The immune system has the capacity to “remember” particular viruses and store those details in B memory cells that reside in the lungs to help ward off future infections. But a new study shows the flu virus takes advantage of this and uses the way the memory cells store its details to recognize and kill them, thus wiping out the immune system’s first wave of defense against virus re-infection.
The study, which was led by the Whitehead Institute for Biomedical Research in Cambridge, MA, is published online in a recent issue of Nature.
When a virus enters the body, the immune system sets about creating virus-specific B cells that make antibodies specific to the pathogen so they can bind to it and disarm it.
These memory cells multiply and give off antibodies that slow down virus proliferation and it eventually dies away.
In the case of the flu virus, the immune system then retains a population of virus-speficic B cells in the lungs – they are on “standby” should the virus try to reinfect at a later date.
The memory B cells hold their virus-specific information in high-affinity virus-specific receptors on their cell surfaces, so they are ready to spot and bind to that particular virus when it arrives.
But it seems that their strength is also their weakness, because the flu virus uses this show of arms as a way to locate those very cells, gain entry into them, and set about destroying their antibody factories, and eventually destroy the cells themselves.
Having thus disarmed the immune system’s first line of defense, the virus has now bought enough time to replicate itself to a sufficient level to cause infection before the immune system has time to respond with a second wave.
Study co-author and postdoctoral researcher Joseph Ashour says:
“We can now add this to the growing list of ways that the flu virus has to establish infection.”
To demonstrate this sequence of events, the team used mice they had bred to have B cells that were specific to a particular strain of flu.
The procedures they used were complex, but they enabled them to track the interaction of a specific flu virus with B memory cells in an unprecedented way to establish exactly how the virus neutralizes B cells specific to itself.
The team sees no reason why this might not work for other types of virus, as co-author Stephanie Dougan, also a postdoctoral researcher, explains:
“We can now make highly effective immunological models for a variety of pathogens. This is actually a perfect model for studying memory immune cells.”
Dr. Ashour says the study could lead to more effective vaccines for seasonal flu and may even suggest new ways to create immunity.
Funds from the Cancer Research Institute, the National Institutes of Health, the Pancreatic Cancer Action Network and the Human Frontiers Science Program helped finance the study.
In 2012, researchers from Northwestern University published a study that gave another example of how the flu virus disrupts the immune system. They showed the virus decreases the production of key immune system-regulating proteins by altering the expression of genetic switches in human lung cells.