July 24, 2014 |
Treatment of HIV patients co-infected with the hepatitis C virus (HCV) with an anti-retroviral drug therapy not only tackles HIV, but also reduces HCV replication, according to a new study led by a University of Cincinnati researcher.
The results were published Wednesday, July 23, 2014, in Science Translational Medicine
Previously, physicians treating co-infected patients worried that HIV antiretroviral therapy might injure the liver to the detriment of patient health, says Kenneth Sherman, MD, PhD, Gould Professor of Medicine and Director in the UC Division of Digestive Diseases in the College of Medicine.
Literature in the 2000s seemed to support that stance, prompting Sherman and the team of researchers from UC and elsewhere to intensively study the two-year experiences of 17 patients co-infected with HIV and hepatitis C. The patients received already approved HIV antiretroviral drug therapies, but underwent frequent evaluation and sampling of blood so that minor changes in the virus and the immune response could be captured.
In a subset of patients there was an initial increase in serum ALT (a marker of liver injury), hepatitis C or both during the first 16 weeks. However, over a period of 18 months researchers found that viral loads for HCV returned to what was expected in a mono-infected patient suffering from HCV without HIV, says Sherman. Initial liver injury actually resulted from effective HIV treatment and not from toxicity.
“The drop in HCV viral levels was a big surprise and not what we necessarily expected,” Sherman says.
In the United States, 200,000 to 300,000 people have HCV/HIV co-infection, while worldwide estimates range from 4 million to 8 million people, according to Sherman. Physicians can use Sherman’s study results to better plan treatment for HIV patients co-infected with hepatitis C.
“There is a complex interaction of biological effects when patients are infected with both HIV and the hepatitis C virus,” Sherman explains. “Initial response to HIV treatment results in a transient increase in HCV viral replication and evidence of liver injury. However, over time HIV suppression leads to reduced HCV replication.”
“This process is highly modulated by down regulation of the interferon-responsive gene family,” adds Sherman, who led the study. “The findings suggest that HIV suppression with antiretroviral medications play an important role in the management of individuals with HCV and HIV infection. It supports the concept that in those with HCV/HIV infection early and uninterrupted HIV therapy is a critical part of preventing liver disease.”
Other UC researchers who were part of the study included: Mohamed Tarek Shata, MD, PhD, associate professor in the division of digestive diseases; Jason Blackard, PhD, associate professor in the division of digestive diseases; Judith Feinberg, MD, professor of infectious diseases; Susan Rouster, principal research assistant in the division of digestive diseases; and Bruce Aronow, PhD, professor of pediatrics.
The study was funded by the National Institute of Allergy and Infectious Diseases. It also received support for clinical aspects of the study such as drug initiation and liver biopsy from UC’s Center for Clinical and Translational Science and Training (CCTST). CCTST is the academic home of the university’s institutional Clinical and Translational Science Award from the National Institutes of Health.
The project was also supported by the National Center for Research Resources and the National Center for Advancing Translational Sciences. Portions of this work were performed under the auspices of the U.S. Department of Energy. Bristol-Myers Squibb and Gilead Sciences provided antiretroviral medications at no charge. They had no role in the design, performance or interpretation of this study.