Beth Jamieson

Beth D. Jamieson, PhD

Associate Professor, Department of Medicine, Hematology/Oncology



Contact Information

Scientific Interests

Dr. Beth Jamieson's research focuses on the immune response to HIV-vaccination and natural infection.

Specifically, Jamieson investigates the HLA-B57 restricted CD8+ T-cell response to HIV to determine why most HIV-1 infected individuals that fail to progress to AIDS within 10 years are HLA-B57+ individuals. As CD8+ T-cells are class I restricted, this association between the class I antigen, HLA-B57, and the lack of disease progression, strongly argues for a role of CD8+ T-cells in determining rates of disease progression. This newly funded project is in the early stages of development.

In addition, Jamieson recently received National Institutes of Health (NIH) funding to investigate and compare the immune response to HIV-1 in women and men. While women and men have been reported to progress to AIDS with similar rates, in the first 4.5 years of infection, women have been reported to have a HIV-1 RNA copies per ml of plasma that are a log lower than found in men. At approximately 4.5 years, the viral burden in women becomes similar to that found in men. As uninfected women and men exhibit several differences in general immune system parameters, it is possible that the early difference in viral burden is due to better immune control of HIV replication early in infection compared to men. Alternatively, women and men may have differences in target cell availability that influences viral replication in the first four years of infection. This is somewhat supported by the findings of others that women tend to have more diverse viral populations than men soon after infection. These possibilities are currently under investigation in Jamieson's laboratory.

Lastly, Jamieson's laboratory continues to study the role of the thymus in T-cell reconstitution in HIV infected individuals, extending her earlier findings that the thymus continues to function well into adulthood despite the earlier misconception that this organ ceased to generate new T-cells after puberty.

Highlighted Publications

Hultin LE, Menendez FA, Hultin PM, Jamieson BD, O'gorman MR, Borowski L, Matud JL, Denny TN, Margolick JB. Assessing immunophenotyping performance: Proficiency-validation for adopting improved flow cytometry methods. Cytometry B Clin Cytom. 2007.

Cole SR, Hernan MA, Anastos K, Jamieson BD, Robins JM. Determining the Effect of Highly Active Antiretroviral Therapy on Changes in Human Immunodeficiency Virus Type 1 RNA Viral Load using a Marginal Structural Left-censored Mean Model. Am J Epidemiol. 2007; 166(2): 219-27.

Gupta SB, Jacobson LP, Margolick JB, Rinaldo CR, Phair JP, Jamieson BD, Mehrotra DV, Robertson MN, Straus WL. Estimating the benefit of an HIV-1 vaccine that reduces viral load set point. J Infect Dis. 2007; 195(4): 546-50.

Yang OO, Ferbas JJ, Hausner MA, Hultin LE, Hultin PM, McFadden D, Sawicki M, Detels R, Majchrowicz M, Matud JL, Giorgi JV, Jamieson BD. Effects of HIV-1 infection on lymphocyte phenotypes in blood versus lymph nodes. J Acquir Immune Defic Syndr. 2005; 39(5): 507-18.

Yang OO, Daar ES, Jamieson BD, Balamurugan A, Smith DM, Pitt JA, Petropoulos CJ, Richman DD, Little SJ, Brown AJ. Human immunodeficiency virus type 1 clade B superinfection: evidence for differential immune containment of distinct clade B strains. J Virol. 2005; 79(2): 860-8.