Sohaib Butt Rose Hills
Investigating ERAP Downregulation In RhCMV Macaque Infected Cells
Studies have shown that human cytomegalovirus (HCMV) establishes lifelong infection in 50% of the human population. One reason for its success in infection of host cells is its ability to evade immune responses, which is what a large majority of herpesvirus genomes are devoted to: evading the immune response. An immune evasion tactic identified by our lab is ERAP protein downregulation, an aminopeptidase required for peptide trimming prior to loading on MHC-I. ERAP protein is essential for antigen processing and recognition of infected cells by cytotoxic T lymphocytes (CTLs), cells responsible for killing infected cells. ERAP downregulation is an immune evasion mechanism of HCMV that evades CTL immune surveillance and our lab wonders if other CMV homologs exhibit a conserved immune evasion mechanism.
In recent studies, Rhesus macaque CMV (RhCMV) vector based vaccines have yielded strong and efficient unconventional CTL responses against simian immunodeficiency virus (SIV) infected macaques. I propose that viral RhCMV effectors may downregulate ERAP in a conserved model. I hypothesize that ERAP downregulation is conserved in RhCMV, as observed in existing HCMV and MCMV models.
Message To Sponsor
Thank you so much for all of your support for my project, I'm very grateful and humble to have this opporutnity. In order to further our investigation of immune evasion pathways and better our understanding of the microbiological world, research support is a gift and i'm very thankful. Thank you to my mentor, Laurent, for working with me and supporting me in pursuit of this project. And thank you to OURS and the SURF staff members for all of the hard work they have put in day in and day out!