Influenza viruses are distinct from other viruses that infect and affect the respiratory tract. Their genetic material—the stuff that acts as the blueprint to make and assemble their proteins—comes in multiple pieces instead of one strand. An influenza virus is the sum of its parts.

Virus genomes

First, let’s take a quick look at how a few of the viruses that infect us use the proteins they produce to replicate more of themselves after commandeering our cells for their nefarious purposes.

Rhinoviruses

These viruses cause the common cold and trigger numerous asthma exacerbations.

Inside their protein shells, they carry their genetic material on a single strand of about 7,000 joined-together molecules called the genome.

That one strand encodes the genetic blueprint to produce a protein (called a polyprotein). That stand is also used as a template to make more of itself.

The polyprotein gets broken into the bits (peptides) that are assembled into a new virion (single virus) and includes pieces that form the shell structure and pieces that have enzymatic functions to help replicate more of itself.

Coronaviruses

Some of these viruses cause the common cold and croup, while others are infamous for causing SARS, COVID-19 and MERS. Coronaviruses have a layer of fat (envelope) outside their protein shell that’s embedded with club-shaped protein spiked that give them their crown-like appearance. They have a much bigger genome strand than the rhinoviruses.

The coronavirus genome acts as a template to produce more copies of itself. Still, it also generates a range of shorter RNA strands that serve as templates for the production of different proteins through more complex processes.

Influenza viruses

So far, we’ve talked about single-stranded genomes. One thread of many joined molecules, the order determines what protein product, structure, or function will be produced. They are examples of monopartite (one part) genomes.

Influenza viruses have multipartite genomes (meaning they have multiple parts). Their genome is the sum of its seven or eight parts. Each piece encodes one or more proteins.

There are four known influenza virus (flu) types: influenza A virus, influenza B virus, influenza C virus, and influenza D virus (shorthand: IFAV, IFBV, IFCV, and IFDV).

IFDV is a cattle and swine virus, but it can also infect humans exposed to an infected animal. IFCV infects humans in childhood but is not identified in epidemics. These viruses have 7 genes.

The flu viruses we identify most frequently are the seasonal IFAVs and IFBVs that infect humans in epidemic proportions each year. These have 8 genes.

The two influenza virus genes we obsess over

We expend a lot of energy examining the H and N genes. With good reason. These produce proteins (Hemagglutinin and Neuraminidase) that protrude from the surface of the flu virus. They help the flu virus bind to a new cell and infect it, and they let newly produced flu viruses break free of an infected cell after they’ve assembled at its surface.

H&N are recognised by and are a major target of our immune response to flu viruses. We track them at both the protein and genetic levels. Each year, labs test the H and N proteins from some of the circulating flu viruses detected in ill patients to ensure that these viruses remain similar to those contained in our seasonal vaccines, thereby verifying a close match.

H and N are also used when discussing IFAV subtypes. You’ll know this if you’ve read about H1N1 or H3N2 viruses in the news. Or when “bird flu” was in the news more, H5N1 and H7N9.

The As have a lot of H and N

Influenza A is a diverse type of flu. There are 18 quite distinct H genes and 11 different N genes. They make their distinguishable proteins, and the diversity doesn’t end there. Within any given H or N gene, whether it’s H1 or H18, there is ongoing mutation changing the proteins enough for them to appear different to our immune system over time. This is a way that viruses produce new variants that can thrive because they can evade the patrolling response.

And the rest of the genes?

We also know that mutations in other flu virus strands can have a range of effects on the new variant viruses that result. However, we don’t monitor those other genes to the same extent as we do H and N. It might be time to dif that more than we have. We have the tools. There are questions that might be answered if we consider the whole virus and not just some of its parts

Updates

• 01MAY2025 – Fixed some typos and added to SEO.