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Noncytopathic type 2 bovine viral diarrhea virus 96B2222 induces upregulation of type-I interferon and chemokine receptor 4 expression in bovine peripheral blood mononuclear cells during in vitro infection

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dc.contributor.authorWeiner, Cristina M., author
dc.contributor.authorVandewoude, Sue, advisor
dc.contributor.authorHansen, Thomas R., advisor
dc.contributor.authorVan Campen, Hana, committee member
dc.date.accessioned2022-07-11T20:01:51Z
dc.date.available2022-07-11T20:01:51Z
dc.date.issued2010
dc.description.abstractBovine viral diarrhea virus (BVDV) infection leads to monetary losses in cattle operations due to morbidity and impaired growth. IT is not currently possible to identify pregnant cattle carrying fetuses persistently infected (PI) with BVDV. We previously described a type-I interferon (IFN-I) response to acute non-cytopathic (ncp) BVDV infection in PI fetuses. It was hypothesized that infection of peripheral blood mononuclear cells (PBMC) with ncp-2 96b2222 BVDV would: (1) up-regulate IFN-stimulated genes (IFN-(3, ISG 15), antiviral molecules (retinoic acid inducible gene I, RIG- 1) and chemokine receptor four (CXCR4); (2) viral entry would be mediated through CXCR4; and (3) differentially affect immune cell populations and expression of CXCR4. After optimization of in vitro conditions, PBMCs isolated from a BVDV-naive steer were infected with ncp-2 96b2222 BVDV and treated with AMD3100 and/or CXCR4's ligand, chemokine ligand 12 (CXCL12). Cells were collected and processed for RT-PCR and flow cytometry staining post-infection. At 32 hours post-infection (hpi), mRNA expression of IFN-I pathway genes (IFN-(3, ISG-15), antiviral molecules (RIG-I), CXCR4, CXCLJ 2 and CD8 increased (P < 0.05). Treatment of PBMCs with AMD3100 prior to BVDV infection did not affect BVDV mRNA replication but caused a decrease in CXCR4 mRNA and cell surface expression. CXCL12 treatment increased the concentration of BVDV, CXCR4, IFN- ß, ISG15, and RIG-I transcription. Blocking CXCR4 with AMD3100 and/or CXCL12 did not prevent viral entry and/or replication, but abrogated a BVDV-induced increase in CXCR4 mRNA expression while CXCL12 modulated infection. During PBMC infection in vitro, BVDV may induce release of IFN- ß which then activates ISGs to increase CXCR4 mRNA and protein. Flow cytometry data suggest trends in immune cell populations during ncp-2 96b2222 BVDV infection.
dc.format.mediummasters theses
dc.identifier.urihttps://hdl.handle.net/10217/235425
dc.languageEnglish
dc.language.isoeng
dc.publisherColorado State University. Libraries
dc.relationCatalog record number (MMS ID): 991014241179703361
dc.relationSF967.M78.W455
dc.relation.ispartof2000-2019
dc.rightsCopyright and other restrictions may apply. User is responsible for compliance with all applicable laws. For information about copyright law, please see https://libguides.colostate.edu/copyright.
dc.subject.lcshBovine viral diarrhea virus
dc.titleNoncytopathic type 2 bovine viral diarrhea virus 96B2222 induces upregulation of type-I interferon and chemokine receptor 4 expression in bovine peripheral blood mononuclear cells during in vitro infection
dc.typeText
dcterms.rights.dplaThis Item is protected by copyright and/or related rights (https://rightsstatements.org/vocab/InC/1.0/). You are free to use this Item in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s).
thesis.degree.disciplineMicrobiology, Immunology, and Pathology
thesis.degree.grantorColorado State University
thesis.degree.levelMasters
thesis.degree.nameMaster of Science (M.S.)

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