Anti-AIDS Drugs Could Worsen Hepatitis C, Study Finds
Researchers fear that some new anti-AIDS drugs could exacerbate existing hepatitis C infections or promote new ones.
At least one promising new family of anti-AIDS drugs targets a cellular receptor which, when disabled, makes hepatitis C infections much more serious, German researchers said here Tuesday. The drugs mimic a genetic mutation that inhibits the entry of the AIDS virus into human cells, the researchers said.
About 30% of HIV-positive people are also infected with the hepatitis C virus, which can be deadly in its own right. The discovery could prevent use of the new drugs in this population, sharply limiting their utility.
But the discovery also could provide new insights into how to control hepatitis C infections, said Dr. David Ho of the Aaron Diamond AIDS Research Center in New York City. “This is certainly a novel observation” that highlights the way genetic differences between people affect the progression of AIDS, he said.
The receptor in question is called CCR5 and was discovered about five years ago. It is not the primary site through which HIV invades cells, but its participation is essential for the most common type of AIDS virus to initiate a productive infection.
About 1% of the population--mostly Caucasians--carries a mutant form of CCR5 called delta-32 that is associated with resistance to HIV. Such people generally do not become infected with HIV, and if they do, the infection does not progress to full-blown AIDS.
It has not been clear, however, what, if any, adverse effects the mutation has for the person carrying it.
Dr. Rainer P. Woitas and his colleagues at the University of Bonn studied the mutation in patients who were infected with HIV alone, with hepatitis C alone, or with both.
They reported at the eighth annual Retrovirus Conference here what Woitas called “a striking increase” in mutations in the hepatitis C patients.
They found that the delta-32 mutation was three to five times more common in patients with hepatitis C infections than it was in the population at large. And patients who carried two copies of the delta-32 gene had significantly higher levels of hepatitis C virus in their blood than those who had the normal form. Higher virus levels are associated with more rapid progression of the disease and more severe symptoms.
A new family of drugs called entry inhibitors--none of which have yet been approved for marketing--are designed to block HIV’s use of CCR5 to enter the cells. But using these drugs in patients who are also infected with the hepatitis C virus, Woitas warned, “would likely only exacerbate the hepatitis C infection.”
No one knows yet how the mutation produces its effects on hepatitis C.
