H1N1 weakness discovered that could lead to its defeat
Scientists from Rice University have discovered a weakness in the H1N1 flu virus that could lead to its defeat. The researchers discovered how the H1N1 virus invades and attacks the immune system. The findings could lead to new ways to defeat H1N1 influenza as well as other flu viruses.
The researchers went back to 1918 to study the genetic sequence of the 1918 flu to find the H1N1 flu weakness. They discovered that the virus attacks and holds on to its host through a “bottleneck” effect – an unexpected finding.
H1N1 flu residues were found by the scientists that bind to receptor sites and cause infection. It has been known that H1N1 flu attaches to its host with hemagglutinin (HA), the protein "hook". The surprise H1N1 weakness found was that the scientists discovered that both antigenic and receptor sites constantly change to avoid antibodies.
H1N1 genetic mapping was performed by Jianpeng Ma and graduate student Jun Shen and Qinghua Wang. Jianpen Ma explains, “The site is known, but no one thought it was involved in the immune system. In order to recognize the receptor, that particular region has to be robust," Ma said. "But it turns out this region is not only variable, but also interacts with the immune system."
In order for the H1N1 virus to avoid antibodies, the researchers say all five antigenic sites would have to mutate. The new research points to evidence that all five of the receptor-binding residues would also have to mutate, but not to the point that the virus detaches.
"If the binding is abolished, the virus dies," said Ma. “The virus's bottleneck [in the receptor binding residues] is our opportunity." The weak link found in the H1N1 virus provides an opportunity for scientists to monitor the virus as it constantly varies and reacts with the immune system.
The findings that H1N1 flu antigenic sites and receptor sites constantly shift to survive could lead to the development of new vaccines. "An underlying implication is that this may not be restricted to H1N1," Wang said. "It may apply to other influenza viruses as well. If studying viral evolution can help predict what will cause a severe problem in humans, you can actually pre-stock vaccines, which will save time."
The newly found H1N1 weakness seems to be in the receptor binding sites that must change to evade antibodies. It was previously thought that five sites of the H1N1 virus’s hemagglutinin (HA) were responsible for triggering an immune response. The current study shows H1N1 flu’s surprise weakness is in the receptor binding sites, that also must constantly change to survive. The findings could lead to defeating the virus as it shifts to survive and avoid antibodies.