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Host cell antigen and T-lymphocyte subset contribution to simian immunodeficiency virus pathogenicity

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dc.contributor.authorStump, Debora Shawn, author
dc.contributor.authorVandeWoude, Sue, advisor
dc.date.accessioned2024-03-13T20:27:59Z
dc.date.available2024-03-13T20:27:59Z
dc.date.issued2008
dc.description.abstractThe continuity of the host cell plasma membrane and the simian immunodeficiency virus (SIV) envelope at the time of budding results in the incorporation of host membrane antigens. Of these host antigens, major histocompatibility complex class II (MHCII), is abundantly represented on the virion surface. In Chapter 1, the investigation the potential of antibodies specific for MHCII to block viral infection by binding viral envelope MHCII in vitro is presented. Our results did not demonstrate viral neutralization associated with anti-MHCII antibodies but illustrate that viral infectivity is influenced by target cell membrane and immunological signaling characteristics. In Chapter 2 we investigated the utility of alloimmunization of genetically divergent rhesus macaques in eliciting immune responses specific for host cell antigens capable of limiting SIV infectivity in vivo. Our results suggest that alloimmune responses are not sufficient to protect animals from SIV challenge. We were also able to assess differences in response to pathogenic SIV infection in rhesus macaques of Chinese origin (ChRh) compared to Indian origin (InRh) in Chapter 3. ChRh in our study were better able to control viral replication and resist disease progression compared to InRh. Peripheral immunocyte kinetics were evaluated using four color flow cytometry in order to define parameters of the differential immune response. No consistent differences were evident, demonstrating that peripheral immune correlates of viral control and disease progression remain unknown. Natural SIV infection has been identified exclusively in primate species inhabiting continental Africa. Serological evidence of exogenous lentiviral infection has been noted in wild lemurs in Madagascar. In Chapter 4, we investigated evidence of a naturally occurring lentivirus, possibly related to African SIVs, in samples from a captive population of L. catta at the Indianapolis Zoo. We show confirmatory serological reactivity to diverse lentiviral antigens but failed to amplify lentiviral specific sequences using established degenerate primer sets. In total, this work represents investigations that interrogate important aspects of nonhuman primate lentiviral pathogenicity. While results were primarily negative in nature, these studies provide important new information and point to additional studies required that will continue investigations into the complex nature of lentiviral host: virus relationships.
dc.format.mediumborn digital
dc.format.mediumdoctoral dissertations
dc.identifierETDF_Stump_2008_3346471.pdf
dc.identifier.urihttps://hdl.handle.net/10217/237973
dc.languageEnglish
dc.language.isoeng
dc.publisherColorado State University. Libraries
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.rights.licensePer the terms of a contractual agreement, all use of this item is limited to the non-commercial use of Colorado State University and its authorized users.
dc.subjectalloimmunity
dc.subjectHIV vaccine development
dc.subjecthost cell antigen
dc.subjectSIV pathogenicity
dc.subjectsimian immunodeficiency virus
dc.subjectT lymphocytes
dc.subjectcellular biology
dc.subjectvirology
dc.titleHost cell antigen and T-lymphocyte subset contribution to simian immunodeficiency virus pathogenicity
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.levelDoctoral
thesis.degree.nameDoctor of Philosophy (Ph.D.)

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