Zana Lukic, PhD
Dr. Zana Lukic is a postdoctoral fellow in the Department of Internal Medicine in Dr. Kathleen Collins' laboratory at the University of Michigan. Before joining the University of Michigan in August of 2014, Dr. Lukic received her Ph.D. degree in Cell Biology, Neurobiology, and Anatomy at Loyola University-Chicago in May of 2014. While at Loyola University-Chicago, Dr. Lukic was in Dr. Edward Campbell's laboratory where she studied early events of the HIV-1 life cycle.
Human Immunodeficiency Virus (HIV) is a pandemic and a huge health burden. HIV-1 is difficult to eradicate due to its’ ability to establish a life-long infection in the host; therefore, patients need to remain on life-long antiretroviral treatment. The two main cell types that are infected by HIV-1 are T cells and macrophages. As antigen-presenting cells, macrophages are important for both innate and adaptive immunity to viral infections. These cells express interferon (IFN)-inducible restriction factors that target various stages of the viral replication cycle to restrict infection. However, HIV-1 encodes accessory proteins that counteract these restriction factors and avoid immune detection to establish persistent infection. My research project focuses on understanding the pathways that the virus utilizes in macrophages in order to evade the host responses.
In vitro culture of primary human cells, qRT-PCR, ELISA, Western blot, lentiviral transduction
Collins DR, Lubow J, Lukic Z, Mashiba M, Collins KL (2015) Vpr Promotes Macrophage-Dependent HIV-1 Infection of CD4+ T Lymphocytes. PLoS Pathog 11(7): e1005054. doi:10.1371/journal.ppat.1005054
Lukic Z, Dharan A, Fricke T, Diaz-Griffero F, Campbell EM (2014). HIV-1 Uncoating is Faciliated by Dynein and Kinesin 1. Journal of Virology 88(23): 13613-25. doi: 10.1128/JVI.02219-14.
Jaya Sastri, Laura Johnsen, Sabrina Imam, Zana Lukic, Alberto Brandariz-Nunez, Nikolai Smolin, Seth L. Robia, Felipe Diaz-Griffero, Christopher Wiethoff, and Edward M. Campbell (August 2014). The Linker 2 region of Rhesus TRIM5alpha governs the assembly of antiparallel dimers during HIV-1 restriction. JVI 88(16):8911-23. doi: 10.1128/JVI.01134-14
David Freeman, Rudy Cedillos, Sam Choyke, Zana Lukic, Katie McGuire, Shauna Marvin, Andrew M. Burrage, Stacey Sudholt, Ajay Rana, Christopher O’Connor, Christopher M. Wiethoff, and Edward M. Campbell (April 2013). Alpha-synuclein induces lysosomal rupture and cathepsin dependent reactive oxygen species following endocytosis. PLoS One 25; 8(4) doi: 10.1371/journal.pone.0062143
Zana Lukic*, Gloria Arriagada*, Stephen P. Goff, Edward M. Campbell (February 2013). The Role of SUMO-1 and SUMO Interacting Motifs in rhTRIM5α-Mediated Retroviral Restriction. Retrovirology 1:10 doi: 10.1186/1742-4690-10-10 *authors equally contributed
Zana Lukic, and Edward M. Campbell (March 2012). The Cell Biology of TRIM5α. Current HIV/AIDS Reports DOI: 10.1007/s11904-011-0102-8
Zana Lukic, Stephane Hausmann, Sarah Sebastian, Justin Rucci, Jaya Sastri, Seth L. Robia, Jeremy Luban, and Edward M. Campbell (November 2011). TRIM5alpha associates with proteasomal subunits in cells while in complex with HIV-1 virions. Retrovirology 8:93 doi: 10.1186/1742-4690-8-93