HIV is a retrovirus that causes acquired immunodeficiency syndrome (AIDS), and even though it's one of the most studied viruses there're still many unknowns that impede developing a cure for AIDS. Viral protein R (Vpr) is an accessory protein of HIV. In this project, we will research how an HIV-1 isolate with an R77Q mutation in the Vpr gene induces apoptosis in contrast to the uncontrolled cell death that other variants produce. This will be done by analyzing the viral DNA in the nucleus and the cytoplasm. Within R77Q infection, we expect to see an increased amount of viral DNA in the cytoplasm and a fewer amount in the nucleus as opposed to other infections featuring wild-type Vpr and other Vpr mutants. When DNA is found in the cytoplasm it is normal for cells to start innate immune responses, but it has also been found that cytosolic DNA triggers biological pathways of programmed cell death. In previous research performed in our lab, we have seen that the R77Q mutation causes cell death by apoptosis at higher rates compared to wild-type viruses and other mutations. This project presents an opportunity to potentiate previous research in understanding how the mutation induces apoptosis.
University / Institution: Brigham Young University
Format: In Person
SESSION C (1:45-3:15PM)
Area of Research: Science & Technology
Faculty Mentor: Bradford Berges