RNA viruses like influenza are prone to mutation (DNA-based lifeforms are much better proofreaders), and type A influenza has become a master shapeshifter, depending on its instability for its very survival. Since animals that survive viral infections develop anitbodies that prevent further attack by the same virus, it’s only by changing the nature of its surface proteins that influenza can keep tricking its hosts’ cells into letting it in year after year. The virus itself can change so quickly that it becomes unrecognizable to the immune system of animals over the course of a single season. That’s why humans — and influenza-prone animals, like this chicken — need a new flu vaccine each fall.

Influenza can mutate in response to environmental changes (exposure to antiviral drugs, for example) but it also changes its genetic identity as a matter of habit as it replicates within cells. If two different strains of influenza virus attack the same cell, they end up “sharing” in the takeover of the cell’s reproductive machinery, and in the process of producing new virus particles they end up sharing genetic information. If they simply exchange a few amino acids, the process is known as recombination. If the two strains swap entire RNA strands, the process is known as reassortment.

Small changes in the flu’s genetic code are known as antigenic drift, and it is the constant drift in flu viruses that accounts for yearly seasonal epidemics. Wholesale reshufflings of the virus (such as the swapping of one HA- or NA-protein for another) are referred to as antigenic shift. While antigenic drift within a flu subtype can result in wide variations in virulence, antigenic shifts are thought to be the events that trigger pandemics, since they can result in entirely new subtypes that can “jump” to new species which have no natural immunity to their combinations of surface proteins.

Credit: FAO