Influenza is caused by influenza viruses, a family of RNA viruses that infect the respiratory tract. There are four types: A, B, C, and D. Influenza A and B are responsible for the seasonal flu epidemics that sweep through populations almost every winter, while influenza C causes only mild illness and influenza D primarily affects cattle without making people sick.
The Virus Behind the Flu
Influenza viruses are studded with two key surface proteins that determine how they behave. The first, hemagglutinin (H), acts like a lock pick: it latches onto sugar molecules on the surface of your respiratory cells, allowing the virus to attach and break in. The second, neuraminidase (N), does the opposite job. Once the virus has hijacked a cell and forced it to produce thousands of copies, neuraminidase strips away those same sugar molecules so the freshly made viruses can detach and spread to neighboring cells.
These two proteins are why you see flu strains labeled with H and N numbers. The current seasonal vaccine for 2025–2026, for example, targets an H1N1 strain, an H3N2 strain, and a B/Victoria lineage strain. Each combination behaves slightly differently, and the mix circulating in any given year determines how severe the flu season will be.
How the Virus Gets Into Your Cells
Once an influenza particle lands on the lining of your nose, throat, or lungs, hemagglutinin binds it to the cell surface. The cell essentially swallows the virus, pulling it inside a tiny compartment. As that compartment becomes more acidic, the virus undergoes a shape change that lets it fuse with the compartment wall and dump its genetic material into the cell.
From there, the virus commandeers the cell’s machinery. It copies its own RNA, builds new viral proteins, and assembles thousands of new virus particles that burst out to infect more cells. This cycle repeats rapidly, which is why symptoms can escalate quickly once they start.
How Influenza Spreads Between People
The primary route is respiratory droplets. When someone with the flu coughs, sneezes, or talks, they release droplets carrying the virus. These can land in the mouths or noses of people nearby or be inhaled directly. Aerosol transmission, where smaller particles linger in the air longer, also plays a role, particularly in enclosed spaces. The virus can survive on hard, nonporous surfaces for up to 48 hours, so touching a contaminated doorknob or phone and then touching your face is another way it spreads.
Timing matters. Most adults become contagious the day before symptoms appear, which means you can spread the virus before you even know you’re sick. Infectiousness peaks during the first three to four days of illness and is higher in people running a fever. Viral shedding typically continues for five to seven days after symptoms begin.
The Incubation Period
After exposure, symptoms usually appear within one to four days. That short incubation period, combined with the fact that people are contagious before they feel ill, is a big part of why the flu spreads so efficiently through workplaces, schools, and households.
Why You Can Get the Flu More Than Once
Influenza viruses change constantly through two distinct processes. The first, called antigenic drift, involves small, ongoing mutations in the genes that code for the virus’s surface proteins. These gradual tweaks mean the version of the flu your immune system learned to recognize last year may look different enough this year to slip past your defenses. Drift is the reason flu vaccine formulas are reviewed and updated every year for both the Northern and Southern Hemispheres.
The second process, antigenic shift, is far more dramatic and far less common. Shift happens when an influenza A virus undergoes an abrupt, major change, picking up entirely new surface proteins. This can occur when a flu virus from birds or pigs acquires the ability to infect humans. Because the resulting virus is so different from anything people have encountered before, most of the population has little or no immunity. Antigenic shift is what triggers pandemics. There have been four flu pandemics in the past 100 years, including the 2009 H1N1 pandemic.
Animal Reservoirs and Crossover Risk
Wild aquatic birds are the natural reservoir for influenza A viruses, which makes the virus impossible to eradicate. From waterfowl, influenza A can spill over into domestic poultry, pigs, horses, and dogs. Each host species tends to circulate its own adapted strains, but the virus occasionally jumps to humans. Avian influenza strains like H5 and H7N9 have infected people who had direct contact with infected birds, whether through handling, slaughtering, or visiting live bird markets. Swine influenza viruses pose a similar risk for people who work closely with pigs or visit places where pigs are exhibited.
These crossover events don’t typically lead to sustained human-to-human transmission, but they’re closely monitored because any one of them could spark the next antigenic shift. Properly cooked poultry and eggs do not transmit avian flu viruses.
How the Virus Sets Up Secondary Infections
One of the more dangerous things about influenza isn’t the virus itself but what it leaves behind. The virus damages the lining of the respiratory tract in two ways: it directly kills epithelial cells, and it triggers inflammatory immune cells that cause further destruction. It also degrades the mucus layer that normally traps bacteria before they can reach deeper tissue.
As the lungs begin to heal, which can take several weeks, there’s a window of heightened vulnerability. Opportunistic bacteria that normally live harmlessly in the upper airways, particularly Streptococcus pneumoniae and Staphylococcus aureus, can take advantage of the weakened barrier and suppressed local immune defenses to cause secondary bacterial pneumonia. This complication is one of the leading causes of serious illness and death during flu seasons, and it was a major factor in the mortality of past pandemics.