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.
Swan ZD, Wonderlich ER, & Barratt-Boyes SM (2016). Macrophage accumulation in gut mucosa differentiates AIDS from chronic SIV infection in rhesus macaques. Eur J Immunol; 46: 446-454. (Cover art).
Wonderlich ER, Swan ZD, Bissel SJ, Hartman AL, Carney JP, O’Malley KJ, Obadan AO, Santos J, Walker R, Sturgeon TJ, Frye LJ Jr., Maiello P, Scanga CA, Bowling JD, Bouwer AL, Duangkhae PA, Wiley CA, Flynn JL, Wang J, Cole KS, Perez DR & Barratt-Boyes SM. (2017). Widespread virus replication in alveoli drives acute respiratory distress syndrome in aerosolized H5N1 influenza infection of macaques. J Immunol; 198: 1616-1626.
- Swan ZD, Bouwer AL, Wonderlich ER & Barratt-Boyes SM (2017). Persistent accumulation of gut macrophages with impaired phagocytic function correlates with SIV disease progression in macaques. Eur J Immunol; 47: 1925-1935.
Duangkhae P, Erdos G, Ryman KD, Watkins SC, Falo LD Jr., Marques ETA Jr. & Barratt-Boyes SM (2018). Interplay between keratinocytes and myeloid cells drives dengue virus spread in human skin. J Invest Dermatol; 138: 618-626.
We have research programs in three main areas: influenza, dengue and SIV. Highly pathogenic avian influenza viruses including H5N1 and H7N9 strains cause severe pneumonia and acute respiratory distress syndrome in humans, and infections are often fatal. Our understanding of the pathogenesis of infection and how we might best prevent severe disease are hampered by the lack of a large animal model that truly reproduces human illness. We have overcome this significant problem by developing an aerosol challenge model of H5N1 influenza virus infection in nonhuman primates, working in the University of Pittsburgh’s Regional Biocontainment Laboratory. Aerosolization delivers virus to the lower respiratory tract and induces acute respiratory distress syndrome in macaques. With this model we can now test novel strategies targeting the over-exuberant innate immune response to prevent acute lung injury. These new therapeutic approaches could prevent the tens of thousands of influenza deaths each year and could be used as the first line of defense to contain an influenza pandemic. Dengue is the most important insect-borne viral disease of humans worldwide and is expanding rapidly on a global scale. The Zika epidemic in the Americas in 2015-16 caused microcephaly and other serious congenital defects, and Zika infections continue at a low level in Brazil today. Both viruses are transmitted via the skin, but the early events that take place following inoculation into skin are poorly understood. We have addressed this problem by developing an ex vivo model of dengue and Zika virus infection in human skin explants. We have recently shown that keratinocytes are a major target of dengue virus infection, and that innate responses by infected keratinocytes lead to recruitment of virus-permissive myeloid cells including dendritic cells and macrophages that serve to expand infection and disseminate virus out of skin. We have now developed the first model of antibody-dependent enhancement of dengue and Zika virus infection in human skin. This new model will allow us to understand how immunity to one virus induced either by infection or vaccination impacts infection with a second virus, be it dengue or Zika. The laboratory also addresses the relationship between dendritic cells and macrophages and progression or control of SIV infection in the rhesus macaque model of HIV/AIDS. We have defined dendritic cell populations in the macaque model and studied the trafficking of ex vivo propagated cells after injection into donor animals. We have also found that myeloid dendritic cells in SIV infected monkeys produce cytokines in response to virus-encoded TLR ligands but that tissue myeloid dendritic cells and macrophages lose the capacity to stimulate T cells in SIV infection associated with reduced production of IL-12 and IFN-α. We have shown that macrophages accumulate in the gut mucosa in monkeys with AIDS but are not present in such large numbers in these tissues in chronic infection without disease.