The drug, bavituximab, takes a novel tack in confronting viruses, which are notorious for mutations that evade or resist conventional pharmaceutical molecules.
Instead of confronting the intruder head-on, bavituximab waits until the virus has infected the cell.
At that point, a fatty molecule called phosphatidylserine, which is normally positioned on the cell wall’s internal surface, flips to the outside of the cell.
Bavituximab then latches onto the phosphatidylserine, sending a red flag to the body’s immune system to dispatch white blood cells to destroy the infected cell.
In a study in Nature Medicine, published by the London-based Nature group, bavituximab was put through its paces among guinea pigs infected with Pichinde virus—a close relative of the Lassa fever virus, considered a potential bioterror weapon by the Pentagon.
Animals that had not been inoculated with bavituximab were all killed; those who had received the injection had a 50-percent survival rate. By giving the bavituximab group an additional injection with a standard anti-virus drug called ribavirin, the survival rate rose to 63 percent.
The drug also provided 100-percent protection amongst mice exposed to a virus called cytomegalovirus (CMV), whereas only 25 percent of untreated animals survived.
Co-author Philip Thorpe, a professor of pharmacology at UT Southwestern Medical Center in Texas, said the findings were exciting, for they raised the prospect of a “completely new class” of anti-viral drugs that may also sidestep the problem of mutation.
“By targeting a property of the host cell rather than the virus itself, anti-PS [phosphatidylserine] antibodies have the potential to treat a range of viral infections,” he said in a press release.
“They should be less susceptible to the viral mutations that contribute to the development of drug resistance.”
Bavituximab, a monoclonal antibody, is currently in clinical trials by Peregrine Pharmaceuticals Inc. of California to treat patients with hepatitis C.
Previous research has shown that phosphatidylserine-flipping occurs in cells infected with influenza, the herpes simplex virus, viruses in the families of the smallpox and rabies viruses as well as HIV, UT Southwestern Medical Center said.
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