Effects of Knocking Down Raptor on mTORC1 Activity and HBV Replication

School Name

South Carolina Governor's School for Science and Mathematics

Grade Level

12th Grade

Presentation Topic

Cell and Molecular Biology

Presentation Type

Mentored

Abstract

Hepatitis B Virus (HBV) is a major global health concern, and understanding significant factors that regulate virus replication is essential for developing cure or treatments. The purpose of this project was to explore the role of Raptor, a key component of the mTORC1 signaling pathway, in HBV replication. We hypothesized that a knockdown of Raptor will disrupt mTORC 1 activity resulting in an increase in HBV replication. To test this, HepG2 cells were transfected with HBV and then reduced the amount of the Raptor protein inside the transferred cells. After that, Western blotting was used to confirm protein expression levels, while HBV replication assays measured nucleocapsid formation and relaxed circular DNA (rcDNA). Both sh1-Raptor and sh2-Raptor constructs were evaluated for efficiency. The results showed that sh1-Raptor did not effectively reduce Raptor protein, while sh2-Raptor successfully knocked down Raptor expression. Surprisingly, effective knockdown of Raptor with sh2 correlated with an increase in HBV replication, as indicated by higher levels of nucleocapsid and rcDNA compared to controls. These findings suggest that, rather than inhibiting HBV replication, loss of Raptor promotes HBV replication. In conclusion, this study demonstrates that Raptor plays a significant role in HBV replication, where suppressing it enhances viral activity. These results highlight the complexity of host–virus interactions and provide new insights that may inform future therapeutic strategies targeting the mTORC1 pathway in HBV infection.

Location

Furman Hall 106

Start Date

3-28-2026 10:45 AM

Presentation Format

Oral Only

Group Project

No

COinS
 
Mar 28th, 10:45 AM

Effects of Knocking Down Raptor on mTORC1 Activity and HBV Replication

Furman Hall 106

Hepatitis B Virus (HBV) is a major global health concern, and understanding significant factors that regulate virus replication is essential for developing cure or treatments. The purpose of this project was to explore the role of Raptor, a key component of the mTORC1 signaling pathway, in HBV replication. We hypothesized that a knockdown of Raptor will disrupt mTORC 1 activity resulting in an increase in HBV replication. To test this, HepG2 cells were transfected with HBV and then reduced the amount of the Raptor protein inside the transferred cells. After that, Western blotting was used to confirm protein expression levels, while HBV replication assays measured nucleocapsid formation and relaxed circular DNA (rcDNA). Both sh1-Raptor and sh2-Raptor constructs were evaluated for efficiency. The results showed that sh1-Raptor did not effectively reduce Raptor protein, while sh2-Raptor successfully knocked down Raptor expression. Surprisingly, effective knockdown of Raptor with sh2 correlated with an increase in HBV replication, as indicated by higher levels of nucleocapsid and rcDNA compared to controls. These findings suggest that, rather than inhibiting HBV replication, loss of Raptor promotes HBV replication. In conclusion, this study demonstrates that Raptor plays a significant role in HBV replication, where suppressing it enhances viral activity. These results highlight the complexity of host–virus interactions and provide new insights that may inform future therapeutic strategies targeting the mTORC1 pathway in HBV infection.