By determining the genetic sequence of influenza viruses over a decade, scientists learn how the flu is evolving.
A major obstacle to combating influenza is the virus causing the flu is quickly evolving. Every flu season, the virus is different enough from the previous season that a new vaccine needs to be produced and redistributed. This is a major public health concern. Vaccinating everyone each time a new vaccine comes out is not an option, so the elderly and more vulnerable populations are prioritized. Additionally, since predictions need to be made for the upcoming flu season, the vaccine might not be perfectly effective. If the evolution of the influenza virus could be better understood, a more comprehensive approach to preventing flu outbreaks could potentially be developed.
To get a better idea of influenza viral evolution, scientists at Duke-NUS Graduate Medical School studied the genetic composition of 900 flu viral samples that infected humans over the last thirteen years. Specifically, they examined two strains of influenza type B viruses named “Victoria” and “Yamagata.”
By looking at the genetic content of Victoria and Yamagata (The DNA that makes each virus unique), it turned out that Victoria and Yamagata have very distinct evolutionary pasts. The Victoria virus has been quickly evolving over the past decade. Although different Victoria viruses are related to each other, they are not exactly the same. Specific varieties of Victoria viruses last for only a few years before they were overtaken by other variations of Victoria. This constant evolution of Victoria is what is seen in a well known type A strain of influenza, H3N2.
Conversely, Yamagata has been under less pressure to evolve. A large variety of Yamagata viruses have been present at all times, but each variety persisted for many years. This led to very little evolution of Yamagata over the last decade. Without much change to genetic composition, Yamagata has been circulating in the human population for over a decade.
While studying the evolution of influenza, the scientists also noticed a striking difference in the patients that Victoria and Yamagata infected. For the Victoria virus, more than 75% of cases were in children less than 18 years old. In addition to infecting youth, the Yamagata virus was able to infected the elderly to a significant extent. Over 50% of Yamagata infections were in patients over 18 years old, with 30-50 year olds being additionally susceptible. The link between age of infection and rates of evolution in Victoria and Yamagata remain unclear.
These insights into how the influenza virus evolves have direct implications for how the flu could be contained in future seasons. Since the Yamagata virus is slow to evolve over many years, targeted vaccines that would not need to be updated every season might be sufficient to control the spread of Yamagata. Currently, influenza vaccinations do not target Yamagata strains, so incorporating Yamagata strains into the vaccination could be beneficial. In contrast, the quickly evolving Victoria might require a novel approach to contain.