{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/87647"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/87647","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Pseudorabies Virus Infection of Porcine Peripheral Blood Leukocytes","abstract":"Pseudorabies virus (PRV) is an alphaherpesvirus of swine that causes significant morbidity in adult populations, morbidity and mortality in young pigs, and economic losses to the swine industry each year. Evidence suggests that PRV causes immunosuppression in infected swine with resultant risk of secondary viral and bacterial infections. Virus was recovered from peripheral blood leukocytes (PBL) collected from infected swine, as well as from immune cells isolated from various lymphoid tissues (e.g., lymph node, tonsil, thymus). Lymphocytes stimulated with T cell mitogens, but not B cell mitogens, were permissive to PRV infection in vitro, as evidenced by the expression of PRV antigens on the surface of these cells and by the production of low titers of infectious PRV. Monocytes were highly permissive to PRV infection in vitro, and 75% of monocytes in culture expressed viral antigens on the cell surface. T lymphoblasts are also permissive, and several important functional phenotypes expressed PRV surface antigens after infection. Twenty percent of CD2-bearing lymphoblasts (total T cells) expressed viral antigens on the cell surface after infection, including 15% of CD4-bearing lymphoblasts (helper T cells) and 13% of CD8-bearing lymphoblasts (cytotoxic T cells and natural killer cells). Up to 90% of cells in culture of an immortal lymphoblastoid cell line expressed viral antigens on the cell surface after infection. Both purified CD4-bearing lymphoblasts and purified CD8-bearing lymphoblasts, as well as the lymphoblastoid cell line, replicated PRV to low titers after infection. These findings suggest that evidence of immunosuppression in PRV-infected swine may be the result of direct infection of lymphocyte effectors of immune function. Infected leukocytes may also play a role in dissemination of PRV to organ sites distant from the initial site of infection (i.e., beyond the respiratory tract).","abstract_html":"Pseudorabies virus (PRV) is an alphaherpesvirus of swine that causes significant morbidity in adult populations, morbidity and mortality in young pigs, and economic losses to the swine industry each year. Evidence suggests that PRV causes immunosuppression in infected swine with resultant risk of secondary viral and bacterial infections. Virus was recovered from peripheral blood leukocytes (PBL) collected from infected swine, as well as from immune cells isolated from various lymphoid tissues (e.g., lymph node, tonsil, thymus). Lymphocytes stimulated with T cell mitogens, but not B cell mitogens, were permissive to PRV infection in vitro, as evidenced by the expression of PRV antigens on the surface of these cells and by the production of low titers of infectious PRV. Monocytes were highly permissive to PRV infection in vitro, and 75% of monocytes in culture expressed viral antigens on the cell surface. T lymphoblasts are also permissive, and several important functional phenotypes expressed PRV surface antigens after infection. Twenty percent of CD2-bearing lymphoblasts (total T cells) expressed viral antigens on the cell surface after infection, including 15% of CD4-bearing lymphoblasts (helper T cells) and 13% of CD8-bearing lymphoblasts (cytotoxic T cells and natural killer cells). Up to 90% of cells in culture of an immortal lymphoblastoid cell line expressed viral antigens on the cell surface after infection. Both purified CD4-bearing lymphoblasts and purified CD8-bearing lymphoblasts, as well as the lymphoblastoid cell line, replicated PRV to low titers after infection. These findings suggest that evidence of immunosuppression in PRV-infected swine may be the result of direct infection of lymphocyte effectors of immune function. Infected leukocytes may also play a role in dissemination of PRV to organ sites distant from the initial site of infection (i.e., beyond the respiratory tract).","abstract_has_math":false,"creators":["Page, Gregory Raymond"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Veterinary Pathobiology","degree_department":null,"school":null,"contributors":["Hahn, Edwin C."],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2015,"date_issued":"2015-09-28T16:21:49Z","date_published":"2015-09-28T16:21:49Z","updated_at":"2026-07-22T22:26:30Z","subjects":["Health Sciences, Immunology"],"languages":["eng"],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["(MiAaPQ)AAI9990104"],"render_values":[{"text":"(MiAaPQ)AAI9990104","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/87647","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Hahn, Edwin C."]},{"key":"dc:creator","label":"Author","values":["Page, Gregory Raymond"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2015-09-28T16:21:49Z","10000-01-01","2000"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Veterinary Pathobiology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois at Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Health Sciences, Immunology"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/2142/87647","(MiAaPQ)AAI9990104"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Pseudorabies virus (PRV) is an alphaherpesvirus of swine that causes significant morbidity in adult populations, morbidity and mortality in young pigs, and economic losses to the swine industry each year. Evidence suggests that PRV causes immunosuppression in infected swine with resultant risk of secondary viral and bacterial infections. Virus was recovered from peripheral blood leukocytes (PBL) collected from infected swine, as well as from immune cells isolated from various lymphoid tissues (e.g., lymph node, tonsil, thymus). Lymphocytes stimulated with T cell mitogens, but not B cell mitogens, were permissive to PRV infection in vitro, as evidenced by the expression of PRV antigens on the surface of these cells and by the production of low titers of infectious PRV. Monocytes were highly permissive to PRV infection in vitro, and 75% of monocytes in culture expressed viral antigens on the cell surface. T lymphoblasts are also permissive, and several important functional phenotypes expressed PRV surface antigens after infection. Twenty percent of CD2-bearing lymphoblasts (total T cells) expressed viral antigens on the cell surface after infection, including 15% of CD4-bearing lymphoblasts (helper T cells) and 13% of CD8-bearing lymphoblasts (cytotoxic T cells and natural killer cells). Up to 90% of cells in culture of an immortal lymphoblastoid cell line expressed viral antigens on the cell surface after infection. Both purified CD4-bearing lymphoblasts and purified CD8-bearing lymphoblasts, as well as the lymphoblastoid cell line, replicated PRV to low titers after infection. These findings suggest that evidence of immunosuppression in PRV-infected swine may be the result of direct infection of lymphocyte effectors of immune function. Infected leukocytes may also play a role in dissemination of PRV to organ sites distant from the initial site of infection (i.e., beyond the respiratory tract).","Made available in DSpace on 2015-09-28T16:21:49Z (GMT). No. of bitstreams: 2 license.txt: 4848 bytes, checksum: 96035ab3f5e1c23cc7138a224ce498bd (MD5) 9990104.pdf: 6045452 bytes, checksum: e38bc4db30931734ffd116318b02a7ab (MD5) Previous issue date: 2000","Embargo set by: Seth Robbins for item 88928 Lift date: Forever Reason: Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","U of I Only","132 p.","Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2000."]},{"key":"dc:title","label":"Title","values":["Pseudorabies Virus Infection of Porcine Peripheral Blood Leukocytes"]}]}],"canonical_facts":{"dc:contributor":["Hahn, Edwin C."],"dc:creator":["Page, Gregory Raymond"],"dc:date":["2015-09-28T16:21:49Z","10000-01-01","2000"],"dc:description":["Pseudorabies virus (PRV) is an alphaherpesvirus of swine that causes significant morbidity in adult populations, morbidity and mortality in young pigs, and economic losses to the swine industry each year. Evidence suggests that PRV causes immunosuppression in infected swine with resultant risk of secondary viral and bacterial infections. Virus was recovered from peripheral blood leukocytes (PBL) collected from infected swine, as well as from immune cells isolated from various lymphoid tissues (e.g., lymph node, tonsil, thymus). Lymphocytes stimulated with T cell mitogens, but not B cell mitogens, were permissive to PRV infection in vitro, as evidenced by the expression of PRV antigens on the surface of these cells and by the production of low titers of infectious PRV. Monocytes were highly permissive to PRV infection in vitro, and 75% of monocytes in culture expressed viral antigens on the cell surface. T lymphoblasts are also permissive, and several important functional phenotypes expressed PRV surface antigens after infection. Twenty percent of CD2-bearing lymphoblasts (total T cells) expressed viral antigens on the cell surface after infection, including 15% of CD4-bearing lymphoblasts (helper T cells) and 13% of CD8-bearing lymphoblasts (cytotoxic T cells and natural killer cells). Up to 90% of cells in culture of an immortal lymphoblastoid cell line expressed viral antigens on the cell surface after infection. Both purified CD4-bearing lymphoblasts and purified CD8-bearing lymphoblasts, as well as the lymphoblastoid cell line, replicated PRV to low titers after infection. These findings suggest that evidence of immunosuppression in PRV-infected swine may be the result of direct infection of lymphocyte effectors of immune function. Infected leukocytes may also play a role in dissemination of PRV to organ sites distant from the initial site of infection (i.e., beyond the respiratory tract).","Made available in DSpace on 2015-09-28T16:21:49Z (GMT). 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