Rama Rao Amara, Ph.D.
Area of Research: HIV/AIDS
As a research associate in the laboratory of
Dr. Harriet Robinson, Dr. Amara played a major role in the preclinical
development
of the AIDS vaccine now in Phase I clinical trials. Now as
an EVC faculty member, Dr. Amara is working to develop a version
of this vaccine that could be used to control AIDS on the Indian
subcontinent, where the strains of HIV that predominant differ
from those most frequently transmitted in the U.S. and other
Western countries.
Dr. Amara is a Research Associate Professor in the Division
of Microbiology and Immunology of the Yerkes
National Primate Research Center of Emory
University, and Associate Professor
in the Emory School
of Medicine Department of Microbiology and
Immunology. He received his Ph.D. in molecular
biology and immunology from the Indian Institute of Science
in Bangalore, India, and did his post-doctoral training at Emory.
research
The goal of our lab is to develop vaccines for
HIV/AIDS with a major emphasis on therapeutic vaccines. There
are currently about 40 million individuals living with HIV worldwide,
with 16,000 people newly infected every day. Without question
the AIDS epidemic represents a major threat to public health,
economic development, and cultural stability worldwide. The introduction
of drugs that control virus replication and improved treatment
regimens like HAART have succeeded only in prolonging the lives
of some infected individuals fortunate enough to have access
to the medications. These anti-viral drugs do not cure infection,
and are associated with several significant problems, including
serious side effects, prohibitively high cost, the need for rigorous
adherence and the potential for developing viral resistance.
For these reasons, development of a safe and effective HIV vaccine
is imperative.
Cellular immune responses are critical for the
control of HIV replication. In particular, CD8 T cells play a
major role in
restricting the growth of virus and eliminating virus-infected
cells. In the presence of antigen and inflammatory signals, cognate
naïve CD8 cells expand and traffic to infection sites, where
they lyse virus-infected host cells. However, CD8 T cells from
HIV-infected individuals have been shown to be non-functional.
Our efforts are focused on understanding the phenotypes of protective
CD8 T cells and the mechanisms of their generation and maintenance.
CD4 T cell help is critical for raising effective anti-viral
CD8 T cells. Following viral infection, CD8 T cells generated
in the absence of CD4 help do not expand and kill virus-infected
cells efficiently. Individuals with AIDS loose their anti-viral
helper CD4 T cells due to preferential killing of these cells
by HIV. This becomes a major limitation when therapeutically
vaccinating AIDS patients to generate functional CD8 T cells.
To overcome this problem, we are currently developing strategies
that can substitute the requirement of CD4 T cell help for
generating functional CD8 T cells.
These above discussed strategies
will enormously improve our ability to develop effective therapeutic
vaccines and vaccine
regimens against HIV/AIDS.

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