By the time she is about three years old, a child has usually endured her first influenza infection. If it’s a nasty bout, her temperature will rise and her muscles will ache. She’s probably young enough that she won’t recall the illness — but her immune system will.
When the virus enters her body, its presence prompts a pool of immature, unprogrammed immune cells to start competing to become the flu’s tracker and assassin. The winners — cells that bind most strongly to the virus — store a memory of the pathogen, ready to recognize and attack it the next time it strikes.
But influenza is an inveterate shape-shifter. Regions of its outer proteins can mutate as it replicates, allowing it to avoid immune detection. When infections with new flu strains occur later in life, the immune system will mount a response based on that first encounter, reacting strongly to recognized regions of the virus, but not to any that have changed. Immune cells can’t tailor any novel antibodies that could help.
How exactly the immune system ‘imprints’ on its first-encountered strains presents a tantalizing puzzle to flu researchers — and solving it could help to combat the virus and improve vaccines.