Murine Model of Cryptococcus-associated Immune Reconstitution Inflammatory Syndrome (IRIS)

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dc.contributor.advisorWormley, Floyd
dc.contributor.authorMendoza, Christopher
dc.contributor.committeeMemberYu-Hung, Chiung
dc.contributor.committeeMemberLopez-Ribot, Jose
dc.date.accessioned2024-02-12T15:39:51Z
dc.date.available2019-08-13
dc.date.available2024-02-12T15:39:51Z
dc.date.issued2018
dc.descriptionThis item is available only to currently enrolled UTSA students, faculty or staff. To download, navigate to Log In in the top right-hand corner of this screen, then select Log in with my UTSA ID.
dc.description.abstractCryptococcus neoformans is an opportunistic fungal pathogen that is able to cause pneumonia and life-threatening infections of the central nervous system. This pathogen is particularly problematic for immunocompromised individuals, such as those with AIDS or undergoing immunosuppressive therapies. Since the initial outbreak of HIV/AIDS, controlling the infection is now possible through combination antiretroviral therapy (ART) which helps to restore immune function in this population. However, approximately 30% of patients who have recieved ART treatment can develop an uncontrolled inflammatory response following reconstitution of the immune system while they still have a latent HIV infection. This poorly understood inflammatory response is known as Immune Reconstitution Inflammatory Syndrome (IRIS) and can be caused by C. neoformans. Our aim is to develop a clinically relevant small animal model of Cryptococcus-related IRIS using wild type mice, as opposed to current murine models of IRIS using genetically immune deficient mice. We established a Cyrptococcus-related IRIS model using immune competent BALB/c mice that were depleted of T cells via complement-fixing antibodies and challenged with a small infectious dose of C. neoformans yeast. The T cell depletions were continued for several weeks post infection, before allowing for the immune system to reconstitute, mimicking what occurs in the IRIS patient population. The mice were monitored for mortality, fungal burden and cytokine production in the CNS. Establishment of this model will allow for the characterization of therapies designed to reduce the mortality associated with Cryptococcus-related IRIS in humans.
dc.description.departmentIntegrative Biology
dc.format.extent38 pages
dc.format.mimetypeapplication/pdf
dc.identifier.urihttps://hdl.handle.net/20.500.12588/4490
dc.languageen
dc.subject.classificationBiology
dc.titleMurine Model of Cryptococcus-associated Immune Reconstitution Inflammatory Syndrome (IRIS)
dc.typeThesis
dc.type.dcmiText
dcterms.accessRightspq_closed
thesis.degree.departmentIntegrative Biology
thesis.degree.grantorUniversity of Texas at San Antonio
thesis.degree.levelMasters
thesis.degree.nameMaster of Science

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