To study infectious disease outbreaks, one of the first things researchers do is to sequence the genome. We did this in real time with the Ebola outbreak in 2014, we’re doing it right now with SARS-CoV-2, and we constantly do this with the influenza virus to predict when the flu season is approaching and how well our vaccine is going to do for the upcoming year.
Understanding the genome helps scientists and doctors to determine what makes a virus so infectious or lethal. For example, the 1918 flu pandemic killed 50-100 million people, so what made that particularly flu virus so much more devastating than any other season?
The 1918 Spanish Flu
Aside from the close quarter confinements during WW1 (which undoubtedly was a catalyst for global spread), researchers needed to sequence the genome to unlock the virus’s functional profile. But genomic sequencing didn’t exist in 1918. Heck, researchers didn’t even know what a virus was in 1918!
Because the flu is no longer circulating in the population, how and collecting and storing samples was almost impossible to achieve during this time period, the only way to collect lung tissue from people that succumbed to the flu and were buried beneath the permafrost! Researchers literally went up in Alaska and found some bodies that (incredibly) still preserved viable lung tissue that harbored the virus.
If you enjoyed this so far, this is just the tip of the iceberg in what was a crash course about the flu in Dr. Jeremy Brown’s “Influenza.” In the book, Brown takes us on an influenza journey starting with its history, how people forecast the flu, vaccine predictions, our immune response, pandemic potential, and more in just under 200 pages.
Influenza
What I really appreciated was how Brown was able to so elegantly describe very complex subjects in such simple terms. For instance, in Chapter 2 he relates our innate immune phagocyte cells to traffic police: always on patrol looking for prior criminals (previous pathogens). He then immediately compares our adaptive immune antigen presenting T cells to detectives: they profile a suspect (new pathogen) to present to other cells for disposal.
Brown also touches on policy related issues regarding the flu. One topic was the potential of “dual-use” research and its implications in biosecurity. For example, when researchers sequenced the 1918 pandemic flu strain, they uncovered why it was devastating to humans across the world (if you want to know I suggest reading the book!). But doing so allows modern researchers to perform “gain of function” experiments, where researchers can manipulate the flu genome (just 8 simple genes) to see what happens in its overall functional: Is it more or less lethal? Can it go airborne? Is it more or less infectious?
Essentially, this opens the door to creating a new biological superbug. One in which could get out and risk causing another devastating global pandemic, whether by accident or on purpose.
Policymakers must to determine the impact of these factors when they consider implementing laws about scientific vigor and emerging technologies. Additionally, we have so much more to learn about infectious diseases that it could be argued that it behooves us to do as much research as possible to further our understanding and save potential lives that become infected.
If these types of questions interest you, especially in light of COVID-19, this book is for you. I give it a solid 4/5, solid quick read.