Simon Barratt-Boyes is a 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. Dr Barratt-Boyes 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. He earned his PhD in comparative pathology from UC Davis in 1993 prior to post-doctoral training in immunology at the University of Pittsburgh. He joined the faculty of the University of Pittsburgh in 1998. His research interests are in viral immunology and pathogenesis with an emphasis on infectious diseases of importance to global human health.
- Kader M, Smith AP, Guiducci C, Wonderlich ER, Normolle D, Watkins SC, Barrat FJ, Barratt-Boyes SM (2013). Blocking TLR7 and TLR9 mediated IFN-α production by plasmacytoid dendritic cells does not diminish immune activation in early SIV infection. PLoS Pathogens; 9: e1003530
- Wonderlich ER, Wijewardana V, Liu X, Barratt-Boyes SM (2013) Virus-encoded TLR ligands reveal divergent functional responses of mononuclear phagocytes in pathogenic simian immunodeficiency virus infection. Journal of Immunology; 190 (5):2188-98.
- Garcia-Bates TM, Cordeiro MT, Nascimento EJM, Smith AP, Soares de Melo KM, McBurney SP, Evans JD, Marques ETA Jr & Barratt-Boyes SM (2013) Association between magnitude of the virus-specific plasmablast response and disease severity in dengue patients. Journal of Immunology 190: 80-87.
- Wonderlich ER & Barratt-Boyes SM (2012) A dendrite in every pie: Myeloid dendritic cells in HIV and SIV infection. Virulence; 3: 647-653
- Soloff AC, Weirbeck HK, Ross TM & Barratt-Boyes SM (2012) Plasmacytoid dendritic cell depletion leads to enhanced mononuclear phagocyte response in lungs of mice with lethal influenza virus infection. Comparative Immunology, Microbiology and Infectious Diseases; 35: 309-317.
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.