Simon M. Barratt-Boyes, PhD
Office: Dept. of IDM
Lab: Room 7046 BST 3
Pittsburgh, PA 15261
- B.V.Sc. - Massey University (1984)
- Ph.D. - University at California at Davis (1993)
- Postdoc - University of Pittsburgh School of Medicine (1997)
- Associate Professor, Department of Infectious Diseases and Microbiology
- Associate Professor, Department of Immunology
Mononuclear phagocytes in simian immunodeficiency virus (SIV) infection Mononuclear phagocytes are important innate immune cells that include monocytes, macrophages, and dendritic cells, which in the human and nonhuman primate consist of two major subsets, myeloid and plasmacytoid. Given their function in antiviral immunity, dendritic cells are thought to play a protective role in HIV and SIV infection, and loss of both subsets is associated with disease progression. However, recently emphasis has been placed on the potential role of the innate immune response in chronic, generalized immune activation that is a hallmark of AIDS. In this scenario, over-active mononuclear phagocytes produce pro-inflammatory cytokines that drive chronic interferon production and inflammation in lymphoid and gut tissues. Hence there is a basic unanswered question in HIV pathogenesis: are dendritic cells, monocytes and macrophages beneficial or detrimental to the infected host? The Barratt-Boyes lab uses the model of SIV infection of rhesus macaques, which replicates the pathogenesis of HIV-1 infection in humans and leads to simian AIDS, to address this question. Dendritic cell responses in influenza virus infection Influenza virus is a respiratory pathogen that targets the lung, and innate immune responses serve a key role in providing early antiviral immunity and limiting disease in acute infection. However, the relationship between dendritic cells and immunity in the lung is not well defined. The lab has used the murine model to examine the impact of plasmacytoid dendritic cells in the early immune response to influenza virus infection. The group is also studying the dynamics of the dendritic cell response to highly pathogenic avian influenza virus infection in nonhuman primates, which serves as a robust model of this serious infection of humans. B cells in the immunity and pathogenesis of dengue Dengue is an emerging pathogen of humans that has become a major global public health concern. Dengue virus infection can manifest as either a self-limiting febrile illness or a fulminant systemic disease with plasma leakage and death. The factors that contribute to these divergent outcomes are not well defined. Antibodies have been linked to the pathogenesis of severe dengue, but little is known about the response of B cells themselves. To address this gap in knowledge, the Barratt-Boyes lab is studying the plasmablast response in humans with acute dengue virus infection using a cohort of patients in Brazil, in collaboration with Dr. Ernesto Marques. Investigations are also underway to define the cellular targets of dengue virus infection in human skin.
Brown, K.N., Trichel, A. & Barratt-Boyes, S.M. (2007) Parallel loss of myeloid and plasmacytoid dendritic cells from blood and lymphoid tissues in simian AIDS. J. Immunol. 178: 6958-6967.
Melhem, N.M., Liu, X.D., Boczowski, D., Gilboa, E. & Barratt-Boyes, S.M. (2007) Robust CD4+ and CD8+ T cell responses to SIV using mRNA-transfected dendritic cells expressing autologous viral antigen. Eur. J. Immunol. 37: 2164-2173.
Gambotto, A., Barratt-Boyes, S.M., de Jong, M.D., Neumann, G., & Kawaoka, Y. (2008) Human infection with highly pathogenic H5N1 influenza virus. The Lancet 371: 1464-1475.
Qin, S., Sui, Y., Soloff, A.C., Junecko, B.A., Kirschner, D.E., Murphey-Corb, M., Watkins, S.C., Tarwater, P.M., Pease, J.E., Barratt-Boyes, S.M., & Reinhart, T.A. (2008) Chemokine and cytokine mediated loss of regulatory T cells in lymph nodes during pathogenic simian immunodeficiency virus infection. J. Immunol. 180: 5530-5536.
Melhem, N.M., Liu, X.D., Gleason, S.M., Liu, X. & Barratt-Boyes, S.M. (2008) High-level antigen expression and sustained antigen presentation in dendritic cells nucleofected with wild-type vial mRNA but not DNA. Clin. Vacc. Immunol. 15: 1337-1344.
Professor in the Department of Infectious Diseases and Microbiology in the Graduate School of Public Health with a secondary appointment in the Department of Immunology in the School of Medicine. Graduated with a bachelor of veterinary science from Massey University in New Zealand in 1984 and did residency training at the University of California at Davis. Earned a PhD in comparative pathology from UC Davis in 1993 prior to post-doctoral training in immunology at the University of Pittsburgh. Joined the faculty of the University of Pittsburgh in 1998. Research interests are in viral immunology and pathogenesis with an emphasis on infectious diseases of importance to global human health.