Okeoma, Chioma, Ph.D.

Assistant Professor
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Our laboratory studies intrinsic host virus restriction factors involved in all aspects of virus infection with emphasis on mechanism(s) of action and regulation.

Mammalian hosts are susceptible to infection by retroviruses including human immunodeficiency virus (HIV) and mouse mammary tumor virus (MMTV), in part, because retroviruses possess unique strategies designed specifically to evade the host innate and adaptive immune systems. In response, the hosts have developed a number of cellular based defense systems such as apolipoprotein B mRNA-editing enzyme (APOBEC3, A3), and bone marrow stromal cell antigen 2 (BST-2), also known as tetherin or CD317 that play a role in virus restriction. Both A3 and BST-2 proteins are expressed in immune cells and both are regulated by cytokines especially the type 1 interferon.

The long term goal of our laboratory is to elucidate the mechanism(s) by which A3 and BST-2 inhibit virus infection in vivo and utilize this knowledge in developing more effective therapeutics and control strategies against retroviral infection. Currently we are focused on three main projects. In one project, we are using different inhibitors and mutant mice to determine the signaling events and pathways involved in 1) IFN-dependent A3 regulation and 2) virus-mediated A3 regulation. In another project, we are using biochemical and immunological techniques to evaluate the mechanism(s) of A3 modulation during HIV-1 infection. In the third project, we are using biochemical, cellular and in vivo assays to determine the mechanism(s) of BST-2 inhibition of virus replication. We are hopeful that the findings and knowledge developed in these projects will significantly improve our capacity to design and develop more effective antiretroviral therapeutics.

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