%) to PI-3V; and 81/104 (77.9%) to BRSV. In several cases, the BVDV type 2 antibody titers may have been due to crossreacting BVDV type 1 antibodies; however, in 7 calves the BVDV type 2 antibodies were higher, indicating BVDV type 2 infection. At the outset of the study, the 120 calves were at risk (susceptible to viral infections) on day 0 because they were seronegative to the viruses: 98/120 (81.7%), < 1:4 to BVDV type 1; 104/120 (86.7%) < 1:4 to BVDV type 2; 86/120 (71.7%) < 1:4 to PI-3V; 87/120 (72.5%) < 1:4 to BRSV; and 111/120 (92.5%) < 1:10 to BHV-1. The results of this study indicate that BVDV types 1 and 2 are involved in acute respiratory disease of calves with pneumonic pasteurellosis. The BVDV may be detected by virus isolation from sera and/or lung tissues and by serology. The BVDV infections occurred in conjunction with infections by other viruses associated with respiratory disease, namely, PI-3V and BRSV. These other viruses may occur singly or in combination with each other. Also, the study indicates that purchased calves may be highly susceptible, after weaning, to infections by BHV-1, BVDV types 1 and 2, PI-3V, and BRSV early in the marketing channel.

Animals↗
PubMed1987

Pathogenesis of bronchiolitis and pneumonia induced in neonatal and weanling rats by parainfluenza (Sendai) virus.

The objective of this research was to identify potential mechanisms that might account for the greater susceptibility of neonatal rats (5 days old) as compared with weanling rats (25 days old) to viral-induced lung injury. Sites of viral replication, the sequential development of bronchiolitis and pneumonia, and systemic humoral immune responses were compared between neonatal and weanling rats from 2 to 17 days after being inoculated intranasally with parainfluenza Type 1 (Sendai) virus. In both neonatal and weanling rats, viral antigen was demonstrated by immunoperoxidase technique and viral nucleocapsids, and budding virions were demonstrated by transmission electron microscopy in bronchiolar ciliated and nonciliated epithelial cells as early as 2 days after inoculation. Similar evidence of viral replication was also demonstrated in both ages of rats in alveolar Type I and Type II epithelial cells and in macrophages. Neither virus nor viral antigens was identified in endothelial cells or interstitial cells of interalveolar septa. Bronchiolitis was induced as early as 2 days after inoculation in both ages of rats and was characterized by necrosis, erosion, and hyperplasia of epithelial cells. Multifocal to locally extensive interstitial pneumonia centered on bronchioles, was characterized by alveolar epithelial cell damage and by infiltration of neutrophils, macrophages, and lymphocytes in alveolar septa and spaces and was observed as early as 2 days after inoculation in both age groups of rats. Interstitial pneumonia of maximal severity occurred in weanling rats at 5 days after inoculation, whereas maximal pneumonia of comparable severity occurred in neonatal rats at 8 days after inoculation. Epithelial repair and resolution of bronchiolitis and pneumonia were largely complete in both ages of rats by 17 days after inoculation. Virus was recovered from lung homogenates of neonatal and weanling rats as early as 2 days after inoculation. In weanling rats, infective virus could not be recovered from lung beyond 6 days after inoculation, whereas in neonatal rats virus could be recovered from lung as late as 10 days after inoculation. Viral persistence in neonatal rats was associated with a delayed onset of serum antibody to the virus, compared with weanling rats. The results indicate that the cellular sites of viral replication and the pattern of inflammatory reactions are closely comparable between neonatal and weanling rats inoculated with Sendai virus.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed2007

Compatibility of a bivalent modified-live vaccine against Bordetella bronchiseptica and CPiV, and a trivalent modified-live vaccine against CPV, CDV and CAV-2.

Eight puppies (group 1) were vaccinated once with a bivalent modified-live vaccine against infectious tracheobronchitis by the intranasal route and at the same time with an injectable trivalent vaccine against canine parvovirus, canine distemper virus and canine adenovirus; a second group of eight puppies (group 2) was vaccinated only with the intranasal bivalent vaccine, and a further eight puppies (group 3) were vaccinated only with the injectable trivalent vaccine. Three weeks later they were all challenged with wildtype Bordetella bronchiseptica and canine parainfluenza virus by the aerosol route, and their antibody responses to the five vaccine organisms were determined. Oronasal swabs were taken regularly before and after the challenge for the isolation of bacteria and viruses, and the puppies were observed for clinical signs for three weeks after the challenge. There were no significant differences in the puppies' titres against canine parvovirus, canine distemper virus and canine adenovirus type 2 between the groups vaccinated with or without the bivalent intranasal vaccine. After the challenge the mean clinical scores of the two groups vaccinated with the intranasal vaccine were nearly 90 per cent lower (P=0.001) than the mean score of the group vaccinated with only the trivalent injectable vaccine, and the puppies in this group all became culture-positive for B bronchiseptica and canine parainfluenza virus. There were only small differences between the rates of isolation of B bronchiseptica from groups 1, 2 and 3, but significantly lower yields of canine parainfluenza virus were isolated from groups 1 and 2 than from group 3.

Adenoviridae Infections↗
PubMed1993

Parainfluenza (Sendai) virus infects ciliated cells and secretory cells but not basal cells of rat tracheal epithelium.

Sendai virus is a common respiratory pathogen in rodents. In the airways of rats infected with Sendai virus, viral antigen is present in epithelial cells, but whether all types of epithelial cells are infected is unknown. Because each type of epithelial cell has specific functions that could be affected by viral infection, we asked whether ciliated cells, secretory cells, and basal cells of the rat tracheal epithelium become infected by Sendai virus. We inoculated pathogen-free rats intranasally with Sendai virus, killed the rats 1 to 12 days after inoculation, and prepared the tracheas for double-labeling immunohistochemistry and for electron microscopy. In other studies, we maximized the infection by inoculating rats with a 100-fold higher titer of the virus, by inoculating weanling rats, or by inoculating tracheal explants with Sendai virus in vitro. We also determined whether Sendai virus can infect basal cells of tracheal explants after removal of the overlying columnar epithelial cells. Immunohistochemical studies showed that at the peak of the infection (5 days after inoculation), 30% of the surface epithelial cells stained for Sendai virus antigen, but no basal cells were stained. Electron microscopic examination confirmed the presence of viral particles in ciliated cells and secretory cells, but none were found in basal cells. No basal cells were infected under the conditions that maximized the infection. We conclude that ciliated cells and secretory cells of the rat tracheal epithelium become infected by Sendai virus, but basal cells do not become infected.

Analysis of Variance↗
PubMed1987

Efficiency of immunofluorescence for rapid detection of common respiratory viruses.

Rapid immunofluorescence (FA) methods for the detection of common respiratory viruses were compared with culture results over a 3-year period to assess the relative efficiency of FA in a clinical laboratory setting. For respiratory syncytial virus, efficiencies were high (sensitivity, 90 to 95%; specificity, 92 to 95%). The sensitivity of FA for detection of parainfluenza virus type 1, parainfluenza virus type 3, influenza A virus, and adenoviruses ranged from 28 to 63%, but specificities for these viruses were uniformly 98 to 100%. The observations form a basis for consideration of selective reduction of routine culture procedures for specimens with initial positive rapid FA results; however, the possibility of dual viral infection in some situations must also be considered.

Adenoviridae Infections↗
PubMed2006

Variants of the paramyxovirus Simian virus 5 with accelerated or delayed viral gene expression activate proinflammatory cytokine synthesis.

Our previous results have shown that the parainfluenza virus SV5 is a poor inducer of proinflammatory cytokines interleukin-8 (IL-8) and macrophage chemoattractant protein 1 (MCP-1). By contrast, an engineered P/V mutant rSV5-P/V-CPI- and a naturally-occurring variant WF-PIV (Wake Forest-Parainfluenza Virus) are both potent activators of IL-8 and MCP-1. In the present study, we addressed the question of why rSV5-WT is such a poor inducer of host cytokine responses relative to the two SV5 variants, and we used the CC chemokine RANTES as a measure of host responses. Time course experiments showed high-level secretion of IL-6 and RANTES following infections of human A549 lung epithelial cells with the P/V-CPI- mutant and WF-PIV. By contrast, SV5-WT induced very low cytokine responses, with the notable exception of moderate induction of RANTES. The mechanism of RANTES induction by the two SV5 variants shared common properties, since RANTES secretion from infected cells had similar kinetics, depended on virus replication, correlated with increased RANTES mRNA levels and promoter activation, and was reduced by inhibitors of the p38 MAPK, ERK, and PI3K pathways. Despite the similar mechanisms of RANTES induction, the two SV5 variants differed dramatically in their growth and gene expression kinetics. By comparison to the P/V mutant rSV5-P/V-CPI- which has accelerated viral gene expression, WF-PIV infection showed a prolonged delay in viral replication, and infected cells did not show high-level viral RNA and protein expression until approximately 12-24 hpi. Sequence analysis revealed that the N, P, V, and M genes from WF-PIV differed by 3, 8, 5, and 10 amino acids compared to rSV5-WT, respectively. Chimeric viruses harboring the WF-PIV P/V or M genes in the context of the other rSV5 genes had growth properties similar to rSV5-WT but had a RANTES-inducing phenotype similar to that of the bone fide WF-PIV virus. Our data indicate a role for both the P/V and the M gene products as determinants of RANTES induction in response to SV5 infection.

Animals↗
PubMed1975

The fate of protein subunits of parainfluenza (Sendai) virus after adsorption to NIL8 hamster embryo cells.

Adsorption of u.v.-inactivated Sendai virus on to NIL8 hamster cells causes fusion of the cells into polykaryocytes within 2 h. "Infected" cells were incubated at 37 degrees C for periods of 10 min to 8 h and their surface proteins iodinated with [125I] catalysed by peroxidase. Structural components of the viral envelope, such as haemagglutin-neuraminidase (HN) and probably also the fusion protein (F) were detected in the cell membrane for periods up to 4 h post infection.

Adsorption↗