The influenza viruses are a bit different from other viruses that infect and affect our respiratory tract. Their genetic material – the stuff that acts as the blueprint to make and assemble its proteins – comes in multiple pieces instead of one strand. An influenza virus is the sum of its parts.
First up, let’s take a quick look at how a few of the viruses that infect us, make the proteins they use to replicate more of themselves after they’ve commandeered our cells for their nefarious purposes.
These viruses cause the common cold and trigger a lot of 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 assemble into the shell structure and pieces that have enzymatic functions to help make more of itself.
Some of these viruses cause the common cold and croup while others infamously cause SARS 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 used to make more of itself but also makes a range of shorter RNA strands that each serve as templates from which different proteins are produced through more complex processes.
So far we’ve talked about single-stranded genomes. One thread of many joined molecules the order or which determines what protein product, or structure, or function will is produced. They are examples of monopartite (one part) genomes.
Influenza viruses have multipartite (many part) genomes. Their genome is the sum of its seven or eight parts. Each piece encodes one or more proteins.
There are 4 known influenza virus (flu) types called 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 infect humans exposed to an infected animal as well. 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 lots of energy looking at the H and N genes. With good reason. These produce proteins (Hemagglutinin and Neuraminidase) that stick out of 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 noticed by and are a major target for, our immune response to flu viruses. We track them both at the protein level and the genetic level. Each year, labs test the H and N proteins from some of the circulating flu viruses detected from ill patients to make sure those viruses remain similar to those contained in our seasonal vaccines; to ensure that they are a close match.
H and N are also used when we talk about 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 own distinguishable proteins and the diversity doesn’t end there. Within any give H or N gene, whether its H1 of H18, there is ongoing mutation changing the proteins enough for them to look different to our immune system over time. This is a way that viruses produce new variants able to thrive because they can escape 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. But we don’t watch those other genes to the same extent that we watch 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