Research Team Probes Cocaine, HIV/AIDS Drug Interactions
Posted January 31, 2011 | Atlanta, GA
Researchers at Georgia Tech and Emory University are investigating the biochemical mechanisms behind cocaine and anti-retroviral drug interactions in mouse models of AIDS to improve treatment strategies.
Funded through a new $5.7 million grant from the National Institute on Drug Abuse of the National Institutes of Health, the study is being led on the Georgia Tech side by Eva Lee, professor in the H. Milton Stewart School of Industrial and Systems Engineering and director of the Center for Operations Research in Medicine.
Researchers agree cocaine injures the heart and predisposes users to HIV/AIDS because of risky behaviors. The anti-retroviral medicines used to treat HIV/AIDS also may adversely affect the cardiovascular system. Used together, cocaine and anti-retroviral therapy can amplify the injury from each.
Lee is working with cardiac pathologist William Lewis, who is the principal investigator of the study and a professor of pathology and laboratory medicine in Emory University School of Medicine.
“The model must be capable of incorporating large amounts of heterogeneous data, including genomic, biochemical, physiological and pathological,” Lee said. “Identifying the discriminatory features and constructing the predictive systems network will offer fundamental understanding of cocaine, HIV/AIDS and antiretroviral nucleosides interaction at multiple levels. … This will shed light on promising avenues for improving treatment strategies.”
It is estimated that more than 34 million Americans have used cocaine and more than 1.5 million are habitual users. More than a million Americans are infected with HIV or have full-blown AIDS.
For decades, cocaine has been thought to increase the risk for HIV infection, Dr. Lewis said.
“HIV/AIDS, along with the use of cocaine and NRTIs [nucleoside reverse transcriptase inhibitors] may lead to cardiomyopathy, a prevalent, life-threatening illness,” he said.
Researchers want to formulate a testable hypothesis on what mechanisms lead to cardiomyopathy and heart failure in AIDS and non-AIDS conditions.