Benjamin J. Burwitz

  • Research Assistant Professor, Oregon National Primate Research Center


Dr. Burwitz's research is two-pronged, focusing on Hepatitis B virus/HIV co-infections, as well as hematopoietic stem cell transplation.

Dr. Burwitz graduated from the University of Wisconsin-Madison in 2004 with a B.S. in molecular biology and psychology. He joined the Department of Cellular and Molecular Pathology at the University of Wisconsin-Madison in 2006 as a graduate student and received his Ph.D. in 2010. In 2011, he joined VGTI as a staff scientist in the lab of Jonah Sacha, and in 2016 was promoted to Research Assistant Professor.

HBV/SIV co-infection of rhesus macaques
The Australia antigen, now known as Hepatitis B virus (HBV) surface antigen, was discovered over 50 years ago. Researchers quickly identified and characterized HBV during the late 1960s and early 1970s, yet no macaque model of HBV infection exists today. Early experiments in the 1970s showed that macaques could not be infected by HBV, and no endogenous hepatitis B-like virus has been discovered in these populations.

HIV/HBV co-infection is common due to highly similar routes of transmission, with an estimated 10-20% of HIV+ individuals also infected with HBV. In addition to their similar routes of transmission, HIV and HBV also share the ability to drive chronic infection, liver dysfunction, liver fibrosis, and immune exhaustion. For these reasons, co-infection with HIV and HBV is associated with higher probabilities of health complications, particularly liver cirrhosis and hepatocellular carcinoma (HCC).

Clinicians and researchers are currently forming an International Coalition to Eliminate Hepatits B Virus (ICE-HBV) to stimulate the development of international working groups on HBV virology, immunology, innovative tools and clinical trials. I believe that any new rhesus macaque model of HBV infection will be on the forefront of efforts to cure HBV, and will be a key component of this new coalition. Therefore, I am continuing to build a rhesus macaque model of HBV infection at VGTI.

Hematopoietic stem cell transplantation in Mauritian cynomolgus macaques

The first hematopoietic stem cell transplantation (HSCT) in humans was reported in 1965. Great progress has been made over the last 50 years improving HSCT techniques and patient care, but despite these advancements, gaft-versus-host disease (GVHD) remains a common cause of morbidity and mortality. A recent report by the Center for International Blood & Marrow Transplant Research listed GVHD as the cause of 20% of deaths following unrelated donor HSCT between 2011 and 2012. Given the remaining hurdles to successfully treating GVHD, a physiologically relevant model of allogeneic HSCT is needed.

Mauritian cynomolgus macaques (MCM) are an insular population that expanded from a small number of founder animals over the last 500 years. The unique natural history of these animals has resulted in exceptionally low genetic diversity. The MHC genetics of this population have been comprehensively characterized and only six common haplotypes exist. Therefore, MCM are the ideal non-human primate model for HSCT as large groups of fully MHC-matched MCM can be readily obtained as donor and recipient pairs. I have successfully co-pioneered a relevant MCM HSCT model at VGTI with Associate Professor Jonah Sacha, which we are now using to answer questions pertaining to GVHD.

Education and training

    • B.S., 2004, University of Wisconsin
    • Ph.D., 2010, University of Wisconsin

Areas of interest

  • Hepatitis B virus/HIV co-infections
  • Hematopoietic stem cell transplantation


Selected publications

  • Ericsen AJ, Lauck M, Mohns MS, DiNapoli SR, Mutschler JP, Greene JM, Weinfurter JT, Lehrer-Brey G, Prall TM, Gieger SM, Buechler CR, Crosno KA, Peterson EJ, Reynolds MR, Wiseman RW, Burwitz BJ, Estes JD, Sacha JB, Friedrich TC, Brenchley JM, O'Connor DH. Microbial Translocation and Inflammation Occur in Hyperacute Immunodeficiency Virus Infection and Compromise Host Control of Virus Replication. PLoS Pathog. 2016 Dec 7;12(12):e1006048. doi: 10.1371/journal.ppat.1006048. 
  • Burwitz BJ, Malouli D, Bimber BN, Reed JS, Ventura AB, Hancock MH, Uebelhoer LS, Bhusari A, Hammond KB, Espinosa Trethewy RG, Klug A, Legasse AW, Axthelm MK, Nelson JA, Park BS, Streblow DN, Hansen SG, Picker LJ, Früh K, Sacha JB. Cross-Species Rhesus Cytomegalovirus Infection of Cynomolgus Macaques. PLoS Pathog. 2016 Nov 9;12(11):e1006014. doi: 10.1371/journal.ppat.1006014. eCollection 2016 Nov. PMID: 27829026, PMCID: PMC5102353
  • Greene JM, Dash P, Roy S, McMurtrey C, Awad W, Reed JS, Hammond KB, Abdulhaqq S, Wu HL, Burwitz BJ, Roth BF, Morrow DW, Ford JC, Xu G, Bae JY, Crank H, Legasse AW, Dang TH, Greenaway HY, Kurniawan M, Gold MC, Harriff MJ, Lewinsohn DA, Park BS, Axthelm MK, Stanton JJ, Hansen SG, Picker LJ, Venturi V, Hildebrand W, Thomas PG, Lewinsohn DM, Adams EJ, Sacha JB. MR1-restricted mucosal-associated invariant T cells respond to mycobacterial vaccination and infection in nonhuman primates.
  • Sturgill ER, Malouli D, Hansen SG, Burwitz BJ, Seo S, Schneider CL, Womack JL, Verweij MC, Ventura AB, Bhusari A, Jeffries KM, Legasse AW, Axthelm MK, Hudson AW, Sacha JB, Picker LJ, Früh K. Natural Killer Cell Evasion Is Essential for Infection by Rhesus Cytomegalovirus. PLoS Pathog. 2016 Aug 31;12(8):e1005868. doi: 10.1371/journal.ppat.1005868. eCollection 2016 Aug. PMID: 27580123, PMCID: PMC5006984


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