Báo cáo khoa học: Selective receptor expression restricts Nipah virus infection of endothelial cells
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Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Selective receptor expression restricts Nipah virus infection of endothelial cells
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Báo cáo khoa học: " Selective receptor expression restricts Nipah virus infection of endothelial cells"Virology Journal BioMed Central Open AccessShort reportSelective receptor expression restricts Nipah virus infection ofendothelial cellsStephanie Erbar, Sandra Diederich and Andrea Maisner*Address: Institute of Virology, Philipps University of Marburg, Marburg, GermanyEmail: Stephanie Erbar - erbar@students.uni-marburg.de; Sandra Diederich - sandra.diederich@staff.uni-marburg.de;Andrea Maisner* - maisner@staff.uni-marburg.de* Corresponding authorPublished: 26 November 2008 Received: 30 October 2008 Accepted: 26 November 2008Virology Journal 2008, 5:142 doi:10.1186/1743-422X-5-142This article is available from: http://www.virologyj.com/content/5/1/142© 2008 Erbar et al; licensee BioMed Central Ltd.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0),which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Nipah virus (NiV) is a highly pathogenic paramyxovirus that causes severe diseases in animals and humans. Endothelial cell (EC) infection is an established hallmark of NiV infection in vivo. Despite systemic virus spread via the vascular system, EC in brain and lung are preferentially infected whereas EC in other organs are less affected. As in vivo, we found differences in the infection of EC in cell culture. Only brain-derived primary or immortalized EC were found to be permissive to NiV infection. Using a replication-independent fusion assay, we could show that the lack of infection in non-brain EC was due to a lack of receptor expression. The NiV entry receptors ephrinB2 (EB2) or ephrinB3 were only expressed in brain endothelia. The finding that EB2 expression in previously non-permissive aortic EC rendered the cells permissive to infection then demonstrated that EB2 is not only necessary but also sufficient to allow the establishment of a productive NiV infection. This strongly suggests that limitations in receptor expression restrict virus entry in certain EC subsets in vivo, and are thus responsible for the differences in EC tropism observed in human and animal NiV infections. affected by further tropism to non-vascular tissues (e.g.FindingsNipah virus (NiV) was identified in 1999 after an out- neurons in the brain). In humans, a widespread vasculitisbreak of fatal encephalitis among pig farmers in Malaysia is observed and NiV infection and syncytia formation is[1]. Fruit bats of the genus Pteropus were identified as nat- believed to trigger thrombosis and necrosis in theural reservoir [2]. Together with the closely related Hendra involved vessels. However, the extent of EC destructionvirus, NiV represents the genus Henipavirus within the due to NiV infection varies in different organs, and wasparamyxovirus family [3]. In contrast to most paramyxo- found to be most prominent in small vessels in the centralviruses, henipaviruses cause diseases in many mammalian nervous system (CNS), the lung and the spleen, whereasspecies including pigs, cats, horses, hamsters, guinea pigs other organs are less or not at all affected (liver) [1]. Theand humans [4-7], and are classified as biosafety level 4 capacity of EC in different organs to support virus replica-(BSL-4) pathogens. tion is thus an important determinant for the clinical out- come of NiV infection. Aim of this study was to elucidateHistopathological studies of NiV infections revealed that which cellular factor(s) determine what kind of EC can bevascular endothelial cells (EC) are the predominant target productively infected. Properties of EC from differentcells of NiV [4,5,8,9]. Clinical disease, however, was organs are known to be heterogenous ...
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Báo cáo khoa học: " Selective receptor expression restricts Nipah virus infection of endothelial cells"Virology Journal BioMed Central Open AccessShort reportSelective receptor expression restricts Nipah virus infection ofendothelial cellsStephanie Erbar, Sandra Diederich and Andrea Maisner*Address: Institute of Virology, Philipps University of Marburg, Marburg, GermanyEmail: Stephanie Erbar - erbar@students.uni-marburg.de; Sandra Diederich - sandra.diederich@staff.uni-marburg.de;Andrea Maisner* - maisner@staff.uni-marburg.de* Corresponding authorPublished: 26 November 2008 Received: 30 October 2008 Accepted: 26 November 2008Virology Journal 2008, 5:142 doi:10.1186/1743-422X-5-142This article is available from: http://www.virologyj.com/content/5/1/142© 2008 Erbar et al; licensee BioMed Central Ltd.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0),which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Nipah virus (NiV) is a highly pathogenic paramyxovirus that causes severe diseases in animals and humans. Endothelial cell (EC) infection is an established hallmark of NiV infection in vivo. Despite systemic virus spread via the vascular system, EC in brain and lung are preferentially infected whereas EC in other organs are less affected. As in vivo, we found differences in the infection of EC in cell culture. Only brain-derived primary or immortalized EC were found to be permissive to NiV infection. Using a replication-independent fusion assay, we could show that the lack of infection in non-brain EC was due to a lack of receptor expression. The NiV entry receptors ephrinB2 (EB2) or ephrinB3 were only expressed in brain endothelia. The finding that EB2 expression in previously non-permissive aortic EC rendered the cells permissive to infection then demonstrated that EB2 is not only necessary but also sufficient to allow the establishment of a productive NiV infection. This strongly suggests that limitations in receptor expression restrict virus entry in certain EC subsets in vivo, and are thus responsible for the differences in EC tropism observed in human and animal NiV infections. affected by further tropism to non-vascular tissues (e.g.FindingsNipah virus (NiV) was identified in 1999 after an out- neurons in the brain). In humans, a widespread vasculitisbreak of fatal encephalitis among pig farmers in Malaysia is observed and NiV infection and syncytia formation is[1]. Fruit bats of the genus Pteropus were identified as nat- believed to trigger thrombosis and necrosis in theural reservoir [2]. Together with the closely related Hendra involved vessels. However, the extent of EC destructionvirus, NiV represents the genus Henipavirus within the due to NiV infection varies in different organs, and wasparamyxovirus family [3]. In contrast to most paramyxo- found to be most prominent in small vessels in the centralviruses, henipaviruses cause diseases in many mammalian nervous system (CNS), the lung and the spleen, whereasspecies including pigs, cats, horses, hamsters, guinea pigs other organs are less or not at all affected (liver) [1]. Theand humans [4-7], and are classified as biosafety level 4 capacity of EC in different organs to support virus replica-(BSL-4) pathogens. tion is thus an important determinant for the clinical out- come of NiV infection. Aim of this study was to elucidateHistopathological studies of NiV infections revealed that which cellular factor(s) determine what kind of EC can bevascular endothelial cells (EC) are the predominant target productively infected. Properties of EC from differentcells of NiV [4,5,8,9]. Clinical disease, however, was organs are known to be heterogenous ...
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