The influenza virus is a microscopic agent that causes the flu, a highly contagious respiratory illness. Each year, it leads to widespread outbreaks affecting millions of people globally and placing a burden on healthcare systems. The virus invades cells in our respiratory tract, using them to create countless copies of itself. Understanding the molecular components of this virus reveals how it is built, how it functions, and why it remains a persistent public health challenge.
The Architecture of the Influenza Virus
The infectious particle of the influenza virus, known as a virion, is a microscopic, spherical structure about 80 to 120 nanometers in diameter. Its outermost layer is a lipid membrane that acts as a protective envelope. This envelope is borrowed from the membrane of the host cell it last infected, which helps it camouflage itself from the host’s immune system.
Embedded within this lipid envelope are proteins that appear as spikes on the virion’s surface. Beneath the envelope lies a rigid shell made of a viral protein called M1, or matrix protein. This M1 layer provides structural integrity, giving shape to the lipid membrane. It acts as a scaffold, holding the virion together in a stable package.
Within the protective M1 shell is the virus’s core, which contains its genetic material. For influenza A and B viruses, this material is organized into eight separate segments of RNA. This collection of genetic segments is what the virus needs to replicate once it successfully enters a host cell.
Key Surface Molecules
The surface of the influenza virion is studded with two main types of glycoprotein spikes: Hemagglutinin (HA) and Neuraminidase (NA). These proteins are the virus’s primary tools for interacting with host cells and are used to name different influenza A subtypes, such as H1N1 or H3N2. The numbers refer to the specific variant of the HA and NA protein on that virus.
Hemagglutinin acts like a key, enabling the virus to attach to and enter a host cell. The HA protein binds to sialic acid molecules on the surface of respiratory cells. This binding triggers the host cell to engulf the virus through endocytosis. Once inside, a change in acidity causes the HA protein to alter its shape, fusing the viral envelope with an internal membrane and releasing the virus’s genetic material into the cell.
After the virus has replicated inside the host cell, new virions need a way to escape. This is the role of neuraminidase, which functions like molecular scissors. As new virus particles bud from the cell surface, their HA proteins can get stuck to sialic acid receptors. NA cleaves these connections, cutting the new virions free so they can disperse and continue the infection cycle.
The Genetic Core
Unlike humans, the influenza virus uses ribonucleic acid (RNA) as its genetic blueprint, not DNA. The viral RNA is “negative-sense,” meaning it must first be copied into a “positive-sense” strand before it can be used to make new viral proteins. This copying process is performed by an enzyme the virus carries with it.
A distinctive feature of the influenza virus’s genome is its segmentation. Its blueprint is broken into eight separate RNA segments for influenza A and B viruses, rather than one continuous strand. Each segment carries the code for one or more proteins the virus needs to replicate, such as HA, NA, and M1. This structure is like an instruction manual divided into eight unbound pages.
This segmented structure is a characteristic of the Orthomyxoviridae family, to which influenza viruses belong. Each of the eight RNA segments is packaged as an individual ribonucleoprotein complex (RNP). The virus has a mechanism to ensure one copy of each of the eight unique segments is packaged into a new particle. This organization is central to the virus’s ability to evolve rapidly.
How Flu Molecules Drive Viral Evolution
The constant evolution of the influenza virus is why a new flu vaccine is often needed each year. One primary mechanism for this change is antigenic drift, which involves small, gradual mutations in the genes for the HA and NA surface proteins. As the virus replicates, these minor changes accumulate and can alter the shape of the proteins. This prevents antibodies from a previous infection or vaccination from recognizing them effectively.
A more dramatic evolutionary mechanism is antigenic shift, a direct consequence of the virus’s segmented genome. This process occurs when two different influenza A strains, such as a human and an avian strain, infect the same host cell. Inside that cell, the eight RNA segments from both viruses can be mixed and matched as new virions are assembled.
This reassortment can create a hybrid virus with a new combination of HA and NA proteins. If this virus has an HA protein that human immune systems have not encountered, it can spread rapidly through a population with little to no immunity. These rare events are responsible for influenza pandemics, where a new virus achieves widespread, global transmission.