scholarly journals Infected Cell Types in Ovine Lung Following Exposure to Bovine Respiratory Syncytial Virus

1994 ◽  
Vol 31 (2) ◽  
pp. 229-236 ◽  
Author(s):  
J. T. Meehan ◽  
R. C. Cutlip ◽  
H. D. Lehmkuhl ◽  
J. P. Kluge ◽  
M. R. Ackermann

Sixteen adult sheep (ten females, six males obtained from a closed flock at National Animal Disease Center, Ames, IA) were experimentally infected with bovine respiratory syncytial virus strain 375 (BRSV), and lung tissues were stained for viral antigen. Two infected sheep were euthanatized at each of the following post-inoculation times: 12, 24, 36, 48, 72, 96, 144, and 192 hours. Lung, nasal turbinates, trachea, right cranial bronchial and mediastinal lymph nodes, liver, and spleen were collected for histologic evaluation. An indirect immunoperoxidase technique was performed on routine paraffin-embedded sections of lung tissue, trachea, turbinates, and bronchial and mediastinal lymph nodes to determine the location of the BRSV antigen. For lung tissue from each sheep 400 light microscopic fields at 160x magnification were examined for staining for BRSV antigen. Lung tissue was also collected for virus and bacterial isolation. Daily serum samples were taken for determination of anti-BRSV titers. Severe respiratory disease was not produced in any sheep. Bovine respiratory syncytial virus was isolated from lung tissue collected from all sheep up through 144 hours postinoculation. At 12 hours post-inoculation (case No. 2) respiratory syncytial virus antigen was detected in bronchiolar epithelium and a mononuclear cell within an alveolar space. Lung tissue from the sheep necropsied between 24 and 144 hours postinoculattion (case Nos. 3–14) contained BRSV antigen in bronchiolar epithelium, type I pneumocytes, type II pneumocytes. alveolar macrophages, and mononuclear cells within alveolar spaces. Macrophages staining for viral antigen were rare. Bronchiolar and type I epithelial cells comprised the majority of infected cells. In a separate experiment, lung slices inoculated in vitro with either BRSV or ovine adenovirus did not stain for the respective antigens. Slices inoculated with parainfluenzavirus-3 did stain for that viral antigen.

1996 ◽  
Vol 53 (3-4) ◽  
pp. 253-260 ◽  
Author(s):  
R.S. Schrijver ◽  
F. Daus ◽  
J.A. Kramps ◽  
J.P.M. Langedijk ◽  
R. Buijs ◽  
...  

2006 ◽  
Vol 87 (8) ◽  
pp. 2145-2148 ◽  
Author(s):  
Sabine Riffault ◽  
Catherine Dubuquoy ◽  
Nathalie Castagné ◽  
Eric Baranowski ◽  
Bernard Charley ◽  
...  

Bovine respiratory syncytial virus (BRSV) is able to counteract the alpha/beta interferon (IFN-α/β)-mediated antiviral response for efficient replication in a host-specific manner. Mice models have been developed for experimental infection with human, but not bovine, respiratory syncytial virus strains. Here, it is shown that BRSV can replicate efficiently on primary cell cultures derived from type I IFN receptor-deficient, but not from wild-type IFN-competent, mice. However, BRSV infection was not enhanced in mice devoid of the type I IFN receptor. These results show that type I IFN is a major host-range determinant for infection at the cellular level, but that other factors control virus replication and pathology in vivo.


1992 ◽  
Vol 108 (1) ◽  
pp. 135-145 ◽  
Author(s):  
R. Sharma ◽  
Z. Woldehiwet

SUMMARYEnzyme-linked immunoabsorbent assay (ELISA) was used to titrate virus-specific IgG, IgM and IgA levels in nasal secretions, lung lavage fluids and serum samples sequentially obtained from lambs experimentally infected with bovine respiratory syncytial virus (RSV). Virus-specific IgG and IgM responses were measured by the indirect double antibody sandwich ELISA using anti-bovine RSV monoclonal antibody, as capture antibody, and peroxidase-conjugated anti-sheep IgG and anti-sheep IgM. Virus-specific IgA antibodies were measured by antibody capture assay using anti-sheep IgA (α–chain specific) and anti-bovine RSV monoclonal antibodies.Bovine RSV-specific IgM and IgA antibodies were detected in the serum samples within 6 days post-inoculation (p.i.). Virus-specific IgC antibodies appeared in serum samples 4 days later. In nasal secretions, IgA antibodies appeared 7 days p.i. but IgM antibodies were not detected until 12–16 days p.i. In serum samples, IgM titres were predominant for the first 2 weeks p.i. IgC titres becoming predominant thereafter. In nasal secretions and lung lavage fluids, IgA titres were significantly higher than IgM or IgG titres up to 21 days p.i. (0·01).


2007 ◽  
Vol 81 (11) ◽  
pp. 5958-5967 ◽  
Author(s):  
Riny Janssen ◽  
Jeroen Pennings ◽  
Hennie Hodemaekers ◽  
Annemarie Buisman ◽  
Marijke van Oosten ◽  
...  

ABSTRACT Respiratory syncytial virus (RSV) is a common cause of severe lower respiratory tract infection in children. Severe RSV disease is related to an inappropriate immune response to RSV resulting in enhanced lung pathology which is influenced by host genetic factors. To gain insight into the early pathways of the pathogenesis of and immune response to RSV infection, we determined the transcription profiles of lungs and lymph nodes on days 1 and 3 after infection of mice. Primary RSV infection resulted in a rapid but transient innate, proinflammatory response, as exemplified by the induction of a large number of type I interferon-regulated genes and chemokine genes, genes involved in inflammation, and genes involved in antigen processing. Interestingly, this response is much stronger on day 1 than on day 3 after infection, indicating that the strong transcriptional response in the lung precedes the peak of viral replication. Surprisingly, the set of down-regulated genes was small and none of these genes displayed strong down-regulation. Responses in the lung-draining lymph nodes were much less prominent than lung responses and are suggestive of NK cell activation. Our data indicate that at time points prior to the peak of viral replication and influx of inflammatory cells, the local lung response, measured at the transcriptional level, has already dampened down. The processes and pathways induced shortly after RSV infection can now be used for the selection of candidate genes for human genetic studies of children with severe RSV infection.


2014 ◽  
Vol 40 (03) ◽  
pp. 123-130
Author(s):  
Shyh-Shyan Liu ◽  
Hsiu-Yen Shen ◽  
Jai-Wei Lee ◽  
Show-Win Lin ◽  
Hunter Chen ◽  
...  

A dairy farm with 300 Holstein cattle in Hsin-Chu County, Taiwan, had an outbreak of a respiratory disease from the end of September to November, 2013. Adult animals (1–5-year-old) showed clinical symptoms of anorexia, depression, fever, and dropped milk production during the early stage of infection. In severe cases, animals suffered from dyspnea with frothy saliva at the edge of opened mouth. Samples were collected from eight sick animals, amplified in the baby hamster kidney cell-21 (BHK-21), and the cytopathic effect (CPE) was confirmed. Primers specific to Bovine respiratory syncytial virus (BRSV), Bovine viral diarrhea virus (BVDV), Bovine herpesvirus type I (BHV-I), Bovine ephemeral fever virus (BEFV) and Mannheimia haemolytica were used to identify the pathogen responsible for this respiratory disease by polymerase chain reaction (PCR). Results of sequence analysis confirmed that BRSV is the causative pathogen for the respiratory infection. This is, to the best of our knowledge, the first disease case of BRSV reported in Taiwan.


PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0246695
Author(s):  
Maxim Lebedev ◽  
Heather A. McEligot ◽  
Victoria N. Mutua ◽  
Paul Walsh ◽  
Francisco R. Carvallo Chaigneau ◽  
...  

Bovine Respiratory Syncytial virus (BRSV) is one of the major infectious agents in the etiology of the bovine respiratory disease complex. BRSV causes a respiratory syndrome in calves, which is associated with severe bronchiolitis. In this study we describe the effect of treatment with antiviral fusion protein inhibitor (FPI) and ibuprofen, on gene expression in lung tissue of calves infected with BRSV. Calves infected with BRSV are an excellent model of human RSV in infants: we hypothesized that FPI in combination with ibuprofen would provide the best therapeutic intervention for both species. The following experimental treatment groups of BRSV infected calves were used: 1) ibuprofen day 3–10, 2) ibuprofen day 5–10, 3) placebo, 4) FPI day 5–10, 5) FPI and ibuprofen day 5–10, 6) FPI and ibuprofen day 3–10. All calves were infected with BRSV on day 0. Daily clinical evaluation with monitoring of virus shedding by qRT-PCR was conducted. On day10 lung tissue with lesions (LL) and non-lesional (LN) was collected at necropsy, total RNA extracted, and RNA sequencing performed. Differential gene expression analysis was conducted with Gene ontology (GO) and KEGG pathway enrichment analysis. The most significant differential gene expression in BRSV infected lung tissues was observed in the comparison of LL with LN; oxidative stress and cell damage was especially noticeable. Innate and adaptive immune functions were reduced in LL. As expected, combined treatment with FPI and Ibuprofen, when started early, made the most difference in gene expression patterns in comparison with placebo, especially in pathways related to the innate and adaptive immune response in both LL and LN. Ibuprofen, when used alone, negatively affected the antiviral response and caused higher virus loads as shown by increased viral shedding. In contrast, when used with FPI Ibuprofen enhanced the specific antiviral effect of FPI, due to its ability to reduce the damaging effect of prostanoids and oxidative stress.


BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Dayle Johnston ◽  
JaeWoo Kim ◽  
Jeremy F. Taylor ◽  
Bernadette Earley ◽  
Matthew S. McCabe ◽  
...  

Abstract Background Bovine Respiratory Syncytial Virus (BRSV) is a cause of Bovine Respiratory Disease (BRD). DNA-based biomarkers contributing to BRD resistance are potentially present in non-protein-coding regulatory regions of the genome, which can be determined using ATAC-Seq. The objectives of this study were to: (i) identify regions of open chromatin in DNA extracted from bronchial lymph nodes (BLN) of healthy dairy calves experimentally challenged with BRSV and compare them with those from non-challenged healthy control calves, (ii) elucidate the chromatin regions that were differentially or uniquely open in the BRSV challenged relative to control calves, and (iii) compare the genes found in regions proximal to the differentially open regions to the genes previously found to be differentially expressed in the BLN in response to BRSV and to previously identified BRD susceptibility loci. This was achieved by challenging clinically healthy Holstein-Friesian calves (mean age 143 ± 14 days) with either BRSV inoculum (n = 12) or with sterile phosphate buffered saline (PBS) (n = 6) and preparing and sequencing ATAC-Seq libraries from fresh BLN tissues. Results Using Diffbind, 9,144 and 5,096 differentially accessible regions (P < 0.05, FDR < 0.05) were identified between BRSV challenged and control calves employing DeSeq2 and EdgeR, respectively. Additionally, 8,791 chromatin regions were found to be uniquely open in BRSV challenged calves. Seventy-six and 150 of the genes that were previously found to be differentially expressed using RNA-Seq, were located within 2 kb downstream of the differentially accessible regions, and of the regions uniquely open in BRSV challenged calves, respectively. Pathway analyses within ClusterProfiler indicated that these genes were involved in immune responses to infection and participated in the Th1 and Th2 pathways, pathogen recognition and the anti-viral response. There were 237 differentially accessible regions positioned within 40 previously identified BRD susceptibility loci. Conclusions The identified open chromatin regions are likely to be involved in the regulatory response of gene transcription induced by infection with BRSV. Consequently, they may contain variants which impact resistance to BRD that could be used in breeding programmes to select healthier, more robust cattle.


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