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Robert Francis Siliciano, M.D., Ph.D.
Professor of Medicine
Research Interests: Drug therapy for HIV infection
Contact for Research Inquiries
Edward D. Miller Research Building
733 N. Broadway
Baltimore, MD 21205 map
Dr. Robert Siliciano is a Professor of Medicine in the Infectious Diseases Department. He studies HIV, specifically viral reservoirs that prevent curing HIV infection and trying to better understand how the T-cell reservoir is established and maintained.
Dr. Siliciano holds a bachelor’s degree from Princeton University and medical degree and PhD from Johns Hopkins. He completed a postdoctoral fellowship at Harvard Medical School before joining the Johns Hopkins faculty. Dr. Siliciano is an investigator in the Howard Hughes Medical Institute, and his work has been recognized by a Distinguished Clinical Scientist Award from the Doris Duke Charitable Foundation and two merit awards from the National Institutes of Health.
- Professor of Medicine
- Joint Appointment in Molecular Biology and Genetics
- Professor of Pharmacology and Molecular Sciences
- M.D., Johns Hopkins University School of Medicine (Maryland) (1982)
- Ph.D., Johns Hopkins University School of Medicine (Maryland) (1983)
Research & Publications
For the 34 million people infected with HIV-1, the best current hope for avoiding the fatal consequences of the infection lies in treatment antiretroviral therapy (ART), which consists of combinations of three drugs that inhibit specific steps in the virus life cycle. The benefits of ART in reducing the morbidity and mortality are clear, but ART is not curative. In 1995, our laboratory provided the first demonstration that latently infected CD4+ T cells were present in patients with HIV-1 infection. We later found that latently infected cells persist indefinitely even in patients on prolonged ART. These studies indicated that eradication of HIV-1 infection with ART alone would never be possible. The latent reservoir for HIV-1 in resting CD4+ T cells is now widely recognized as the major barrier to curing HIV-1 infection and is the subject of an intense international research effort. Our laboratory has gone on to characterize the different forms of HIV-1 that persist in patients on ART and to explore potential strategies for eradicating the virus. In particular, we are searching for and evaluating drugs that target the latent reservoir. We are also developing assays that can be used to monitor the elimination of this reservoir in patients participating in eradication trials. The laboratory is also interested in the basic pharmacodynamic principles that explain how antiretroviral drugs work. We have recently uncovered a previously unrecognized form of intermolecular cooperatively that explains why certain classes of antiretroviral drugs are so effective at inhibiting viral replication. We are using this discovery along with experimental and computational approaches to develop improved therapies for HIV-1 infection and to understand and prevent drug resistance. Finally, we are studying the immunology of HIV-1 infection, and in particular, the ability of some patients to control the infection without ART.
Lab Website: Robert Siliciano Laboratory
Selected PublicationsView all on Pubmed
Amy F Weil; Devlina Ghosh; Yan Zhou; Lauren Seiple; Moira A McMahon; Adam M Spivak; Robert F Siliciano; James T Stivers. Uracil DNA glycosylase initiates degradation of HIV-1 cDNA containing misincorporated dUTP and prevents viral integration. Proceedings of the National Academy of Sciences of the United States of America 2013;110(6):E448-57. View on Pubmed
Susanne Eriksson; Erin H Graf; Viktor Dahl; Matthew C Strain; Steven A Yukl; Elena S Lysenko; Ronald J Bosch; Jun Lai; Stanley Chioma; Fatemeh Emad; et al. Comparative analysis of measures of viral reservoirs in HIV-1 eradication studies. PLoS pathogens 2013;9(2):e1003174. View on Pubmed
Daniela Boehm; Vincenzo Calvanese; Roy D Dar; Sifei Xing; Sebastian Schroeder; Laura Martins; Katherine Aull; Pao-Chen Li; Vicente Planelles; James E Bradner; et al. BET bromodomain-targeting compounds reactivate HIV from latency via a Tat-independent mechanism. Cell cycle (Georgetown, Tex.) 2013;12(3):452-62. View on Pubmed