Human cytomegalovirus infection and atherothrombosis
Vascular endothelium, as a key regulator of hemostasis, mediates vascular dilatation, prevents platelet adhesion, and inhibits thrombin generation. Endothelial dysfunction caused by acute or chronic inflammation, such as in atherosclerosis, creates a proinflammatory environment which supports leukoc...
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description | Vascular endothelium, as a key regulator of hemostasis, mediates vascular dilatation, prevents platelet adhesion, and inhibits thrombin generation. Endothelial dysfunction caused by acute or chronic inflammation, such as in atherosclerosis, creates a proinflammatory environment which supports leukocyte transmigration toward inflammatory sites, and at the same time promotes coagulation, thrombin generation, and fibrin deposition in an attempt to close the wound. Life-long persistent infection with human cytomegalovirus (HCMV) has been associated with atherosclerosis. In vivo studies have revealed that HCMV infection of the vessel wall affects various cells including monocytes/macrophages, smooth muscle cells (SMCs) and endothelial cells (ECs). HCMV-infected SMCs within vascular lesions display enhanced proliferation and impaired apoptosis, which contribute to
intima
-
media
thickening, plaque formation and restenosis. Monocytes play a central role in the process of viral dissemination, whereas ECs may represent a viral reservoir, maintaining persistent infection in HCMV-infected atherosclerotic patients following the primary infection. Persistent infection leads to dysfunction of ECs and activates proinflammatory signaling involving nuclear factor κB, specificity protein 1, and phosphatidylinositol 3-kinase, as well as expression of platelet-derived growth factor receptor. Activation of these pathways promotes enhanced proliferation and migration of monocytes and SMCs into the
intima
of the vascular wall as well as lipid accumulation and expansion of the atherosclerotic lesion. Moreover, HCMV infection induces enhanced expression of endothelial adhesion molecules and modifies the proteolytic balance in monocytes and macrophages. As a consequence, infected endothelium recruits naive monocytes from the blood stream, and the concomitant interaction between infected ECs and monocytes enables virus transfer to migrating monocytes. Endothelial damage promotes thrombin generation linking inflammation and coagulation. HCMV, in turn, enhances the thrombin generation. The virus carries on its surface the molecular machinery necessary to initiate thrombin generation, and in addition, may interact with the prothrombinase protein complex thereby facilitating thrombin generation. Thus, infection of endothelium may significantly increase the production of thrombin. This might not only contribute to thrombosis in patients with atherosclerosis, but might also induce thrombi |
doi_str_mv | 10.1007/s11239-011-0662-x |
format | Article |
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intima
-
media
thickening, plaque formation and restenosis. Monocytes play a central role in the process of viral dissemination, whereas ECs may represent a viral reservoir, maintaining persistent infection in HCMV-infected atherosclerotic patients following the primary infection. Persistent infection leads to dysfunction of ECs and activates proinflammatory signaling involving nuclear factor κB, specificity protein 1, and phosphatidylinositol 3-kinase, as well as expression of platelet-derived growth factor receptor. Activation of these pathways promotes enhanced proliferation and migration of monocytes and SMCs into the
intima
of the vascular wall as well as lipid accumulation and expansion of the atherosclerotic lesion. Moreover, HCMV infection induces enhanced expression of endothelial adhesion molecules and modifies the proteolytic balance in monocytes and macrophages. As a consequence, infected endothelium recruits naive monocytes from the blood stream, and the concomitant interaction between infected ECs and monocytes enables virus transfer to migrating monocytes. Endothelial damage promotes thrombin generation linking inflammation and coagulation. HCMV, in turn, enhances the thrombin generation. The virus carries on its surface the molecular machinery necessary to initiate thrombin generation, and in addition, may interact with the prothrombinase protein complex thereby facilitating thrombin generation. Thus, infection of endothelium may significantly increase the production of thrombin. This might not only contribute to thrombosis in patients with atherosclerosis, but might also induce thrombin-dependent proinflammatory cell activation. This review summarizes the existing evidence on the role of HCMV in vascular inflammation.</description><identifier>ISSN: 0929-5305</identifier><identifier>EISSN: 1573-742X</identifier><identifier>DOI: 10.1007/s11239-011-0662-x</identifier><identifier>PMID: 22161772</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>1-Phosphatidylinositol 3-kinase ; Apoptosis ; Arteriosclerosis ; Atherosclerosis - immunology ; Atherosclerosis - pathology ; Blood ; Cardiology ; Cell activation ; Cell migration ; Coagulation ; Coagulation factor Xa ; Cytomegalovirus - immunology ; Cytomegalovirus Infections - immunology ; Cytomegalovirus Infections - pathology ; Endothelial cells ; Endothelium ; Endothelium, Vascular - immunology ; Endothelium, Vascular - pathology ; fibrin ; Hematology ; hemostasis ; Human cytomegalovirus ; Humans ; Inflammation ; Leukocyte migration ; Lipids ; Macrophages ; Medicine ; Medicine & Public Health ; Monocytes ; Persistent infection ; Plaques ; Platelet-derived growth factor receptors ; Platelets ; Proteolysis ; restenosis ; Reviews ; Signal transduction ; Smooth muscle ; Thrombin ; thrombolysis ; Thrombosis ; Thrombosis - immunology ; Thrombosis - pathology ; Wounds</subject><ispartof>Journal of thrombosis and thrombolysis, 2012-02, Vol.33 (2), p.160-172</ispartof><rights>Springer Science+Business Media, LLC 2011</rights><rights>Springer Science+Business Media, LLC 2012</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c402t-81a12300574581649324813e8b6f1908806249a55eab26ec49e3f05715e3d9dc3</citedby><cites>FETCH-LOGICAL-c402t-81a12300574581649324813e8b6f1908806249a55eab26ec49e3f05715e3d9dc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11239-011-0662-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11239-011-0662-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22161772$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Popović, Milan</creatorcontrib><creatorcontrib>Smiljanić, Katarina</creatorcontrib><creatorcontrib>Dobutović, Branislava</creatorcontrib><creatorcontrib>Syrovets, Tatiana</creatorcontrib><creatorcontrib>Simmet, Thomas</creatorcontrib><creatorcontrib>Isenović, Esma R.</creatorcontrib><title>Human cytomegalovirus infection and atherothrombosis</title><title>Journal of thrombosis and thrombolysis</title><addtitle>J Thromb Thrombolysis</addtitle><addtitle>J Thromb Thrombolysis</addtitle><description>Vascular endothelium, as a key regulator of hemostasis, mediates vascular dilatation, prevents platelet adhesion, and inhibits thrombin generation. Endothelial dysfunction caused by acute or chronic inflammation, such as in atherosclerosis, creates a proinflammatory environment which supports leukocyte transmigration toward inflammatory sites, and at the same time promotes coagulation, thrombin generation, and fibrin deposition in an attempt to close the wound. Life-long persistent infection with human cytomegalovirus (HCMV) has been associated with atherosclerosis. In vivo studies have revealed that HCMV infection of the vessel wall affects various cells including monocytes/macrophages, smooth muscle cells (SMCs) and endothelial cells (ECs). HCMV-infected SMCs within vascular lesions display enhanced proliferation and impaired apoptosis, which contribute to
intima
-
media
thickening, plaque formation and restenosis. Monocytes play a central role in the process of viral dissemination, whereas ECs may represent a viral reservoir, maintaining persistent infection in HCMV-infected atherosclerotic patients following the primary infection. Persistent infection leads to dysfunction of ECs and activates proinflammatory signaling involving nuclear factor κB, specificity protein 1, and phosphatidylinositol 3-kinase, as well as expression of platelet-derived growth factor receptor. Activation of these pathways promotes enhanced proliferation and migration of monocytes and SMCs into the
intima
of the vascular wall as well as lipid accumulation and expansion of the atherosclerotic lesion. Moreover, HCMV infection induces enhanced expression of endothelial adhesion molecules and modifies the proteolytic balance in monocytes and macrophages. As a consequence, infected endothelium recruits naive monocytes from the blood stream, and the concomitant interaction between infected ECs and monocytes enables virus transfer to migrating monocytes. Endothelial damage promotes thrombin generation linking inflammation and coagulation. HCMV, in turn, enhances the thrombin generation. The virus carries on its surface the molecular machinery necessary to initiate thrombin generation, and in addition, may interact with the prothrombinase protein complex thereby facilitating thrombin generation. Thus, infection of endothelium may significantly increase the production of thrombin. This might not only contribute to thrombosis in patients with atherosclerosis, but might also induce thrombin-dependent proinflammatory cell activation. This review summarizes the existing evidence on the role of HCMV in vascular inflammation.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Apoptosis</subject><subject>Arteriosclerosis</subject><subject>Atherosclerosis - immunology</subject><subject>Atherosclerosis - pathology</subject><subject>Blood</subject><subject>Cardiology</subject><subject>Cell activation</subject><subject>Cell migration</subject><subject>Coagulation</subject><subject>Coagulation factor Xa</subject><subject>Cytomegalovirus - immunology</subject><subject>Cytomegalovirus Infections - immunology</subject><subject>Cytomegalovirus Infections - pathology</subject><subject>Endothelial cells</subject><subject>Endothelium</subject><subject>Endothelium, Vascular - immunology</subject><subject>Endothelium, Vascular - pathology</subject><subject>fibrin</subject><subject>Hematology</subject><subject>hemostasis</subject><subject>Human cytomegalovirus</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Leukocyte migration</subject><subject>Lipids</subject><subject>Macrophages</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Monocytes</subject><subject>Persistent infection</subject><subject>Plaques</subject><subject>Platelet-derived growth factor receptors</subject><subject>Platelets</subject><subject>Proteolysis</subject><subject>restenosis</subject><subject>Reviews</subject><subject>Signal transduction</subject><subject>Smooth muscle</subject><subject>Thrombin</subject><subject>thrombolysis</subject><subject>Thrombosis</subject><subject>Thrombosis - immunology</subject><subject>Thrombosis - pathology</subject><subject>Wounds</subject><issn>0929-5305</issn><issn>1573-742X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkE1Lw0AQhhdRbK3-AC9SvHiKzuxXskcRtULBi4K3ZZts2pQkW3cTaf-9W1oVBPE0h3nmnZmHkHOEawRIbwIiZSoBxASkpMn6gAxRpCxJOX07JENQVCWCgRiQkxCWAKAU0GMyoBQlpikdEj7pG9OO803nGjs3tfuofB_GVVvavKtcOzZtMTbdwnrXLbxrZi5U4ZQclaYO9mxfR-T14f7lbpJMnx-f7m6nSc6BdkmGJt4HIFIuMpRcMcozZDabyRIVZBlIypURwpoZlTbnyrIy0igsK1SRsxG52uWuvHvvbeh0U4Xc1rVpreuDVoJLAUzK_0lU2_0cI3n5i1y63rfxjQhliqVUqgjhDsq9C8HbUq981Ri_0Qh6q17v1OuoXm_V63WcudgH97PGFt8TX64jQHdAiK12bv3P5r9TPwFg0Yyu</recordid><startdate>20120201</startdate><enddate>20120201</enddate><creator>Popović, Milan</creator><creator>Smiljanić, Katarina</creator><creator>Dobutović, Branislava</creator><creator>Syrovets, Tatiana</creator><creator>Simmet, Thomas</creator><creator>Isenović, Esma R.</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7U9</scope><scope>H94</scope></search><sort><creationdate>20120201</creationdate><title>Human cytomegalovirus infection and atherothrombosis</title><author>Popović, Milan ; Smiljanić, Katarina ; Dobutović, Branislava ; Syrovets, Tatiana ; Simmet, Thomas ; Isenović, Esma R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c402t-81a12300574581649324813e8b6f1908806249a55eab26ec49e3f05715e3d9dc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>Apoptosis</topic><topic>Arteriosclerosis</topic><topic>Atherosclerosis - immunology</topic><topic>Atherosclerosis - pathology</topic><topic>Blood</topic><topic>Cardiology</topic><topic>Cell activation</topic><topic>Cell migration</topic><topic>Coagulation</topic><topic>Coagulation factor Xa</topic><topic>Cytomegalovirus - immunology</topic><topic>Cytomegalovirus Infections - immunology</topic><topic>Cytomegalovirus Infections - pathology</topic><topic>Endothelial cells</topic><topic>Endothelium</topic><topic>Endothelium, Vascular - immunology</topic><topic>Endothelium, Vascular - pathology</topic><topic>fibrin</topic><topic>Hematology</topic><topic>hemostasis</topic><topic>Human cytomegalovirus</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Leukocyte migration</topic><topic>Lipids</topic><topic>Macrophages</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Monocytes</topic><topic>Persistent infection</topic><topic>Plaques</topic><topic>Platelet-derived growth factor receptors</topic><topic>Platelets</topic><topic>Proteolysis</topic><topic>restenosis</topic><topic>Reviews</topic><topic>Signal transduction</topic><topic>Smooth muscle</topic><topic>Thrombin</topic><topic>thrombolysis</topic><topic>Thrombosis</topic><topic>Thrombosis - immunology</topic><topic>Thrombosis - pathology</topic><topic>Wounds</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Popović, Milan</creatorcontrib><creatorcontrib>Smiljanić, Katarina</creatorcontrib><creatorcontrib>Dobutović, Branislava</creatorcontrib><creatorcontrib>Syrovets, Tatiana</creatorcontrib><creatorcontrib>Simmet, Thomas</creatorcontrib><creatorcontrib>Isenović, Esma R.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Journal of thrombosis and thrombolysis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Popović, Milan</au><au>Smiljanić, Katarina</au><au>Dobutović, Branislava</au><au>Syrovets, Tatiana</au><au>Simmet, Thomas</au><au>Isenović, Esma R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Human cytomegalovirus infection and atherothrombosis</atitle><jtitle>Journal of thrombosis and thrombolysis</jtitle><stitle>J Thromb Thrombolysis</stitle><addtitle>J Thromb Thrombolysis</addtitle><date>2012-02-01</date><risdate>2012</risdate><volume>33</volume><issue>2</issue><spage>160</spage><epage>172</epage><pages>160-172</pages><issn>0929-5305</issn><eissn>1573-742X</eissn><abstract>Vascular endothelium, as a key regulator of hemostasis, mediates vascular dilatation, prevents platelet adhesion, and inhibits thrombin generation. Endothelial dysfunction caused by acute or chronic inflammation, such as in atherosclerosis, creates a proinflammatory environment which supports leukocyte transmigration toward inflammatory sites, and at the same time promotes coagulation, thrombin generation, and fibrin deposition in an attempt to close the wound. Life-long persistent infection with human cytomegalovirus (HCMV) has been associated with atherosclerosis. In vivo studies have revealed that HCMV infection of the vessel wall affects various cells including monocytes/macrophages, smooth muscle cells (SMCs) and endothelial cells (ECs). HCMV-infected SMCs within vascular lesions display enhanced proliferation and impaired apoptosis, which contribute to
intima
-
media
thickening, plaque formation and restenosis. Monocytes play a central role in the process of viral dissemination, whereas ECs may represent a viral reservoir, maintaining persistent infection in HCMV-infected atherosclerotic patients following the primary infection. Persistent infection leads to dysfunction of ECs and activates proinflammatory signaling involving nuclear factor κB, specificity protein 1, and phosphatidylinositol 3-kinase, as well as expression of platelet-derived growth factor receptor. Activation of these pathways promotes enhanced proliferation and migration of monocytes and SMCs into the
intima
of the vascular wall as well as lipid accumulation and expansion of the atherosclerotic lesion. Moreover, HCMV infection induces enhanced expression of endothelial adhesion molecules and modifies the proteolytic balance in monocytes and macrophages. As a consequence, infected endothelium recruits naive monocytes from the blood stream, and the concomitant interaction between infected ECs and monocytes enables virus transfer to migrating monocytes. Endothelial damage promotes thrombin generation linking inflammation and coagulation. HCMV, in turn, enhances the thrombin generation. The virus carries on its surface the molecular machinery necessary to initiate thrombin generation, and in addition, may interact with the prothrombinase protein complex thereby facilitating thrombin generation. Thus, infection of endothelium may significantly increase the production of thrombin. This might not only contribute to thrombosis in patients with atherosclerosis, but might also induce thrombin-dependent proinflammatory cell activation. This review summarizes the existing evidence on the role of HCMV in vascular inflammation.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>22161772</pmid><doi>10.1007/s11239-011-0662-x</doi><tpages>13</tpages></addata></record> |
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subjects | 1-Phosphatidylinositol 3-kinase Apoptosis Arteriosclerosis Atherosclerosis - immunology Atherosclerosis - pathology Blood Cardiology Cell activation Cell migration Coagulation Coagulation factor Xa Cytomegalovirus - immunology Cytomegalovirus Infections - immunology Cytomegalovirus Infections - pathology Endothelial cells Endothelium Endothelium, Vascular - immunology Endothelium, Vascular - pathology fibrin Hematology hemostasis Human cytomegalovirus Humans Inflammation Leukocyte migration Lipids Macrophages Medicine Medicine & Public Health Monocytes Persistent infection Plaques Platelet-derived growth factor receptors Platelets Proteolysis restenosis Reviews Signal transduction Smooth muscle Thrombin thrombolysis Thrombosis Thrombosis - immunology Thrombosis - pathology Wounds |
title | Human cytomegalovirus infection and atherothrombosis |
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