Urmila Vudali L&S Biological Sciences
Characterizing a Marker of Latent HIV-infected Cells using CRISPR/Cas9
With over 39 million people living with HIV, it is one of the world’s foremost health challenges. While Antiretroviral Therapy has reduced HIV-related mortalities by suppressing viral replication, it fails to eradicate the virus, leaving a latent viral reservoir.
Thus, identifying a marker of latently infected cells is the focus of many researchers. CD30, a transmembrane protein, is primarily found in tumor cells, such as Hodgkin and other lymphomas. It is found on a small percentage of healthy lymphocytes. However, the Henrich Lab has found enhanced CD30 in HIV infected CD4+ T cells. I aim to further characterize the relationship between CD30 expression and HIV infection to establish the viability of CD30 as a reliable target for HIV therapies.
I hypothesize that HIV upregulates CD30 to boost infected cell survival and evade immune-mediated clearance. By using CRISPR/Cas to disable the CD30 gene in human cells and infecting them, I hope to assess the impact on HIV’s ability to infect the cells. Secondly, I propose to knock out CD30 in infected cells, and observe their proliferation over time to determine if CD30 diminishes HIV infected cell survival.
Message To Sponsor
I would like to express my sincere gratitude to the Shin Morgan fund for supporting my research this summer. This experience has given me the opportunity to explore cutting-edge research and further my career goals. I have learned so much about the ups and downs and the research process and have grown immensely as a researcher. I am excited for the be opportunities this project has created and look forward to continuing my work in my senior thesis.