When a person becomes infected with HIV, the immune system kicks into gear: Immune cells called B cells build antibodies, tiny protein warheads that seek out and destroy viruses. But because HIV mutates so rapidly, these antibodies are generally ineffective—by the time B cells learn to build antibodies against one version of HIV, a new viral mutant has already taken over.
In some patients, the immune system manages to make antibodies that actually work against a broad spectrum of HIV mutants, but those antibodies typically emerge only five or six years into the infection. And by that point, their efforts may be too little, too late. “Once you already have an established infection with millions or billions of viral particles in an infected individual, even with a potent antibody response, it's too late to shut everything down,” explains Satish Pillai, a researcher at the Blood Systems Institute of San Francisco.
These more effective antibodies can’t reverse the damage done to other immune cells over the preceding several years, but they can reduce the virus’s numbers and slow down the progression of the infection. Researchers have long speculated that if they kicked in early, they may be able to prevent HIV from gaining a toehold in newly infected individuals. But without knowing where these elite antibodies come from, it’s hard to pursue the idea much further.