Restriction of HIV-1 Infection by the Interferon-Induced Dynamin GTPase Inhibitor, Mx2
The focus of the Aiken lab is to understand the molecular events governing HIV-1 replication in order to develop novel antiviral therapies. My research project is focused on understanding how the interferon-induced dynamin-like GTPase inhibitor, Myxovirus resistance protein 2 (Mx2), restricts the HIV-1 capsid from entering the nucleus. From our current knowledge, once HIV-1 enters the cell and undergoes reverse transcription, the dsDNA is shuttled to the nucleus where it can integrate into the host genome to start replication. It is thought that the resistance protein Mx2 is activated by an interferon-induced response to the virus where it can somehow stop the virus from entering the nucleus.
In my study, we hypothesize that there is a cofactor that helps Mx2 in restricting HIV-1 from entering the nucleus. Using a screen of different cell lines that do and do not endogenously produce Mx2, I am working to understand how Mx2 restricts HIV from entering the nucleus, and if there is a factor that is helping restrict HIV-1. Using infection and binding assays with these cell lines, I will assess the results of these different assays and work to better understand the mechanism of restriction of HIV-1 by Mx2.