CONTACT INFORMATION
Phone:
(608) 890-0843
Mailing Address:

585 Science Dr
Madison, WI 53711

Shelby O'Connor, PhD

  • Associate Professor

Department of Pathology and Laboratory Medicine



Education
2004
PhD, Cellular and Molecular Biology, University of Wisconsin, Madison, WI

Research Interests

Host and vaccine-elicited immune responses to SIV/HIV; SIV/HIV evolution; The dynamic host immune response during HIV/SIV and M.tuberculosis co-infections; Immunology/Immunopatholo

Detail:

My research lab is interested in understanding the host immune response to HIV and the effect that HIV-infection has on host immunity to other pathogens. HIV+ immunocompromised individuals cannot mount robust immune responses like those who are otherwise healthy. We use nonhuman primates with defined host MHC genetics to understand key factors of immunity against SIV, a virus closely related to HIV. We are also developing novel SIV virus stocks to improve our understanding of viral compartmentalization and viral evolution, in vivo. In addition, we are collaborating with others to develop nonhuman primate co-infection models to identify factors that contribute to failed host immunity to M.tuberculosis in animals who have an ongoing SIV infection.

My lab is currently focused on two major research areas:

SIV pathogenesis and vaccine projects: We have two ongoing SIV projects. In one project, we are developing and testing a barcoded SIV virus stock to evaluate viral compartmentalization and viral evolution in macaques. In our second project, we are determining whether CD8 T cells targeting epitopes that are conserved among circulating viral strains are more or less effective at destroying virus particles than CD8 T cells that target epitopes that accumulate immune escape variants. We hope these studies will identify which T cell responses should be elicited by a successful SIV/HIV vaccine.

SIV/Mtb co-infection studies: HIV+ individuals rapidly become sick after co-infection with secondary pathogens, such as Mycobacterium tuberculosis (Mtb). We are interested in understanding why HIV+ immunocomprimised individuals are unable to control bacterial replication. We hope these studies will help identify critical therapeutic interventions to prevent HIV+ individuals from becoming sick with tuberculosis.