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1. Title Page / Table of Contents, Vol. 26, Supplement 4, 1996

Author

I. Elalamy, Sanne Valentin, J.P. Vannier, Martine Renard, Theo Lindhout, C. Soria, Harlan F. Weisman, Bengt Zöller, A.M.H.P. van.den.Besselaar, A. Pruvost, M. Trossaërt, Kalid Azzam, Michel René Boisseau, J. Paysant, Désiré Collen, Andreas Hillarp, M. Martínez, Amparo Vaya, Amparo Vayá, A. Maurel, Barry S. Coller, Ferruccio Berti, Chiara Cerletti, Keaven M. Anderson, J. Conard, Ludovic Drouet, M. Renard, Annie Pruvost, Alexander G.G. Turpie, R.R. Forastiero, A. Del Maschio, Michel Bonneau, J. Dalmau, Francis Belloc, Irene Lluch, G. van Willigen, D. Simon, Helen Ireland, J.W.N. Akkerman, Giovannni de Gaetano, Irene Salemink, M. Verstraete, N. Resnick-Roguel, Reiner Muller-Peddinghaus, Claire Bal dit Sollier, Patrick Andre, Justo Aznar, Alan T. Nurden, M. Pick, M. Vasse, C. Closse, Margareta Hellgren, James H. Chesebro, Lorenzo Gil, Björn Dahlbäck, A. Panet, David A. Lane, Sophie Gandrille, L.O. Carreras, Marcial Martínez, Marie-Claire Boffa, Norma B de Bosch, G. Kunz, Yale Nemerson, M. Korner, M.H. Horellou, Per Morten Sandset, John T. Fallon, David Bergqvist, Rafael Carmena, Patrice Dumain, D. Sela-Donenfeld, M.R. Boisseau, Roberto Marti, Pier Mannuccio Mannucci, J.P. Collet, Angelo Sala, L. Poller, E. Dejana, M. Seigneur, Valentin Fuster, A. Zanetti, Frans Van de Werf, Douglas A. Triplett, Joan E.B. Fox, Armando Tripodi, Christèle Closse, Virgilio Evangelista, Martine Aiach, F. Belloc, M.M. Samama, Rafael Apitz, J. Soria, J. Hirsh, B. Boneu, Giancarlo Folco, Jacques Maclouf, Virgilio Bosch, George M. Willems, Peter Carmeliet, Patricia Hainaud, Giuseppe Rossoni, Konstantinos Kyriakoulis, M. Labios, Steven Vanderschueren, George Pignaud, A. Eldor, JuanJose Badimon, and Martine Seigneur

Subjects
business.industry, Physiology (medical), Medicine, Library science, Table of contents, Hematology, Title page, business
Published
1996
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2. Injury models of the vascular endothelium: apoptosis and loss of thromboresistance induced by a viral protein

Author

Amiram Eldor, M. Korner, M. Pick, D. Sela-Donenfeld, A. Panet, and N. Resnick-Roguel

Subjects
Sarcoma, Avian, Viral protein, viruses, Hemangiosarcoma, Apoptosis, Biology, Vascular endothelial growth inhibitor, medicine.disease_cause, Avian sarcoma virus, Thromboxane A2, Vasculogenesis, Cytopathogenic Effect, Viral, Viral Envelope Proteins, Physiology (medical), medicine, Animals, Aorta, Cells, Cultured, Poultry Diseases, Cell Cycle, Thrombosis, Hematology, Immunity, Innate, Cell biology, Extracellular Matrix, Vascular endothelial growth factor B, Vascular endothelial growth factor A, Vascular endothelial growth factor C, Viral replication, Avian Sarcoma Viruses, Cattle, Endothelium, Vascular, Chickens
Abstract

Endothelial injury caused by viruses usually involves viral replication or transformation. We report a novel mechanism of endothelial damage by a toxic viral protein. We have isolated a new retrovirus from hemangiosarcomas which appeared among layer hens. The isolated avian hemangiosarcoma virus (AHV) is capable of inducing hemangiomas in hens in-vivo and causes a cytopathic effect (CPE) and loss of thromboresistance in cultured bovine aortic endothelial cells (BAEC). These effects do not require viral replication and can be induced by purified AHV envelope glycoprotein (gp85). AHV causes CPE in BAEC through a typical programmed cell death (apoptosis). Quiescent G0/G1-BAEC are much more sensitive to AHV induced apoptosis than actively dividing cells. These experiments demonstrate the capacity of viral proteins to affect the integrity and functionality of vascular endothelial cells.

Published
1996

3. Envelope glycoprotein of avian hemangioma retrovirus induces a thrombogenic surface on human and bovine endothelial cells

Author

Morris A. Blajchman, Moshe Kotler, Israel Vlodavsky, Haim Burstein, Amiram Eldor, E Hy-Am, N. Resnick-Roguel, and Amos Panet

Subjects
Endothelium, Platelet Aggregation, Immunology, Hemangiosarcoma, Thrombogenicity, Microbiology, Thromboplastin, Tissue factor, Retrovirus, Viral envelope, Viral Envelope Proteins, Virology, medicine, Animals, Platelet, Cells, Cultured, biology, Avian Leukosis Virus, Thrombosis, biology.organism_classification, Epoprostenol, Cell biology, Extracellular Matrix, Endothelial stem cell, Kinetics, medicine.anatomical_structure, Viral replication, Insect Science, Cattle, Endothelium, Vascular, Research Article
Abstract

Vascular endothelial cells are a target for blood-borne pathogens which may affect their integrity and thromboresistant properties. Here, we report that cultured bovine and human endothelial cells lose their thromboresistance following interaction with the avian hemangioma-inducing retrovirus. We show that the envelope (env) gene product, glycoprotein 85, is responsible for this effect, which appears soon after infection without viral replication or cell transformation. Induction of thrombogenicity is associated with a reduction in prostacyclin release and increased expression of tissue factor. These observations may explain the occurrence of thrombosis frequently observed in association with the hemangiosarcomas induced by avian hemangioma-inducing retrovirus. These unique endothelial cell-virus interactions may also be a model for the pathogenesis of various vascular diseases.

Published
1990

4. Multifocal vascular tumors in fowl induced by a newly isolated retrovirus

Author

D, Soffer, N, Resnick-Roguel, A, Eldor, and M, Kotler

Subjects
Immunoenzyme Techniques, Microscopy, Electron, Tumor Virus Infections, Retroviridae, Skin Neoplasms, Liver Neoplasms, Animals, Cell Differentiation, Female, Chick Embryo, Cells, Cultured, Poultry Diseases
Abstract

The morphological features of a spontaneous, multifocal vascular neoplasm of chickens are described. Histologically, the tumor was characterized by areas consisting of freely anastomosing vascular channels with prominent papillary appearance and lined by bland-looking endothelial cells, which alternate with areas resembling cavernous hemangioma. Occasionally solid areas composed of plump, pleomorphic cells were also present. Although there was no clear evidence for metastatic spread, some tumors were obviously invasive. Electron microscopy and immunohistochemistry confirmed the endothelial nature of neoplastic cells, demonstrating in particular pinocytic vesicles, well developed junctional complexes, fragmented basal lamina, occasional Weibel-Palade bodies, and patchy factor VIII-related antigen immunoreactivity. The overall appearance of the tumor was that of a cavernous hemangioma with prominent papillary endothelial hyperplasia. Previously we have shown that the tumor was induced by a newly isolated strain of avian hemangioma retrovirus and in this study we demonstrated typical type C retrovirus particles in the tumor by electron microscopy. It is suggested that this retrovirus-induced avian tumor may serve as a useful model for the study of transformed endothelia and other vascular tumorigenesis.

Published
1990

5. Subjects Index, Vol. 26, Supplement 4, 1996

Author

Sophie Gandrille, Amparo Vaya, I. Elalamy, J. Conard, J. Hirsh, Joan E.B. Fox, Alexander G.G. Turpie, Theo Lindhout, Justo Aznar, Patrice Dumain, Konstantinos Kyriakoulis, A. Zanetti, A. Eldor, M. Korner, Helen Ireland, Martine Seigneur, M. Martínez, Andreas Hillarp, Giancarlo Folco, Jacques Maclouf, Reiner Muller-Peddinghaus, R.R. Forastiero, D. Simon, Douglas A. Triplett, Keaven M. Anderson, A. Del Maschio, M.M. Samama, M.R. Boisseau, Pier Mannuccio Mannucci, Ludovic Drouet, M. Seigneur, D. Sela-Donenfeld, Francis Belloc, Sanne Valentin, E. Dejana, Irene Lluch, Martine Renard, G. Kunz, Irene Salemink, John T. Fallon, G. van Willigen, M. Pick, Margareta Hellgren, J.W.N. Akkerman, M. Labios, Per Morten Sandset, Amparo Vayá, David Bergqvist, Roberto Marti, Christèle Closse, Steven Vanderschueren, Patricia Hainaud, JuanJose Badimon, Giuseppe Rossoni, Bengt Zöller, Virgilio Evangelista, L. Poller, A. Pruvost, N. Resnick-Roguel, Lorenzo Gil, Giovannni de Gaetano, J. Soria, Patrick Andre, F. Belloc, Björn Dahlbäck, Rafael Carmena, J.P. Vannier, David A. Lane, L.O. Carreras, B. Boneu, George Pignaud, Rafael Apitz, Chiara Cerletti, Norma B de Bosch, Harlan F. Weisman, M.H. Horellou, Claire Bal dit Sollier, C. Soria, Michel Bonneau, Kalid Azzam, J. Dalmau, Annie Pruvost, A.M.H.P. van.den.Besselaar, M. Trossaërt, Martine Aiach, Ferruccio Berti, Armando Tripodi, J. Paysant, Alan T. Nurden, M. Vasse, C. Closse, Désiré Collen, J.P. Collet, Angelo Sala, A. Maurel, Barry S. Coller, M. Verstraete, Michel René Boisseau, Valentin Fuster, George M. Willems, Yale Nemerson, Peter Carmeliet, A. Panet, Marcial Martínez, Marie-Claire Boffa, Virgilio Bosch, Frans Van de Werf, James H. Chesebro, and M. Renard

Subjects
medicine.medical_specialty, Index (economics), business.industry, Physiology (medical), Internal medicine, medicine, Physiology, Hematology, business
Published
1996
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6. Authors Index, Vol. 26, Supplement 4, 1996

Author

M. Renard, Martine Seigneur, David Bergqvist, J. Hirsh, M.R. Boisseau, Pier Mannuccio Mannucci, M. Seigneur, Lorenzo Gil, Sanne Valentin, Amparo Vayá, Francis Belloc, Irene Lluch, L. Poller, Martine Renard, Giancarlo Folco, George M. Willems, Frans Van de Werf, Jacques Maclouf, Margareta Hellgren, James H. Chesebro, G. van Willigen, I. Elalamy, E. Dejana, Peter Carmeliet, Björn Dahlbäck, Claire Bal dit Sollier, Michel René Boisseau, Norma B de Bosch, JuanJose Badimon, Theo Lindhout, David A. Lane, Bengt Zöller, N. Resnick-Roguel, J. Paysant, L.O. Carreras, Andreas Hillarp, A. Pruvost, Désiré Collen, Patricia Hainaud, Giuseppe Rossoni, Reiner Muller-Peddinghaus, F. Belloc, Rafael Apitz, R.R. Forastiero, A.M.H.P. van.den.Besselaar, M. Trossaërt, D. Simon, M.H. Horellou, Konstantinos Kyriakoulis, John T. Fallon, Ferruccio Berti, Chiara Cerletti, Yale Nemerson, Christèle Closse, Virgilio Evangelista, Virgilio Bosch, Per Morten Sandset, Michel Bonneau, J. Dalmau, A. Panet, Annie Pruvost, Marcial Martínez, Marie-Claire Boffa, Amparo Vaya, M. Verstraete, Roberto Marti, A. Del Maschio, D. Sela-Donenfeld, Alan T. Nurden, M. Vasse, C. Closse, Giovannni de Gaetano, Patrick Andre, Justo Aznar, Douglas A. Triplett, J. Conard, Alexander G.G. Turpie, Helen Ireland, G. Kunz, J.P. Vannier, Harlan F. Weisman, Kalid Azzam, J.W.N. Akkerman, Rafael Carmena, M. Korner, C. Soria, Valentin Fuster, Martine Aiach, M. Pick, M.M. Samama, M. Martínez, J.P. Collet, Angelo Sala, A. Maurel, Barry S. Coller, J. Soria, Keaven M. Anderson, Ludovic Drouet, A. Eldor, Irene Salemink, B. Boneu, Steven Vanderschueren, Sophie Gandrille, George Pignaud, Patrice Dumain, A. Zanetti, Armando Tripodi, Joan E.B. Fox, and M. Labios

Subjects
Gerontology, Index (economics), business.industry, Physiology (medical), Medicine, Physiology, Hematology, business
Published
1996
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8. Cytocidal effect caused by the envelope glycoprotein of a newly isolated avian hemangioma-inducing retrovirus

Author

Judith Hamburger, Amiram Eldor, Moshe Kotler, Haim Burstein, Israel Vlodavsky, Amos Panet, and N. Resnick-Roguel

Subjects
animal structures, viruses, Immunology, Alpharetrovirus, Chick Embryo, Microbiology, Virus, Multiplicity of infection, Viral envelope, stomatognathic system, Cytopathogenic Effect, Viral, Viral Envelope Proteins, Virology, Animals, Cells, Cultured, Poultry Diseases, Cytopathic effect, Glycoproteins, Rous sarcoma virus, biology, Avian Leukosis Virus, urogenital system, biochemical phenomena, metabolism, and nutrition, biology.organism_classification, Molecular biology, Cell killing, Viral replication, Insect Science, Hemangioma, Research Article
Abstract

We isolated a field strain of avian hemangioma retrovirus (AHV) which induces a cytopathic effect (CPE) on cultured avian and mammalian cells shortly after infection. The kinetics of cell killing were dependent on the multiplicity of infection. The CPE on avian and mammalian cells was independent of virus replication, because UV-irradiated virus led to cell death as well. Biochemical and genetic experiments indicated that AHV env gene products were responsible for the CPE. Partially purified AHV envelope glycoproteins (gp85), but not those of the Rous sarcoma virus Prague C strain, induced a CPE. Rous-associated virus type 1, in which the env region was replaced by the AHV gp85 region, induced a CPE on avian and mammalian cultured cells. Therefore, we suggest that CPE is induced by AHV via interaction between viral gp85 and the cell membrane. This mode of CPE is unique among avian sarcoma-leukemia viruses.

Published
1989

9. Injury models of the vascular endothelium: apoptosis and loss of thromboresistance induced by a viral protein.

Author

Eldor A, Sela-Donenfeld D, Korner M, Pick M, Resnick-Roguel N, and Panet A

Subjects
Animals, Aorta cytology, Avian Sarcoma Viruses isolation & purification, Cattle, Cell Cycle, Cells, Cultured, Cytopathogenic Effect, Viral, Endothelium, Vascular pathology, Endothelium, Vascular virology, Extracellular Matrix metabolism, Hemangiosarcoma complications, Hemangiosarcoma virology, Immunity, Innate, Sarcoma, Avian complications, Thromboxane A2 biosynthesis, Apoptosis, Avian Sarcoma Viruses pathogenicity, Chickens virology, Endothelium, Vascular injuries, Hemangiosarcoma veterinary, Poultry Diseases virology, Sarcoma, Avian virology, Thrombosis etiology, Viral Envelope Proteins pharmacology
Abstract

Endothelial injury caused by viruses usually involves viral replication or transformation. We report a novel mechanism of endothelial damage by a toxic viral protein. We have isolated a new retrovirus from hemangiosarcomas which appeared among layer hens. The isolated avian hemangiosarcoma virus (AHV) is capable of inducing hemangiomas in hens in-vivo and causes a cytopathic effect (CPE) and loss of thromboresistance in cultured bovine aortic endothelial cells (BAEC). These effects do not require viral replication and can be induced by purified AHV envelop glycoprotein (gp85). AHV causes CPE in BAEC through a typical programmed cell death (apoptosis). Quiescent G0/G1-BAEC are much more sensitive to AHV induced apoptosis than actively dividing cells. These experiments demonstrate the capacity of viral proteins to affect the integrity and functionality of vascular endothelial cells.

Published
1996
Full Text
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10. Unique sequences in the env gene of avian hemangioma retrovirus are responsible for cytotoxicity and endothelial cell perturbation.

Author

Burstein H, Resnick-Roguel N, Hamburger J, Arad G, Malkinson M, and Kotler M

Subjects
Amino Acid Sequence, Animals, Base Sequence, Cats, Cattle, Cell Aggregation, Cell Survival, Cells, Cultured, Chickens, DNA, Viral genetics, DNA, Viral isolation & purification, Gene Products, env genetics, Hemangiosarcoma microbiology, Molecular Sequence Data, Plasmids, Repetitive Sequences, Nucleic Acid, Restriction Mapping, Sequence Homology, Nucleic Acid, Avian Leukosis Virus genetics, Endothelium, Vascular cytology, Genes, env
Abstract

An avian retrovirus isolated from spontaneous cavernous hemangiomas of layer hens codes for an env protein that induces a cytopathic effect on a wide variety of cultured avian and mammalian cells and also causes thrombogenicity of endothelial cells. Sequence analysis of the avian hemangioma inducing virus revealed unique elements in both its env gene and its LTR. We propose that these elements are responsible for the biological and pathogenic characteristics of the virus.

Published
1990
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11. Envelope glycoprotein of avian hemangioma retrovirus induces a thrombogenic surface on human and bovine endothelial cells.

Author

Resnick-Roguel N, Eldor A, Burstein H, Hy-Am E, Vlodavsky I, Panet A, Blajchman MA, and Kotler M

Subjects
Animals, Cattle, Cells, Cultured, Endothelium, Vascular microbiology, Endothelium, Vascular pathology, Epoprostenol biosynthesis, Extracellular Matrix physiology, Hemangiosarcoma microbiology, Hemangiosarcoma pathology, Hemangiosarcoma physiopathology, Kinetics, Platelet Aggregation, Thromboplastin biosynthesis, Thrombosis microbiology, Viral Envelope Proteins genetics, Avian Leukosis Virus genetics, Endothelium, Vascular physiology, Thrombosis pathology, Viral Envelope Proteins metabolism
Abstract

Vascular endothelial cells are a target for blood-borne pathogens which may affect their integrity and thromboresistant properties. Here, we report that cultured bovine and human endothelial cells lose their thromboresistance following interaction with the avian hemangioma-inducing retrovirus. We show that the envelope (env) gene product, glycoprotein 85, is responsible for this effect, which appears soon after infection without viral replication or cell transformation. Induction of thrombogenicity is associated with a reduction in prostacyclin release and increased expression of tissue factor. These observations may explain the occurrence of thrombosis frequently observed in association with the hemangiosarcomas induced by avian hemangioma-inducing retrovirus. These unique endothelial cell-virus interactions may also be a model for the pathogenesis of various vascular diseases.

Published
1990
Full Text
View/download PDF

12. Multifocal vascular tumors in fowl induced by a newly isolated retrovirus.

Author

Soffer D, Resnick-Roguel N, Eldor A, and Kotler M

Subjects
Animals, Cell Differentiation, Cells, Cultured, Chick Embryo, Female, Immunoenzyme Techniques, Liver Neoplasms microbiology, Liver Neoplasms pathology, Liver Neoplasms ultrastructure, Liver Neoplasms veterinary, Microscopy, Electron, Retroviridae ultrastructure, Skin Neoplasms microbiology, Skin Neoplasms pathology, Skin Neoplasms ultrastructure, Skin Neoplasms veterinary, Tumor Virus Infections pathology, Poultry Diseases, Retroviridae isolation & purification, Tumor Virus Infections veterinary
Abstract

The morphological features of a spontaneous, multifocal vascular neoplasm of chickens are described. Histologically, the tumor was characterized by areas consisting of freely anastomosing vascular channels with prominent papillary appearance and lined by bland-looking endothelial cells, which alternate with areas resembling cavernous hemangioma. Occasionally solid areas composed of plump, pleomorphic cells were also present. Although there was no clear evidence for metastatic spread, some tumors were obviously invasive. Electron microscopy and immunohistochemistry confirmed the endothelial nature of neoplastic cells, demonstrating in particular pinocytic vesicles, well developed junctional complexes, fragmented basal lamina, occasional Weibel-Palade bodies, and patchy factor VIII-related antigen immunoreactivity. The overall appearance of the tumor was that of a cavernous hemangioma with prominent papillary endothelial hyperplasia. Previously we have shown that the tumor was induced by a newly isolated strain of avian hemangioma retrovirus and in this study we demonstrated typical type C retrovirus particles in the tumor by electron microscopy. It is suggested that this retrovirus-induced avian tumor may serve as a useful model for the study of transformed endothelia and other vascular tumorigenesis.

Published
1990

13. Cytocidal effect caused by the envelope glycoprotein of a newly isolated avian hemangioma-inducing retrovirus.

Author

Resnick-Roguel N, Burstein H, Hamburger J, Panet A, Eldor A, Vlodavsky I, and Kotler M

Subjects
Animals, Avian Leukosis Virus pathogenicity, Cells, Cultured, Chick Embryo, Cytopathogenic Effect, Viral, Alpharetrovirus pathogenicity, Glycoproteins toxicity, Hemangioma veterinary, Poultry Diseases etiology, Viral Envelope Proteins toxicity
Abstract

We isolated a field strain of avian hemangioma retrovirus (AHV) which induces a cytopathic effect (CPE) on cultured avian and mammalian cells shortly after infection. The kinetics of cell killing were dependent on the multiplicity of infection. The CPE on avian and mammalian cells was independent of virus replication, because UV-irradiated virus led to cell death as well. Biochemical and genetic experiments indicated that AHV env gene products were responsible for the CPE. Partially purified AHV envelope glycoproteins (gp85), but not those of the Rous sarcoma virus Prague C strain, induced a CPE. Rous-associated virus type 1, in which the env region was replaced by the AHV gp85 region, induced a CPE on avian and mammalian cultured cells. Therefore, we suggest that CPE is induced by AHV via interaction between viral gp85 and the cell membrane. This mode of CPE is unique among avian sarcoma-leukemia viruses.

Published
1989
Full Text
View/download PDF

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