Gregory F. Burton
Office: C203 BNSN
Office Phone: 801-422-4917
Lab Room: E221 BNSN
Lab Phone: 801-422-4085
1975 BS at University of Utah (1975)
1977 MS at Brigham Young University (1985)
1989 PhD at Virginia Commonwealth University (1989)
1989 Fellowship at Virginia Commonwealth University
Career Activities Highlights:
- Member of Simmons Center for Cancer Research (SCCR) at Brigham Young University
Dr. Burton specializes in biochemistry, with particular emphasis placed on immunology and molecular biology, including HIV/AIDS treatment.
The establishment of "reservoirs" or sites where HIV escapes drug or immune system intervention is a major concern in the treatment of HIV infections. These reservoirs permit the virus to linger and spread in the body. Such reservoirs in humans consist of latently infected CD4 T-lymphocytes, monoctyes/macrophages, and follicular dendritic cells (FDCs). Lymphocytes and monocytes/macrophages can be found throughout the body, but FDC are only found in tissue sites like lymph nodes and the spleen. In these areas, FDCs live in close proximity with the HIV's primary target: the CD4 T-lymphocyte. Moreover, macrophages often live close to FDCs.
Dr. Burton's research focuses on the largest HIV reservoir: the FDC.
Shortly after infection, large quantities of HIV cells become trapped on the surfaces of FDCs. Here the virus will persist, unless the FDC network is destroyed. Dr. Burton works to define the contributions of FDCs to HIV pathogenesis. His work has led him to understand that, while FDCs may not be infected by HIV, FDCs allow HIV to survive in a highly infectious form. In contrast, HIV in other reservoir types is internalized, meaning the cells composing those reservoirs are infected with HIV. Because the virus hosted by the FDC does not actively infect the FDC, the virus is not susceptible to treatment by any drugs science currently use. Further, the presence of HIV on FDCs allows the virus to escape immune system responses. When infected subjects generate neutralizing antibodies that could block infection of target cells, FDC virus cells can still cause infection.
Dr. Burton's research has proved that FDCs create a unique microenvironment that enhances HIV infection through increasing the expression of a major HiV co-receptor (CXCR4) on CD4+ lymphocytes. FDCs create this microenvironment by augmenting HIV transcription in infected cells and inhibiting CD4+ T-lymphocyte apoptosis cell death. Dr. Burton's laboratory discovered that the germinal-center T-cells (CD4+ T-cells that reside adjacent to FDCs) cannot migrate to a specific chemokine, CXCL12, when FDCs induce an inhibition signal. This inability to respond to chemokines might increase the likelihood of the T-cells' exposure to infectious HIV on FDCs.
Dr. Burton worked to dissect the signaling molecules that resulted in germinal-center T-cell unresponsiveness. The doctor also studied the genetic composition of FDC-trapped HIVs in order to characterize the contributions of HIV to disease pathogenesis.
Department History Interview:
Dr. Burton participated in an interview celebrating the 100th anniversary of the organization of the BYU Department of Chemistry & Biochemistry.