Influenza is caused by influenza viruses, a family of RNA viruses that come in four types: A, B, C, and D. Types A and B are responsible for the seasonal flu epidemics that sicken roughly one billion people worldwide each year, causing 3 to 5 million cases of severe illness and between 290,000 and 650,000 respiratory deaths annually. Types C and D play almost no role in human disease.
Understanding which virus is behind the flu matters because not all influenza viruses behave the same way. They differ in severity, how fast they mutate, and whether they can jump from animals to humans.
The Four Types of Influenza Virus
Influenza A is the most dangerous and versatile of the four types. It infects humans, birds, pigs, horses, and other animals, and it is the only type capable of triggering pandemics. The two subtypes currently circulating in people are A(H1N1) and A(H3N2). Influenza A is classified by two proteins that sit on the virus’s outer surface: hemagglutinin (H) and neuraminidase (N). There are 18 known versions of hemagglutinin and 11 of neuraminidase, creating a huge number of possible combinations. Most of those combinations circulate in birds, not people.
Influenza B also causes seasonal flu but is limited to humans and seals. It does not have subtypes like A does. Instead, it splits into two lineages, Victoria and Yamagata. Influenza B tends to cause milder illness on average, though it can still be severe, especially in children.
Influenza C causes only mild respiratory infections and doesn’t drive epidemics. Influenza D primarily affects cattle and is not known to infect people.
How the Virus Gets Into Your Cells
The two surface proteins on influenza A give the virus everything it needs to invade and spread. Hemagglutinin acts like a key: it latches onto sugar molecules called sialic acids on the surface of cells lining your respiratory tract, which pulls the virus inside. Once the virus has hijacked the cell’s machinery to make copies of itself, neuraminidase takes over. It snips the connection between newly formed virus particles and the host cell, releasing them to infect neighboring cells. Neuraminidase also prevents freshly made viruses from clumping together, helping them spread more efficiently.
This two-step process of attachment and release is the reason antiviral medications target these specific proteins. Blocking neuraminidase, for example, traps new virus particles on the cell surface and slows the infection’s spread through the body.
Why the Flu Comes Back Every Year
Influenza viruses mutate constantly through a process called antigenic drift. As the virus copies itself, small errors accumulate in the genes encoding its surface proteins. Over time, those proteins change enough that antibodies from a previous infection or vaccination no longer recognize them well. This is why you can catch the flu more than once, and it’s the primary reason flu vaccine formulations are reviewed and updated every year.
A more dramatic change, called antigenic shift, happens only with influenza A. In a shift event, the virus acquires an entirely new version of hemagglutinin or both hemagglutinin and neuraminidase, often by swapping genetic material with a flu virus from birds or pigs. Because the resulting virus is so different from anything the human immune system has seen, most people have little or no protection against it. Antigenic shift is rare, but when it happens, it can spark a pandemic. There have been four flu pandemics in the past century, including the 2009 H1N1 pandemic.
Animal Flu Viruses and Pandemic Risk
Because influenza A circulates in birds and pigs, there is always a chance that an animal strain could adapt to spread among humans. The H5N1 avian influenza virus is a current example. It has infected poultry flocks on every continent and has caused sporadic human cases, mostly through direct contact with infected birds or cattle. Human-to-human transmission of H5N1 has not been reported. For that to happen, the virus would need to change its receptor preference from the type found in bird cells to the type found in human airways. This kind of adaptation has occurred with other subtypes in the past (H1, H2, and H3), which is why public health agencies monitor H5N1 closely.
When a flu virus from pigs infects a person, it’s called a variant virus and is labeled with a “v” after its name, such as A(H3N2)v. These cases are tracked separately because any animal-origin virus has the potential to spark wider outbreaks if it gains the ability to pass easily between people.
Incubation, Shedding, and Contagiousness
After you’re exposed to an influenza virus, symptoms typically appear within one to four days. Most adults become contagious starting the day before symptoms begin and remain infectious for roughly five to seven days after symptoms start. Children, people with weakened immune systems, and those with severe illness can shed the virus for 10 days or longer. This pre-symptomatic contagiousness is one reason flu spreads so effectively: you can pass it along before you even know you’re sick.
How Influenza Is Detected
Rapid influenza diagnostic tests, the kind you might encounter at an urgent care clinic, give results in about 15 minutes but have significant limitations. Their sensitivity sits around 50 to 70 percent, meaning they miss a substantial number of true infections. The FDA now requires newer rapid tests to meet at least 80 percent sensitivity. Molecular tests, which detect viral genetic material, are far more accurate and can return results within 30 minutes in some clinical settings. The specificity of rapid tests is high, around 95 to 99 percent, so a positive result is generally reliable even if a negative one isn’t.
How Vaccines Match the Virus
Because influenza viruses drift genetically from season to season, the World Health Organization convenes expert panels twice a year to decide which strains the next season’s vaccines should target. For the 2025-2026 flu season in the United States, all vaccines are trivalent, meaning they protect against three viruses: an A(H1N1) strain, an A(H3N2) strain, and a B/Victoria lineage strain. The specific strains selected differ slightly depending on how the vaccine is manufactured. Egg-based vaccines use one set of reference viruses, while cell-based and recombinant vaccines use a slightly different set, because the virus can change during egg-based production.
This annual reformulation is a direct consequence of antigenic drift. A vaccine that worked well one winter may offer reduced protection the next if the circulating virus has drifted enough. It’s the same virus family, but with a surface the immune system no longer recognizes as precisely.