Influenza virus is a pretty fascinating virus, primarily because of its tremendous ability to change. The versatility of the virus is described as "the chameleon-like power to mutate keeps them ahead of the game". These creepy RNA viruses, as we know, enjoy negotiating with their hosts. They are not like DNA viruses or bacteria that can cause diseases with high mortality. Instead, they stay with the hosts while performing their amazingly high-speed evolution, by both antigenic shift and antigenic drift.
Antigenic drift refers to mutations in surface glycoproteins of the viruses (hemagglutinin and neuraminidase). The high rate of mutation (an error rate between 1×10−3 and8×10−3 substitutions per site per year) is due to the lack of proofreading mechanism of viral RNA polymerase. The mutations that happen in the receptor binding site of the antigens will result in the failure of host immunity recognition and the subsequent immunity evasion.
Another mechanism that keeps influenza virus changing is antigenic shift, which is known as reassortment of genome segments from different strains. The most telling example of antigenic shift, the swine-origin H1N2 in 2009, is the result of triple reassortment. The virus contains four segments from classic American swine influenza virus, two segments from human influenza virus and two from avian lineage. The reassortment of the virus causes new host adaptation and pandemic formation, posing great threat to public health.
Here is a review article that depics the evolution of influenza A viruses