When the study began, there was no vaccine for the novel 2009 H1N1 strain. The researchers hoped to use the antibodies from patients who recovered as therapy for those who were severely ill with this emerging virus.
The researchers began by analyzing antibody responses from nine patients recruited through the Hope Clinic, the clinical division of the Emory Vaccine Center. In these patients, ages 21 to 45 years old, the virus caused a range of illness, from mild to life-threatening disease.
The researchers identified white blood cells from the patients that made antibodies against the virus, then isolated antibody genes from individual cells. They used the genes to produce antibodiesa total of 86 varietiesand then tested which flu strains the antibodies reacted against.
Five antibodies isolated by the team could bind all the seasonal H1N1 flu strains from the last decade, the devastating "Spanish flu" strain from 1918, plus a potentially lethal H5N1 avian flu strain.
This indicated that "while the flu changes from year to year, some core elements have been consistent for nearly a century," said Wilson.
The cross-reactive antibodies were produced by highly mutated antibody genes. These antibodies appear to have been produced by white blood cells that had been exposed to influenza in previous years and were reactivated by a new viral infection. As the antibody genes, developed to combat one strain, adapted to a new infection, they continued to mutate, increasing their affinity for certain key targets present on both strains.
Half of the cross-reactive antibodies the team identified attached to the virus's "stalk" region, a sort of biochemical drill-bit the virus uses to enter cells. Because this part of the virus doesn't change as much as other regions, scientists have proposed to make it the basis for a vaccine that could provide broader protection.
"Previously, this type of broadly protective
|Contact: John Easton|
University of Chicago Medical Center