A survey of jaagsiekte sheep retrovirus (JSRV) infection in sheep in the three northeastern provinces of China

2021 ◽  
Vol 166 (3) ◽  
pp. 831-840
Author(s):  
Wen Shi ◽  
Shuo Jia ◽  
Xueting Guan ◽  
Xin Yao ◽  
Ronghui Pan ◽  
...  
Keyword(s):  
Jaagsiekte Sheep Retrovirus

scholarly journals Retrovirus Vectors Bearing Jaagsiekte Sheep Retrovirus Env Transduce Human Cells by Using a New Receptor Localized to Chromosome 3p21.3

2000 ◽  
Vol 74 (10) ◽  
pp. 4698-4704 ◽  
Author(s):  
Sharath K. Rai ◽  
James C. DeMartini ◽  
A. Dusty Miller
Keyword(s):  
Host Range ◽  
Chemokine Receptors ◽  
Lung Tumor ◽  
High Titer ◽  
Leukemia Virus ◽  
Human Infection ◽  
Human Cells ◽  
Careful Examination ◽  
Chromosome 3 ◽  
Jaagsiekte Sheep Retrovirus

ABSTRACT Jaagsiekte sheep retrovirus (JSRV) is a type D retrovirus associated with a contagious lung tumor of sheep, ovine pulmonary carcinoma. Other than sheep, JSRV is known to infect goats, but there is no evidence of human infection. Until now it has not been possible to study the host range for JSRV because of the inability to grow this virus in culture. Here we show that the JSRV envelope protein (Env) can be used to pseudotype Moloney murine leukemia virus (MoMLV)-based retrovirus vectors and that such vectors can transduce human cells in culture. We constructed hybrid retrovirus packaging cells that express the JSRV Env and the MoMLV Gag-Pol proteins and can produce JSRV-pseudotype vectors at titers of up to 106 alkaline phosphatase-positive focus-forming units/ml. Using this high-titer virus, we have studied the host range for JSRV, which includes sheep, human, monkey, bovine, dog, and rabbit cells but not mouse, rat, or hamster cells. Considering the inability of the JSRV-pseudotype vector to transduce hamster cells, we used the hamster cell line-based Stanford G3 panel of whole human genome radiation hybrids to phenotypically map the JSRV receptor (JVR) gene within the p21.3 region of human chromosome 3. JVR is likely a new retrovirus receptor, as none of the previously identified retrovirus receptors localizes to the same position. Several chemokine receptors that have been shown to serve as coreceptors for lentivirus infection are clustered in the same region of chromosome 3; however, careful examination shows that the JSRV receptor does not colocalize with any of these genes.

scholarly journals In Vivo and In Vitro Analysis of Factor Binding Sites in Jaagsiekte Sheep Retrovirus Long Terminal Repeat Enhancer Sequences: Roles of HNF-3, NF-I, and C/EBP for Activity in Lung Epithelial Cells

2006 ◽  
Vol 80 (1) ◽  
pp. 332-341 ◽  
Author(s):  
Kathleen McGee-Estrada ◽  
Hung Fan
Keyword(s):  
Epithelial Cells ◽  
Long Terminal Repeat ◽  
Binding Site ◽  
Terminal Repeat ◽  
Lung Epithelial Cells ◽  
Type Ii ◽  
Jaagsiekte Sheep Retrovirus ◽  
Efficient System ◽  
Lung Epithelial

ABSTRACT Jaagsiekte sheep retrovirus (JSRV) is the causative agent of ovine pulmonary adenocarcinoma, a contagious lung cancer of sheep that arises from type II pneumocytes and Clara cells of the lung epithelium. Studies of the tropism of this virus have been hindered by the lack of an efficient system for viral replication in tissue culture. To map regulatory regions important for transcriptional activation, an in vivo footprinting method that couples dimethyl sulfate treatment and ligation-mediated PCR was performed in murine type II pneumocyte-derived MLE-15 cells infected with a chimeric Moloney murine leukemia virus driven by the JSRV enhancers (ΔMo+JS Mo-MuLV). In vivo footprints were found in the JSRV enhancers in two regions previously shown to be important for JSRV long terminal repeat (LTR) activity: a binding site for the lung-specific transcription factor HNF-3β and an E-box element in the distal enhancer adjacent to an NF-κB-like binding site. In addition, in vivo footprints were detected in two downstream motifs likely to bind C/EBP and NF-I. Mutational analysis of a JSRV LTR reporter construct (pJS21luc) revealed that the C/EBP binding site is critical for LTR activity, while the putative NF-I binding element is less important; elimination of these sites resulted in 70% and 40% drops in LTR activity, respectively. Electrophoretic mobility shift assays using nuclear extracts from MLE-15 murine Clara cell-derived mtCC1-2 cells with probes corresponding to the NF-I or C/EBP sites revealed several complexes. Antiserum directed against NF-IA, C/EBPα, or C/EBPβ supershifted the corresponding protein-DNA complexes, indicating that these isoforms, which are also important for the expression of several cellular lung-specific genes, may be important for JSRV expression in lung epithelial cells.

scholarly journals Jaagsiekte Sheep Retrovirus Biology and Oncogenesis

Viruses ◽  
2010 ◽  
Vol 2 (12) ◽  
pp. 2618-2648 ◽  
Author(s):  
Andrew Hofacre ◽  
Hung Fan
Keyword(s):  
Jaagsiekte Sheep Retrovirus

scholarly journals Detection of Jaagsiekte sheep retrovirus in apparently healthy sheep by real-time TaqMan PCR in comparison with histopathological findings

2016 ◽  
Vol 60 (1) ◽  
pp. 7-12 ◽  
Author(s):  
Aliasghar Bahari ◽  
Masoud Sabouri Ghannad ◽  
Omid Dezfoulian ◽  
Fereydon Rezazadeh ◽  
Ali Sadeghi-Nasab
Keyword(s):  
Real Time ◽  
Real Time Pcr ◽  
Mediastinal Lymph Node ◽  
Pulmonary Adenocarcinoma ◽  
Ovine Pulmonary Adenocarcinoma ◽  
Jaagsiekte Sheep Retrovirus ◽  
Tissue Samples ◽  
Blood Samples ◽  
Proviral Dna ◽  
Healthy Sheep

Abstract Introduction: The aim of this study was to use TaqMan real-time PCR technique to investigate Jaagsiekte sheep retrovirus (JSRV) proviral DNA in whole blood samples of sheep, and compare the results to those of histopathological examinations. Material and Methods: Eighty blood samples from clinically healthy sheep were randomly collected before the animals were slaughtered. Ten tissue samples from each lung and associated caudal mediastinal lymph node were taken. Results: Fifteen (18.75%) blood samples were found to contain proviral DNA, and 11 (13.75%) corresponding lung samples showed microscopic changes consistent with ovine pulmonary adenocarcinoma. None of the samples displayed metastases to the caudal mediastinal lymph nodes. The prominent pattern of neoplastic nodules consisted of acinar (alveolar) form. Conclusion: The results indicated the higher sensitivity of real-time PCR compared to histopathological examinations in detection of ovine pulmonary adenocarcinoma.

scholarly journals Expression and Characterization of a Soluble, Active Form of the Jaagsiekte Sheep Retrovirus Receptor, Hyal2

2005 ◽  
Vol 79 (1) ◽  
pp. 79-86 ◽  
Author(s):  
Vladimir Vigdorovich ◽  
Roland K. Strong ◽  
A. Dusty Miller
Keyword(s):  
Cell Surface ◽  
Expression System ◽  
Specific Interaction ◽  
Active Form ◽  
Soluble Form ◽  
Viral Inhibition ◽  
Virus Envelope ◽  
Critical Function ◽  
Jaagsiekte Sheep Retrovirus ◽  
Hyaluronidase Activity

ABSTRACT Retrovirus entry into cells is mediated by specific interactions between virus envelope glycoproteins and cell surface receptors. Many of these receptors contain multiple membrane-spanning regions, making their purification and study difficult. The jaagsiekte sheep retrovirus (JSRV) receptor, hyaluronidase 2 (Hyal2), is a glycosylphosphatidylinositol (GPI)-anchored molecule containing no peptide transmembrane regions, making it an attractive candidate for study of retrovirus entry. Further, the hyaluronidase activity reported for human Hyal2, combined with its broad expression pattern, may point to a critical function of Hyal2 in the turnover of hyaluronan, a major extracellular matrix component. Here we describe the properties of a soluble form of human Hyal2 (sHyal2) purified from a baculoviral expression system. sHyal2 is a 54-kDa monomer with weak hyaluronidase activity compared to that of the known hyaluronidase Spam1. In contrast to a previous report indicating that Hyal2 cleaved hyaluronan to a limit product of 20 kDa and was active only at acidic pH, we find that sHyal2 is capable of further degradation of hyaluronan and is active over a broad pH range, consistent with Hyal2 being active at the cell surface where it is normally localized. Interaction of sHyal2 with the JSRV envelope glycoprotein was analyzed by viral inhibition assays, showing >90% inhibition of transduction at 28 nM sHyal2, and by surface plasmon resonance, revealing a remarkably tight specific interaction with a dissociation constant (KD ) of 32 ± 1 pM. In contrast to results obtained with avian retroviruses, purified receptor was not capable of promoting transduction of cells that do not express the virus receptor.

Jaagsiekte Sheep Retrovirus (JSRV)

2020 ◽  
Author(s):  
James M. Sharp ◽  
Marcelo De las Heras ◽  
Massimo Palmarini ◽  
Thomas E. Spencer
Keyword(s):  
Jaagsiekte Sheep Retrovirus

scholarly journals Jaagsiekte Sheep Retrovirus Env Protein Stabilizes Retrovirus Vectors against Inactivation by Lung Surfactant, Centrifugation, and Freeze-Thaw Cycling

2001 ◽  
Vol 75 (18) ◽  
pp. 8864-8867 ◽  
Author(s):  
David A. Coil ◽  
John H. Strickler ◽  
Sharath K. Rai ◽  
A. Dusty Miller
Keyword(s):  
Gene Therapy ◽  
Lung Surfactant ◽  
Jaagsiekte Sheep Retrovirus ◽  
Freeze Thaw ◽  
Lung Fluid ◽  
Retrovirus Vector ◽  
Improved Stability ◽  
Env Protein ◽  
Virus Adaptation ◽  
Apparent Resistance

ABSTRACT Jaagsiekte sheep retrovirus (JSRV) replicates in the lungs of sheep and causes the secretion of copious lung fluid containing the virus. Adaptation of JSRV to infection and replication in the lung and its apparent resistance to the denaturing activity of lung fluid suggest that vectors based on JSRV would be useful for gene therapy targeted to the lung. We show here that a retrovirus vector bearing the JSRV Env is stable during treatment with lung surfactant while an otherwise identical vector bearing an amphotropic Env is inactivated. Furthermore, the JSRV vector was stable during centrifugation, allowing facile vector concentration, and showed no loss of activity after six freeze-thaw cycles. However, the JSRV vector was inactivated by standard disinfectants, indicating that JSRV vectors pose no unusual safety risk related to their improved stability under other conditions.

scholarly journals Jaagsiekte Sheep Retrovirus Transformation in Madin-Darby Canine Kidney Epithelial Cell Three-Dimensional Culture

2010 ◽  
Vol 84 (10) ◽  
pp. 5379-5390 ◽  
Author(s):  
Chassidy Johnson ◽  
Kiah Sanders ◽  
Hung Fan
Keyword(s):  
Epithelial Cell ◽  
Mdck Cells ◽  
Mapk Pathway ◽  
Three Dimensional ◽  
Bronchioloalveolar Carcinoma ◽  
Envelope Gene ◽  
Madin Darby Canine Kidney ◽  
Jaagsiekte Sheep Retrovirus ◽  
Darby Canine Kidney ◽  
Canine Kidney

ABSTRACT Jaagsiekte sheep retrovirus (JSRV) is the causative agent of a contagious lung cancer in sheep that shares similarities with human bronchioloalveolar carcinoma (BAC). JSRV is unique because the envelope gene (env) is the oncogene, as it can transform cells in culture and induce tumors in animals. The phosphatidylinositol 3-kinase (PI3K)-Akt-mTOR and H/N-Ras-MEK-mitogen-activated protein kinase (MAPK) pathways have been shown to be critical for Env transformation. However, the question still remains of how disruption of these pathways relates to tumor formation. To address this, JSRV Env transformation was studied in the context of epithelial structure, using the polarized Madin-Darby canine kidney (MDCK) epithelial cell three-dimensional (3-D) culture system. The results indicated that JSRV Env-transformed MDCK cells were larger and had full or multiple lumens, in contrast to the single lumens observed in controls. The altered phenotype was largely mediated by an increase in proliferation, in addition to overcoming the proliferative suppression signal. JSRV Env was not found to disrupt polarity or tight junctions or to inhibit lumen apoptosis. The PI3K-Akt-mTOR pathway was important for Env transformation in MDCK cells, although the mechanisms of action differed in 3-D and monolayer cultures. PI3K-dependent signaling to mTOR occurred in monolayers, while PI3K-independent signaling to mTOR occurred in 3-D culture. In contrast, the H/N-Ras-MEK-MAPK pathway was found to be inhibitory to transformation in both normal and transformed MDCK cells in 3-D culture. However, in monolayer culture, inhibition of MEK reverted the transformed phenotype, suggesting a different mechanism(s) of action in monolayer versus 3-D culture.

Sign in / Sign up

Export Citation Format

Share Document