Researchers in Florida have created an artificial molecule which has managed to keep four monkeys free from HIV infection despite being injected with large doses of the virus.
Scientists at the Scripps Research Institute in Jupiter, Florida say the lab-made molecule mimics one of our immune system’s antibodies and may have more protective power than any defence our bodies can currently produce.
Here’s how it works, according to the American Association for the Advancement of Science:
HIV infects white blood cells by sequentially attaching to two receptors on their surfaces.
First, HIV’s own surface protein, gp120, docks on the cell’s CD4 receptor. This attachment twists gp120 such that it exposes a region on the virus that can attach to the second cellular receptor, CCR5.
The new construct combines a piece of CD4 with a smidgen of CCR5 and attaches both receptors to a piece of an antibody.
In essence, the AIDS virus locks onto the construct, dubbed eCD4-Ig, as though it were attaching to a cell and thus is neutralised.
The Scripps Research team infected four monkeys with eCD4-Ig, forcing the monkeys’ cells to mass produce the molecule. The monkeys were then “challenged” with high doses of an AIDS virus for up to 34 weeks. None of the animals became infected.
“The animals had no detectable immune response against the eCD4-Ig, presumably because it is so similar to pieces of their own cells,” Scripps’ viral immunologist Michael Farzan said.
The new study follows a similar gene therapy approach with natural antibodies that also showed promise in monkey experiments, according to AIDS vaccine researcher Nancy Haigwood of Oregon Health & Science University in Beaverton.
“It’s really very creative and a breakthrough as far as I am concerned,” Haigwood said.
However, not everyone is convinced, with Nobel laureate and virologist David Baltimore from the California Institute of Technology noting that the research is restricted to test-tube and animal data.
“It’s perhaps a better construct than the antibodies we’ve been using, but it’s a matter of how it plays out in human trials,” he says.
“I don’t think it’s easy to tell how that will happen.”
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