Ward Building Room 6-314
303 E Chicago Avenue
Chicago IL 60611
Description of Interests
Our research focuses on infection by Human Immunodeficiency Virus type 1 (HIV-1), a retrovirus and causative agent of acquired immunodeficiency syndrome (AIDS). In addition to suppressing the immune system, rendering victims susceptible to opportunistic infections, HIV-1 can cross the blood-brain barrier and cause serious damage to the central nervous system, ultimately leading to HIV-associated dementia.
We are interested in how HIV-1 particles exploit host microtubule (MT) network to move within infected cells, including brain cell types such as microglia. Our earlier work identified a number of host proteins involved in cytoskeletal regulation and motor function as playing key roles in the early stages of HIV-1 infection. This includes Ezrin-Radixin-Moesin (ERM) proteins, which cross-link the actin and MT cytoskeletons. In exploring their role in HIV-1 infection, we identified the first biological function for the host protein, PDZD8, demonstrating that it binds ERMs to control MT stability. Furthermore, we uncovered that PDZD8 is a direct target for the HIV-1 protein, Gag.
Other work in our laboratory has shown that HIV-1 can induce the formation of highly stable MT subsets to facilitate early HIV-1 trafficking to the nucleus. We are interested in the role played in this process by proteins such as PDZD8, as well as a family of specialized MT regulatory proteins called +TIPs. We are also interested in the function of MT motors and cargo adaptor proteins in HIV-1 infection. In particular, we are exploring how Fasiculation and Elongation factor Zeta-1 (FEZ-1), a kinesin-1 adaptor protein that is highly expressed in neurons, functions to control HIV-1 infection.
The ultimate goal of our work is to understand the molecular basis behind how MTs, regulators of MT dynamics and MT motor proteins function to enable HIV-1 movement to and from the nucleus.
AIDS; Cytoskeleton; Infectious Diseases; Viral Pathogenesis; Virology
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