Simon M. Barratt-Boyes, PhD

Simon M. Barratt-Boyes, PhD


9046 Biomedical Science Tower 3
3501 Fifth Avenue
Pittsburgh, PA 15260

Ph: 412-383-7537

Fax: 412-383-8926

My Website »


  • Postdoc, University of Pittsburgh School of Medicine, 1997
  • PhD, University of California at Davis, 1993
  • BVSc, Massey University, 1984

Academic Affiliation

Professor, Department of Infectious Diseases and Microbiology, Graduate School of Public Health

Professor, Department of Immunology, School of Medicine

Member, Center for Vaccine Research

Member, Graduate Program in Microbiology and Immunology (PMI)

About Research

Our research focuses on viral diseases that impact human health, including influenza, dengue and HIV. Highly pathogenic avian influenza viruses cause severe pneumonia and infection is often lethal in humans. Progress in controlling and treating severe influenza is hampered by the lack of a large animal model that truly reproduces human illness. We have now developed an aerosol challenge model of H5N1 influenza virus infection in nonhuman primates, which induces acute respiratory distress syndrome. With this model we are testing novel strategies targeting the over-exuberant innate immune response to prevent acute lung injury. Dengue is the most important insect-borne viral disease of humans worldwide and is expanding rapidly on a global scale. The early events that take place following inoculation into skin are poorly understood. We have developed an ex vivo model of virus infection in human skin explants, and have recently shown that keratinocytes are a major target of dengue virus infection. 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. 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 recently shown that macrophages accumulate in the gut mucosa in monkeys with AIDS but not monkeys with chronic infection without disease; macrophages and dendritic cells from infected monkeys also have diminished capacity to stimulate T cells. 

Selected Publications

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.

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.

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, Wu W-C, Normolle DP & Barratt-Boyes SM. 2015. Macrophages and myeloid dendritic cells lose T cell-stimulating function in simian immunodeficiency virus infection associated with diminished IL-12 and IFN-α production. J Immunol. 195: 3284-3292.

Click here for a full list of publications>