The 2017-2018 flu season was historically severe. Public health officials estimate that 900,000 Americans were hospitalized and 80,000 died from the flu and its complications. For comparison, the previous worst season from the past decade, 2010-2011, saw 56,000 deaths. In a typical season, 30,000 Americans die.
So why was the 2017-2018 season such a bad year for flu? There were two big factors.
First, one of the circulating strains of the influenza virus, A(H3N2), is particularly virulent, and vaccines targeting it are less effective than those aimed at other strains. In addition, most of the vaccine produced was mismatched to the circulating A(H3N2) subtype.
These problems reflect the special biology of the influenza virus and the methods by which vaccines are produced.
Flu virus is a quick change artist, influenza is not a single, static virus. There are three species – A, B and C – that can infect people. A is the most serious and C is rare, producing only mild symptoms. Flu is further divided into various subtypes and strains, based on the viral properties.
Viruses consist of protein packages surrounding the viral genome, which, in the influenza virus, consists of RNA divided into eight separate segments. The influenza virus is enveloped by a membrane layer derived from the host cell. Sticking through this membrane are spikes made up of the proteins haemagglutinin (HA) and neuraminidase (NA), both of which are required for the virus to successfully cause an infection.
Your immune system reacts first to these two proteins. Their properties determine the H and N designations of various viral strains – for instance, the H1N1 “swine flu” that swept the globe in 2009.
Both HA and NA proteins are constantly changing. The process that copies the viral RNA genome is inherently sloppy, plus these two proteins are under strong pressure to evolve so they can evade attack by the immune system. This evolution of the HA and NA proteins, called antigenic drift, prevents people from developing lasting immunity to the virus. Although the immune system may be prepared to shutdown previously encountered strains, even slight changes can require the development of a completely new immune response before the infected person becomes resistant. Thus we have seasonal flu outbreaks.
In addition, various subtypes of influenza A infect animals, the most important of which, for humans, are domestic birds and pigs. If an animal is simultaneously infected with two different subtypes, the segments of their genomes can be scrambled together. Any resulting virus may have new properties, to which humans may have little or no immune defense. This process, called antigenic shift, is responsible for the major pandemics that have swept the world in the last century.
Against this background of antigenic change, every year the World Health Organization predicts which strains of flu virus will be circulating during the next flu season, and vaccines are formulated based on this information.
Jason Sparks@sparksjls
I bet you can't, can you?
