Unpacking Influenza: The Science Behind the Season, Part 1
Answers to the questions you've been wanting to ask.
Welcome to the first in a series where we'll take a deeper look at a familiar foe: the influenza virus. Every year, we hear about the impending "flu season," we're encouraged to get our shots, and we see headlines about rising case numbers. But to truly understand why this seasonal cycle is so relentless and why the threat can sometimes escalate to a global crisis, we first need to understand the virus itself.
This series is about empowering you with knowledge. In this first part, we'll explore the real-world impact of influenza—its burden on our communities—and then zoom in to the microscopic level to decode the virus's blueprint. We'll see how its fundamental structure is the key to understanding everything from how to control its spread to its potential to cause a pandemic.
As usual, here are some notes available for download if you'd like.
More Than "Just the Flu"
Influenza is a significant global health issue, causing up to 650,000 deaths worldwide each year. It's an acute respiratory infection that can lead to severe illness, hospitalization, and death across all age groups.
The 2025 Season in Australia: A Concerning Picture
As of early July 2025, the flu season is well and truly upon us, and the numbers are concerning. Nationally, there have been over 167,000 laboratory-confirmed influenza cases reported. In Western Australia alone, there have been over 11,000 notifications, a figure that is more than 60% higher than the five-year average for the same period.
This surge in cases translates directly to pressure on our healthcare system. In WA, there have been 1,848 flu-related hospitalizations this year, which is over 55% higher than the five-year average. We’ve also seen unnecessary deaths related to influenza in the past few weeks alone.
Compounding this issue is a lag in vaccination uptake. By the end of June 2025, overall flu vaccination coverage in WA was just 26.1%, falling significantly short of the five-year average of 33%. This trend is visible across key age groups when compared to the national average as of early July 2025:
Children (6 months to <5 years): 19.4% in WA vs. 21.9% nationally.
Adults (15 to <50 years): 17.3% in WA vs. 19.4% nationally.
Older Adults (65+ years): 58.4% in WA vs. 59.0% nationally.
This data paints a clear picture: at a time when the virus is circulating more actively, our community's shield of immunity is lower than it should be.
The Viral Envelope: Entry, Evasion, and Easy Destruction
The flu virus is an enveloped virus, meaning its RNA is wrapped in a fatty membrane it hijacks from the host cell. This “cloaked” design, studded with surface proteins, helps it sneak into other cells and sometimes evade immune detection.
But this cloak is also fragile. The envelope is easily broken down by heat, pH changes, and disinfectants—unlike the tougher shells of non-enveloped viruses. It also explains why soap and alcohol-based sanitizers work: they dissolve the lipid membrane, physically tearing the virus apart.
Clean hands = no entry.
The Segmented Genome: The LEGO-Like Blueprint
Inside that envelope lies a segmented, single-stranded RNA genome—eight separate pieces, like eight LEGO blocks.
This setup allows the virus to reassort its segments with those from another flu virus if both infect the same cell. The result? A brand-new virus, with new traits, possibly never encountered by human immune systems. This process, called antigenic shift, is how pandemics are born.
The RNA is also “negative-sense”, meaning it can’t be read directly by the host cell. The virus must first convert it into usable code (mRNA) using its own enzyme, RNA-dependent RNA polymerase. But this enzyme is prone to errors—mutations—which drive the virus’s ability to evolve rapidly and escape immunity.
The Key Proteins: How Flu Infects—and How We Fight Back
Three viral proteins play major roles in both infection and immune targeting:
Hemagglutinin (HA) – The “key” that binds to receptors on our respiratory cells, letting the virus in. This is the main target for neutralizing antibodies after vaccination.
Neuraminidase (NA) – The “scissors” that help the virus escape the cell after replicating. It’s the target for antivirals like oseltamivir (Tamiflu).
M2 Protein – A tiny proton channel that helps the virus release its genome once inside the host cell. It’s targeted by older drugs (adamantanes), although these are now less useful due to resistance.
The Virus on the Move: Drift and Shift
Influenza viruses are constantly changing. This isn’t accidental—it’s a survival strategy.
Antigenic Drift – Small, gradual mutations accumulate over time, especially in HA and NA proteins. This is why seasonal vaccines need updating each year: the virus keeps slightly changing its appearance to stay ahead of our immune memory.
Antigenic Shift – A sudden, major change. When two different flu viruses (say, human and avian) co-infect the same host, their segmented genomes can mix, creating a completely new virus. This has the potential to spark global pandemics, as we saw with the 2009 H1N1 outbreak. Influenza A poses the biggest risk here, given its ability to infect multiple species (e.g. birds, pigs, humans).
Key Clinical Takeaways
Segmented RNA genome allows reassortment (antigenic shift) → potential for pandemics.
High mutation rate from error-prone RNA polymerase → seasonal antigenic drift → annual vaccine updates.
Negative-sense RNA needs conversion to mRNA → requires viral polymerase → target for antivirals.
Lipid envelope makes virus fragile → inactivated by soap and alcohol → hand hygiene is critical.
Ongoing evolution demands vigilant surveillance, timely diagnosis, and early antiviral use.
Coming Up Next…
We’ve unpacked why influenza is no ordinary virus. Its structure makes it infectious, fragile, and ever-changing. Its genome makes it unpredictable, with the ability to drift into seasonal surges—or shift into something far more dangerous.
In Part 2, we’ll explore how we detect and track the flu in real time—from rapid swabs to cutting-edge sequencing—and what these tests can (and can’t) tell us during a flu season.
Stay tuned.