Tricia H. Burdo, PhD
Vice Chair, Department of Microbiology, Immunology and Inflammation
Professor, Microbiology, Immunology and Inflammation
Professor, Center for Neurovirology & Gene Editing
Professor, Neural Sciences
- Contact Information
- About Me
My lab focuses on the role of ongoing chronic immune activation and the role of monocyte/macrophages in HIV-associated peripheral neuropathy (HIV-PN), HIV-associated neurocognitive disorders (HAND) and cardiovascular disease (CVD). It is becoming clear that HIV+ patients on effective antiretroviral therapy (ART) who have non-detectable plasma virus, still have persistent immune activation that includes monocytes and macrophages, accelerated immune aging and senescence, and other co-morbidities including an increased incidence of coronary atherosclerosis and is of great interest in the lab.
We use the SIV-infected rhesus macaque model to study the roles of monocyte traffic, macrophage activation and virus in peripheral neuropathy with and without ART. We have shown that traffic of monocytes (as measured by BrdU+ monocytes) is critical for histopathology in dorsal root ganglia (DRG) and correlates to loss of intraepidermal nerve fibers (IENFD).
We have pioneered work on soluble CD163 (sCD163) as a marker of chronic immune activation in SIV and HIV infection. We have showed that monocyte egress out of the bone marrow correlates with sCD163 in plasma and severity of SIV encephalitis (SIVE). sCD163 was elevated in the plasma of both chronic and early HIV+ patients, which decreased significantly with ART. However, sCD163 in chronically infected patients did not come back to levels found in uninfected demonstrating ongoing monocyte/macrophage activation even with suppressive ART.
The mechanisms of HAND persistence in the ART era are not well understood. It is likely that events occurring early in the CNS set the stage for a future neurological disease that emerges during chronic infection with or without effective ART. We have shown that sCD163 is elevated in HIV+ individuals with HAND and suggest that the persistence of HAND is likely mediated by continual immune activation that includes monocytes and macrophages.
More recently we have been working in conjunction with investigators at Mass General Hospital on immune markers of cardiac disease during HIV infection. We have shown that sCD163 correlated with non-calcified vulnerable plaque. In addition, sCD163 also correlated with the number of inflammatory macrophages in the ascending aorta of HIV infected individuals, as shown by FDG-PET imaging. Currently, Dr. Burdo is an Immunologist measuring immune biomarkers in the Randomized Trial to Prevent Vascular Events in HIV (REPRIEVE) clinical trial (http://reprievetrial.org/). Dr. Burdo is also the lead Immunologist on an ancillary study to examine Sex-Specific Mechanisms of Cardiovascular Disease Risk and Risk Reduction, in which we will assess among HIV-infected individuals ages 40-75 sex-based differences in immune activation and statin-induced immunomodulation in relation to clinical cardiovascular disease events (http://followyourheart.reprievetrial.org/). These are current ongoing projects in the lab.
- Education, Training & Credentials
- Fellowship, The Scripps Research Institute, San Diego, CA, 2007
- PhD, Cell and Molecular Biology, Penn State College of Medicine, Hershey, PA, 2003
- BA, Biology, Saint Anselm College, Manchester, NH, 1998
- International Society for NeuroVirology
- International Society for NeuroImmunology
- Society for Neuroscience
Williams K, Hickey WF, Burdo TH and Soulas C. Mononuclear phagocytes. In: The neurology of AIDS. HE Gendelman, I Grant, IP Everall, HS Fox, HA Gelbard, SA Lipton, S Swindells (eds). 2012 Oxford university press.
Williams KC and Burdo TH. Neuro-AIDS, Immunopathogenesis of, Encyclopedia of AIDS, Editors: Thomas J. Hope, Mario Stevenson, Douglas Richman. Spring Science + Business Media, New York, March 17, 2015.