Faculty

Anthony Amoroso, M.D.
Assistant Professor
Assistant Professor of Medicine, Division of Infectious Diseases, University of Maryland School of Medicine
Director, HIV Care and Infectious Disease Clinic, Baltimore Veterans Hospital
aamoroso@ihv.umaryland.edu

Dr. Amoroso's teaching credits include the supervision and education of fellows, residents and students at the Evelyn Jordan Center clinic, VA hospital, and inpatient teaching service at the University of Maryland Medical System.

Dr. Amoroso was invited to speak at the 12th Annual Maryland Conference on AIDS: A Challenge to Primary Care in Oct 2000 and the State Department Medical Core, Primary Care Conference on AIDS in Africa: Challenges and Limitations held in Petoria, South Africa in April 2001 and 2002. He has authored a chapter in the text book AIDS in Africa, 2nd ed. "The Use of Antiretroviral Therapy in Resource Limited Countries."

Dr. Amoroso graduated with honors from Georgia Institute of Technology and received his M.D. from the Medical College of Georgia, graduating Summa cum Laude. While at the Medical College of Georgia, he received the School of Medicine Academic Scholarship award and the Department of Medicine Clinical Scholar Award. He is board certified in Internal Medicine and Infectious Diseases. In 1999, he received the SHEA/CDC Certification in Hospital Epidemiology.

Education

• M.D. - Medical College of Georgia (summa cum laude)

Research Interests

Currently, Dr. Amoroso is an active investigator in several HIV treatment studies in the Institute's clinical research unit. Dr. Amoroso has designed several trials evaluating the role of G1 cell cycle agents in the treatment of HIV. His primary research interests are developing antiretroviral combination therapy for resource limited countries, chemokine and co-receptor dynamics, and HIV therapeutic vaccine development.

Current Treatment Limitations
Although treatment with antiretroviral therapy causes profound suppression of HIV replication and results in improvements of immune function, it is limited by high costs, toxicities and is difficult to adhere to. Moreover, the chance of achieving long term control of HIV infection with antiretroviral therapy alone seems very unlikely. Multiple studies have indicated that current antiretroviral therapy is insufficient to completely eradicate HIV from infected individuals. The data provides no evidence that the amount of residual virus is decreasing with time on typical antiretroviral therapy (2 NRTI and 1 PI). After stopping antiretroviral therapy, the viral load can rebound to higher levels than pretreatment viral loads. Rebound rates seen after 1 to 5 years of antiretroviral therapy are similar to those seen after short courses of therapy. Antiretroviral therapy demands stringent adherence to complex dosing regimens. The rate of virological failure over a 6-month period of time has been demonstrated to be as high as 60% in patients that cannot achieve greater then 95% adherence. The combination of multiple adverse side effects associated with antiretroviral therapy and the availability of this treatment to only 1 in 40 of the estimated 40 million people infected world wide has prompted us to reconsider the current strategies for achieving the goals of HIV therapy. A more rational approach to therapeutic interactions is needed, with the focus shifted towards maintaining long term, relative viral control.

The Importance of Biological Compartments
The importance of different body compartments (i.e., blood, tissue, central nervous system), cell types (T-cell, macrophages) and cellular compartments (resting or activated) as potential HIV reservoirs has been realized. And although different antivirals have activity in different compartments, to date few trials have focused on treatment agents that are active in all biological compartments. One such strategy would be to use agents that are aimed at decreasing HIV in the active and resting cell compartments. Resting lymphoctyes are a major reservoir for HIV. It is therefore important that antiretroviral therapy be capable of suppressing HIV in both resting and activated cells.

In addition, studies on HIV viral dynamics have shown that from the earliest stages of infection there is massive viral production by actively replicating lymphocytes. There is also evidence that stimulating the immune system increases the viral load. If HIV replication is dependent on the activation of T cells than one should be able to exploit this by using agents, which decrease activated T cells. By using our insight on the importance of cell cycles in the treatment of HIV, it would appear that agents which target cellular cycles could be used successfully in HIV treatment. If such a result could be shown, the impact of cyclic therapy in cost, side effects, and availability could be greatly increased.