The flu is caused by influenza viruses, a family of respiratory viruses that infect the cells lining your nose, throat, and lungs. These viruses spread primarily through tiny droplets released when an infected person coughs, sneezes, or talks. But “what causes the flu” goes deeper than just catching it from someone: the virus itself is constantly changing, jumping between species, and exploiting environmental conditions to trigger seasonal epidemics and occasional pandemics.
The Virus Behind the Flu
Four types of influenza virus exist: A, B, C, and D. Only types A and B cause the seasonal flu epidemics that sweep through populations each winter. Type C produces mild illness and doesn’t cause epidemics. Type D mainly infects cattle and isn’t known to make people sick.
Influenza A is the more dangerous of the two. It’s the only type capable of causing pandemics, and it circulates in both humans and animals, including birds, pigs, and other mammals. Influenza B circulates almost exclusively in humans and tends to cause less severe outbreaks, though it can still lead to serious illness. As of late 2025, the dominant strain circulating worldwide is an influenza A(H3N2) subtype, with A(H1N1) and B viruses circulating at lower levels.
How the Virus Infects Your Cells
The surface of each influenza virus particle is studded with two key proteins. The first acts like a grappling hook: it latches onto sugar molecules on the surface of cells in your respiratory tract, allowing the virus to anchor itself and get pulled inside the cell. The second protein works like a pair of scissors, snipping the virus free from a cell after it has finished making copies of itself so those new virus particles can spread to neighboring cells.
Once inside a cell, the virus does something unusual for a respiratory virus. It sends its genetic material into the cell’s nucleus, essentially hijacking the cell’s own machinery to produce new viral proteins and copies of its genome. The cell becomes a factory, assembling new virus particles that bud off and go on to infect more cells. This cycle of infection, replication, and release is what damages your respiratory lining and triggers the immune response you experience as fever, body aches, and coughing.
How the Flu Spreads Between People
Respiratory droplets are the primary route. When someone with the flu coughs, sneezes, or even talks, they release droplets containing virus particles. Those droplets can land in the mouths or noses of people nearby, or potentially be inhaled into the lungs. Less commonly, you can pick up the virus by touching a contaminated surface and then touching your mouth, nose, or eyes.
The timing of contagiousness matters. After exposure, it typically takes one to four days before symptoms appear. But you can start spreading the virus a full day before you feel sick. You’re most contagious during the first three to four days after symptoms begin, especially if you have a fever. Most adults remain infectious for about five to seven days after getting sick. Children, people with weakened immune systems, and those with severe illness can shed the virus for 10 days or more. Even people who are infected but never develop symptoms can spread it to others.
Why the Flu Keeps Coming Back
Unlike many infections that grant lasting immunity, the flu returns year after year because the virus is constantly evolving. This happens through two distinct processes.
The first is a slow, steady accumulation of small genetic mutations. Every time the virus copies itself inside a host, tiny errors creep into its genetic code. Over time, these errors change the shape of the proteins on the virus’s surface just enough that your immune system no longer recognizes it. Antibodies you built up from a previous flu infection or vaccination may bind poorly, or not at all, to the altered virus. This gradual drift is why you can catch the flu multiple times throughout your life and why flu vaccine formulas are reviewed and updated every year.
The second process is rarer but far more dangerous. It involves a sudden, major reshuffling of the virus’s genetic material, producing a dramatically different version of the virus. This typically happens when two different influenza strains infect the same animal (often a pig or bird) and swap genetic segments, creating a hybrid virus with surface proteins that human immune systems have never encountered. When this new virus gains the ability to spread efficiently between people, the result can be a pandemic. The 2009 H1N1 pandemic, for example, emerged from a virus carrying gene segments originating from North American swine, Eurasian swine, human, and bird influenza viruses. Only four flu pandemics have occurred in the past century, but each one caused widespread illness because most people had little or no preexisting immunity.
The Role of Animals in Creating New Strains
Wild aquatic birds are the natural reservoir for influenza A viruses, harboring at least 16 different subtypes. Mammals, including humans, have minimal preexisting immunity to most of these bird-adapted viruses. Pigs have long been considered a “mixing vessel” because their respiratory cells have receptors that can bind both bird-adapted and human-adapted viruses, creating opportunities for genetic reassortment.
The current global concern centers on highly pathogenic avian influenza H5N1 viruses. These viruses have been circulating widely in wild bird populations and have spilled over into multiple mammalian species. Some of these mammalian isolates have already acquired genetic changes that help the virus replicate more efficiently in mammalian cells. During one outbreak in farmed mink, the virus picked up mutations typically seen in human-adapted influenza strains. Between January 2022 and April 2023, eight human cases of H5N1 from this viral lineage were reported, many of them severe or fatal. If such a virus were to infect domestic pigs and reassort with strains already circulating in swine, the risk of a new virus capable of spreading easily among people would increase significantly.
Why Flu Thrives in Winter
Cold, dry air creates ideal conditions for influenza transmission, and this holds true even in subtropical climates where humidity is typically high. Research from New Zealand found that spikes in influenza and pneumonia deaths followed periods of unusually cold or dry air by up to 19 days. Several factors work together to explain this pattern.
Low humidity helps the virus survive longer on surfaces and in the air. Dry air also dries out the mucous membranes in your nose and throat, weakening a key physical barrier against infection. Indoor heating without humidification compounds the problem by dropping indoor humidity further. And cold weather drives people indoors into closer contact with one another, increasing the chance of both airborne and direct transmission. Notably, it’s the relative departure from normal conditions that seems to matter most. An unusually cold, dry stretch in a warm climate can trigger the same uptick in transmission as winter in a cold one.
Vaccine Effectiveness Against Current Strains
Because the virus changes every year, the flu vaccine is a moving target. For the 2024-2025 season, preliminary data from the CDC shows the vaccine reduced outpatient flu visits by roughly 42 to 56% across all ages, depending on the surveillance network. Protection was strongest in children: the vaccine was 60 to 63% effective at preventing outpatient visits and 63 to 78% effective at preventing hospitalization in kids under 18.
Effectiveness varied by strain. The vaccine performed better against H1N1 viruses, with 53 to 72% effectiveness in children and 39 to 42% in adults. Against H3N2, the dominant strain this season, protection was lower: 16 to 42% for outpatient visits in children, and 25 to 51% in adults depending on the setting. For adults 65 and older, overall vaccine effectiveness ranged from 18 to 57%, with the broadest protection seen in hospital-based studies. Even when the vaccine doesn’t prevent infection entirely, it consistently reduces the severity of illness and the likelihood of hospitalization.