Influenza Virus Explained — How Seasonal Flu Actually Works

The World Health Organization estimates that seasonal influenza causes around a billion cases a year, including 3 to 5 million severe cases and 290,000 to 650,000 respiratory deaths. The virus keeps coming back because it is a moving target: it makes frequent copying errors, it can swap whole gene segments with other flu viruses, and the antibodies you built last winter recognize it a little less well each year. This article explains how influenza infects a cell, why it changes, how the yearly vaccine is chosen, and why some seasons are far worse than others.

Educational content, not medical advice. Talk to your doctor before changing any medication, treatment, or routine. Information here reflects current research but every person's situation differs.

What influenza is, and what the four types mean

Influenza is a family of RNA viruses. Its genome is single-stranded RNA split into eight separate pieces, and the whole thing is wrapped in a lipid envelope studded with two kinds of surface protein. That detail, the split genome, explains most of what is unusual about the virus, and we will return to it more than once.

There are four types, labeled A through D. WHO and the US Centers for Disease Control and Prevention (CDC) describe them in nearly identical terms.

Type	Hosts	Public health role
Influenza A	Humans, birds, pigs, horses, other mammals	Causes seasonal epidemics; the only type known to cause pandemics
Influenza B	Humans (mainly)	Causes seasonal epidemics; not divided into subtypes, only lineages
Influenza C	Humans	Mild infections; minor public health importance
Influenza D	Mainly cattle	Not known to infect people

Types A and B are the ones that fill clinics every winter. Type A is further sorted into subtypes by its two surface proteins, hemagglutinin (H) and neuraminidase (N). CDC lists 18 hemagglutinin subtypes and 11 neuraminidase subtypes, and more than 130 combinations have been identified in nature. Only two combinations, A(H1N1) and A(H3N2), routinely circulate in people.

Type B works differently. It has no subtypes. Instead it is divided into two lineages, B/Victoria and B/Yamagata. CDC notes that B/Yamagata viruses have not been detected after March 2020, which is why seasonal vaccines in the United States are now formulated against three viruses (one A(H1N1), one A(H3N2), and one B/Victoria) rather than the four-virus formulas used earlier in the decade.

Think of the naming system as a license plate. The letter tells you the make (type), the H and N numbers tell you the model, and the clade or lineage tells you the specific production run. Two viruses can share a plate prefix and still behave differently enough that immunity to one gives only partial protection against the other.

The H and N proteins: a key and an exit door

Every influenza A virus is named for the two proteins that jut out of its envelope.

Hemagglutinin (H) is the key. It binds sialic acid, a sugar found on the surface of cells lining the airway, and that binding is what lets the virus attach. Hemagglutinin is made as an inactive precursor called HA0, which has to be cut by host proteases (protein-cutting enzymes) into two linked pieces, HA1 and HA2, before the virus is infectious. This is one reason the type of cells and enzymes in a given tissue influence where a flu strain can grow.

Neuraminidase (N) is the exit door. After new virus particles assemble, they remain stuck to the cell by the same sialic acid bonds that hemagglutinin loves. Neuraminidase snips those bonds so the particles can leave and infect neighbors. It also helps virions move through the mucus that coats the airway.

Both proteins are what your antibodies mostly learn to recognize, which is exactly why they are also the parts of the virus under the greatest pressure to change.

Historical pandemic names tell you which combinations have caused trouble in humans: H1N1 in 1918 and again in 2009, H2N2 in 1957, and H3N2 in 1968. Each emerged carrying at least one surface protein that most people had never encountered.

How influenza infects a cell, step by step

The cycle from attachment to the release of new particles takes on the order of hours, and a single infected cell can produce a very large number of new virions. The sequence is the same in every strain.

1. Attachment. Hemagglutinin binds sialic acid on an airway epithelial cell. Human-adapted viruses bind best to the sialic acid linkage common in the upper airway, while many avian viruses prefer a different linkage that is found mostly deeper in the human lung and abundantly in birds. That mismatch is part of why bird flu rarely spreads from person to person.
2. Entry. The cell swallows the virus into a bubble called an endosome. As the endosome acidifies, to a pH of roughly 5 to 6, hemagglutinin snaps into a new shape and fuses the viral envelope with the endosome membrane. This is the molecular equivalent of a spring-loaded hook.
3. Uncoating. The M2 protein forms an ion channel in the viral envelope, letting protons flow in and loosening the genome segments so they can be released into the cell.
4. Trip to the nucleus. The eight RNA segments travel into the cell nucleus. As the Influenza A virus overview puts it, replication here, "unlike most other RNA viruses," takes place in the nucleus. The segments never travel alone: each is bundled with the polymerase proteins PB1, PB2, and PA, which form the machine that copies viral RNA.
5. Cap-snatching and copying. To make messenger RNA that the cell's ribosomes will read, the viral polymerase grabs and cleaves the caps from the host cell's own messenger RNAs and uses them as primers. The virus essentially steals a start signal. The polymerase also makes full copies of each segment for new virions.
6. Assembly. New proteins and genome segments gather at the cell membrane. Packaging eight different segments into each particle is a delicate sorting job, and it is where reassortment can later occur.
7. Release. Neuraminidase cuts the sialic acid tethers, and the new virions bud off to infect adjacent cells.

Each step offers a drug target. Oseltamivir (Tamiflu), zanamivir, and peramivir work at the exit step by inhibiting neuraminidase. Baloxavir marboxil works earlier, interfering with the polymerase's cap-snatching activity. Older drugs aimed at the M2 channel are no longer useful against most circulating strains because of resistance.

The lesson for non-specialists is that influenza is not just a "droplet that makes you sick." It is a small, efficient program that hijacks the nucleus of a cell, uses the cell's machinery to copy itself, and times its release carefully.

Why you feel sick: the immune system does most of the work

Many of the symptoms people call "the flu" come from the body's response rather than direct damage by the virus. When infected cells detect viral RNA through internal sensors, they release signaling proteins called interferons and cytokines. These molecules recruit immune cells to the airway, raise body temperature, and trigger the fatigue and aching that make you want to lie down.

CDC describes the typical picture: fever or chills, cough, sore throat, runny or stuffy nose, muscle or body aches, headaches, and fatigue, with vomiting and diarrhea more common in children. Symptoms usually come on suddenly, and most people recover in a few days to less than two weeks. Not everyone has a fever.

The comparison with a cold is the one patients ask about most often.

Feature	Cold	Flu
Onset	Gradual	Abrupt
Fever	Rare	Common; lasts 3 to 4 days
Aches	Slight	Common; often severe
Fatigue	Sometimes	Usual
Headache	Rare	Common
Stuffy nose	Common	Sometimes
Sore throat	Common	Sometimes

Source: CDC, "Flu Symptoms."

Fever is not simply a side effect. Raising body temperature changes how the immune system and the pathogen interact, a topic covered in our explainer on why fevers help fight infections. The same inflammatory machinery that clears the virus can also injure the lung when it overshoots, which is one reason severe influenza can cause pneumonia even after viral levels start to fall.

CDC lists pneumonia as the most serious common complication, with sinus and ear infections as more moderate ones. Other possible complications include inflammation of the heart, brain, or muscles, multi-organ failure, and sepsis. Flu can also make asthma and chronic heart disease worse.

Who is at higher risk

CDC and WHO identify groups at increased risk of severe illness. They include adults 65 and older, young children (CDC lists those younger than 2, with the highest risk in infants under 6 months), pregnant people, people with chronic lung, heart, kidney, liver, or metabolic disease, people with weakened immune systems, people with severe obesity, and residents of nursing homes and other long-term care facilities. Health and care workers are also at higher risk of infection because of exposure.

For these groups, early treatment with an antiviral prescribed by a clinician is generally recommended. That is a medical decision, so the point here is only that risk is not evenly distributed.

Transmission: how it spreads and how long people are contagious

Most experts think influenza spreads mainly through droplets made when people with flu cough, sneeze, or talk. Those droplets can land in the mouths or noses of people nearby or be inhaled. Less often, a person touches a surface with virus on it and then touches their mouth, nose, or eyes.

Timing matters because it undermines the instinct to "stay away from people who look sick." According to CDC, flu can be detected in most infected people starting about one day before symptoms develop, and detection can last up to five to seven days after becoming sick. People with flu are most contagious during the first three days of illness. Young children and people with weakened immune systems may be contagious for longer.

Symptoms typically begin about two days after infection, with a range of one to four days. That short incubation period, combined with infectiousness before symptoms, is why flu can sweep through a school or office in a matter of days. Our guide to how viruses work from infection to replication puts these timing features in a broader context.

Why flu is seasonal

In temperate regions flu cases surge in winter. No single cause explains this. Researchers point to a combination of factors: indoor crowding, school calendars, colder and drier air that may help respiratory droplets and virus particles persist, and changes in how the immune system and airway lining behave in cold conditions. Tropical regions often show a less sharp pattern, with activity in more than one part of the year. The safest summary is that seasonality is real, multi-factorial, and still being studied.

Antigenic drift: why last year's immunity fades

Influenza's polymerase does not proofread well, so copying errors are frequent, a trait typical of RNA viruses. Most mutations are neutral or harmful to the virus. A few change the shape of hemagglutinin or neuraminidase just enough that existing antibodies bind less tightly.

CDC defines this as antigenic drift: small changes in the genes of influenza viruses that can alter the surface proteins and make existing antibodies less effective. Drift is a main reason people can catch the flu multiple times in their lives.

Picture a lock whose shape is changed a fraction of a millimeter each year. Your old key (the antibody) still slides in, but it no longer turns smoothly. After enough years, it stops working.

Drift is not uniform across types. CDC notes that influenza B viruses generally change more slowly than influenza A viruses, and that A(H3N2) viruses have formed many genetically different clades that continue to co-circulate. That diversity is one reason H3N2 is a notoriously hard target for vaccine designers.

Drift also shapes the immune memory of individuals. Immune systems tend to respond most strongly to the version of a virus they met first, a phenomenon discussed in immunology literature under the name original antigenic sin or imprinting. How strongly early exposure shapes later protection remains an active research area, so treat claims about it with caution unless they cite specific studies.

Antigenic shift and reassortment: how pandemics begin

Drift is a slow leak. Shift is a burst pipe.

CDC defines antigenic shift as an abrupt, major change in a flu A virus that can produce new hemagglutinin or neuraminidase proteins in human-infecting viruses, sometimes introducing a new subtype to people. Shift is rare: CDC counts four flu pandemics in the past 100 years.

The mechanism is reassortment, enabled by the segmented genome. When two different flu viruses infect the same cell, the cell produces segments from both, and some newly assembled virions can carry a mixed set. It is like shuffling two half-decks of cards into a single deck. Most hybrids are less fit than either parent, but occasionally one combines a novel surface protein (so nobody has immunity) with internal genes that let it spread well among people.

A pandemic can occur when a new influenza A virus emerges that infects people, spreads efficiently among them, and meets a population with little or no immunity.

The four pandemics of the past century

Pandemic	Dates	Subtype	Estimated worldwide deaths	Notes
Spanish flu	1918 to 1920	H1N1	17 to 100 million	Estimates vary enormously; origin still debated
Asian flu	1957 to 1958	H2N2	1 to 4 million	Avian-derived genes combined with a human strain
Hong Kong flu	1968 to 1969	H3N2	1 to 4 million (some sources lower)	Descended from H2N2 by reassortment
Swine flu	2009 to 2010	H1N1 (pdm09)	151,700 to 575,400	Reassortment of human, avian, and two swine lineages

Source: summary table in Wikipedia's "Influenza pandemic," which compiles published estimates; CDC for the reassortment description of the 2009 virus.

Death estimates for old pandemics rest on incomplete records, so the ranges are wide. The 1918 range spans a factor of nearly six, and even sources that agree on the order of magnitude disagree on the details. The 2009 range comes from modeling studies that tried to account for deaths never confirmed in a laboratory, which is also why it is higher than the laboratory-confirmed counts reported at the time.

The 2009 virus is a clean example of how shift works. CDC describes an H1N1 virus carrying genes from swine, bird, and human influenza viruses that emerged in people, spread quickly, and caused a pandemic because most people had little or no immunity. Its descendants, called A(H1N1)pdm09, now circulate as one of the seasonal subtypes.

Pigs, birds, and the mixing vessel idea

Pigs are often called "mixing vessels" because they can be infected by avian, swine, and human flu viruses. The Influenza A virus overview treats pigs as a possible, though not certain, intermediate host for reassortment, and that caution is warranted: reassortment can also occur in humans and other animals.

What matters for risk is the interface between humans and animals. For more on how animal viruses cross over, see our explainer on how viruses jump from animals to humans and our guide to the avian strain that has dominated headlines, H5N1 bird flu.

As of CDC's situation summary updated October 15, 2026, 72 human cases of A(H5) bird flu had been reported in the United States since February 2024, seven detected through national flu surveillance and 65 through monitoring of exposed people. CDC described the current public health risk as low. That risk assessment can change, which is why surveillance of animal outbreaks continues.

Global surveillance and how vaccine strains are chosen

The yearly vaccine is not designed in a single meeting. It rests on a continuous global process.

Laboratories around the world collect samples from patients, sequence the viruses, and test how well antibodies raised against candidate vaccine viruses neutralize current strains. WHO then issues recommendations twice a year: a February meeting covers the Northern Hemisphere, and a September meeting covers the Southern Hemisphere. WHO's recommendations page lists the most recent decisions as those for the 2026 to 2027 Northern Hemisphere season and the 2027 Southern Hemisphere season. WHO states that annual vaccination is recommended because immunity wanes over time.

Selection depends on several kinds of evidence:

• Genetic data. Sequencing shows which clades are growing.
• Antigenic data. Laboratory tests measure whether antibodies from vaccinated or previously infected animals and people still neutralize new strains.
• Epidemiology. Surveillance shows which strains are actually spreading.
• Forecasting. Scientists estimate how strains might change over the several months before the season arrives.

That forecasting is the weak point. The decision has to be made months before the season, because the manufacturing pipeline takes time, and the virus continues to evolve during that period.

How vaccines are made

CDC describes three FDA-approved production methods in the United States.

Method	How it works	Notes
Egg-based	Candidate viruses are injected into fertilized chicken eggs; virus-containing fluid is harvested, then inactivated and purified	Used for most flu vaccines for more than 70 years
Cell culture-based	Viruses are grown in cultured mammalian cells	Does not require eggs; currently used only for inactivated vaccines
Recombinant	A gene for hemagglutinin is delivered into a qualified cell line, which produces the antigen	Does not use eggs at any stage

The familiar flu shot is inactivated (made from killed virus or from purified proteins). The nasal spray is a live attenuated vaccine, made from live but weakened virus.

Egg production has one persistent drawback. Viruses can pick up small mutations while adapting to grow in eggs, and those mutations can make the vaccine strain a slightly worse match for the virus circulating in people. This is one reason researchers have invested in egg-independent platforms. Our article on mRNA vaccines explains the technology that many flu candidates now use, though no mRNA flu vaccine should be assumed to be a replacement for existing options without checking current regulatory status.

How well do flu vaccines work?

Vaccine effectiveness (VE) is measured in observational studies. Researchers compare how often vaccinated and unvaccinated people with flu-like illness test positive for flu, then adjust for factors such as age, sex, underlying conditions, and the time between symptom onset and enrollment.

CDC reports adjusted overall VE estimates that ranged from 10% in 2004 to 2005 to 60% in 2010 to 2011. Across the 21 seasons with estimates, the median is 40%. Recent values include 36% (2021 to 2022), 30% (2022 to 2023), 44% (2023 to 2024), 56% (2024 to 2025, preliminary), and 36% (2025 to 2026, preliminary). The 2020 to 2021 season has no estimate because of low influenza circulation.

Season	Adjusted overall VE	95% confidence interval
2004 to 2005	10%	−36 to 40
2010 to 2011	60%	53 to 66
2021 to 2022	36%	21 to 48
2022 to 2023	30%	−9 to 54
2023 to 2024	44%	36 to 51
2024 to 2025 (preliminary)	56%	54 to 58
2025 to 2026 (preliminary)	36%	33 to 39

Source: CDC, "Flu Vaccine Effectiveness Studies."

Two reading tips. First, a confidence interval that includes zero (as in 2004 to 2005 and 2022 to 2023) means the study could not rule out no effect for that season, not that the vaccine did nothing. Second, a vaccine with 40% effectiveness does not mean "it works for 40% of people." It means that vaccinated people had, on average, about 40% lower odds of laboratory-confirmed flu than comparable unvaccinated people.

Why does effectiveness vary so much? Several reasons overlap:

1. Strain match. If the dominant circulating virus has drifted from the vaccine strain, protection falls.
2. Which subtype dominates. Vaccines tend to perform differently against H1N1, H3N2, and B viruses.
3. Host factors. Age and prior exposure shape the response. Older adults often respond less strongly.
4. Egg adaptation. As noted above, production can alter the antigen.
5. Measurement. Studies differ in design and population, so estimates can differ even for the same season.

A middling number can be a misleading summary of the benefit. Even when a vaccine does not prevent infection, vaccinated people who still get flu may have milder illness, and public health agencies emphasize that prevention of severe outcomes is a major goal. Check current agency guidance for the specific benefit figures for your region, since these vary by season.

For the immunology behind this, our articles on how vaccines work, how vaccines train memory B cells, and antibody structure explain how a shot produces antibodies and why the target's shape matters so much.

Why some flu seasons are much worse than others

Severity is not a single dial. It reflects an interaction between virus, population, and circumstances.

Which subtype dominates. Seasons dominated by A(H3N2) have often been associated with more severe disease in older adults, in part because H3N2 changes quickly and has diversified into many co-circulating clades. Seasons dominated by H1N1 or B can look different. Treat this as a tendency rather than a rule.

How well the vaccine matches. As the VE table shows, effectiveness swings from season to season. A poor match leaves more people susceptible.

Population immunity. A subtype that has been absent for several years meets a population with fewer recently boosted antibodies. Children, who have had fewer exposures, can be especially susceptible.

Co-circulating infections. When flu, RSV, COVID-19, and other respiratory viruses surge together, hospitals can be strained beyond what any single virus would cause.

Behavior and timing. School schedules, travel, crowding, and public health measures change the speed of spread. The 2020 to 2021 season is the clearest example: CDC could not estimate vaccine effectiveness because there was so little influenza circulating.

CDC estimates that between 2010 and 2025 flu caused 9.4 million to 51 million illnesses, 120,000 to 710,000 hospitalizations, and 6,300 to 52,000 deaths each year in the United States. Note how wide the ranges are. The upper end is more than five times the lower end for illnesses and more than eight times for deaths, even in a single country with strong surveillance.

Antiviral treatment: what it does and when it works

CDC recommends four FDA-approved antivirals for treating flu: oseltamivir, zanamivir, peramivir, and baloxavir marboxil. According to CDC, antiviral drugs work best when started within 1 to 2 days after symptoms begin, and they can lessen symptoms and shorten illness by about a day. Later starts can still help, especially for people at higher risk or those who are hospitalized with severe illness.

The timing makes biological sense. Viral replication in the airway tends to peak early, so blocking release or copying matters most when the viral population is still growing. By the time a person has been sick for several days, the immune response is doing most of the work.

CDC emphasizes that it is very important to start antivirals as soon as possible for patients who are hospitalized, very sick, or at increased risk of complications, such as people with asthma, chronic lung disease, diabetes, or heart disease, and pregnant women. Most otherwise healthy people with mild illness do not need antivirals. Whether to take one is a decision for a clinician.

Resistance is a long-term concern with any antiviral. Because influenza mutates, strains can acquire changes that reduce a drug's effect, which is why surveillance programs test circulating viruses for resistance markers.

Common misconceptions about influenza

"The flu is just a bad cold." The two are caused by different viruses and differ in severity. CDC's comparison table shows abrupt onset, common fever, and severe aches as hallmarks of flu, while colds are typically gradual and milder.

"The flu shot gave me the flu." Inactivated vaccines contain killed virus or purified proteins and cannot cause influenza. Some people feel sore or run a mild fever for a day or two after a shot, which reflects the immune system responding. And since flu and other respiratory viruses circulate widely during vaccination season, some people catch an unrelated infection just after being vaccinated and wrongly blame the shot.

"If the vaccine is only 40% effective, it isn't worth it." This misreads what VE measures and ignores the severity of outcomes. Public health agencies weigh a vaccine's ability to lower the risk of illness across an entire population, including high-risk groups, rather than judging it person by person.

"Flu is a stomach bug." What people call "stomach flu" is usually gastroenteritis caused by other pathogens such as norovirus. Influenza is a respiratory infection, although vomiting and diarrhea occur, mainly in children.

"Getting flu once makes you immune." Drift and the circulation of multiple subtypes and lineages mean immunity to one infection does not guarantee protection against another virus, or even the same subtype a few years later. CDC notes drift is a main reason people can catch flu multiple times.

"Pandemics are always more lethal than seasonal flu." The table of past pandemics shows that the 2009 pandemic had death estimates in the same general range as a bad seasonal epidemic. What defines a pandemic is novelty and global spread, not just lethality.

Where flu research is heading

Several lines of work are underway. Some results are established and some are still hoped for.

Broadly protective vaccines. The goal is a vaccine that targets parts of the virus that change less than the head of hemagglutinin, so that protection lasts across drift and possibly across subtypes. This is a long-standing research priority, but no universal influenza vaccine is licensed for general use. Reports of promising trials should be read with attention to the stage of the trial and what was actually measured.

Faster manufacturing platforms. Cell-based and recombinant methods avoid some egg-related problems. Nucleic-acid platforms like mRNA could shorten the time between strain selection and production, though the practical benefits and regulatory status of specific products need to be checked individually.

Better forecasting. Computational models that predict which clades will expand are an active field, and so are efforts to improve the laboratory assays on which strain selection depends. The challenge is inherent: evolution has a stochastic component, so even excellent models will sometimes miss.

Zoonotic surveillance. Monitoring influenza in birds, pigs, and other animals aims to detect dangerous reassortants early. The H5N1 situation illustrates why: even when human cases are sporadic, each one is a data point about how the virus is adapting.

None of these makes the existing annual vaccine obsolete in the near term. They are better thought of as ways to reduce the gap between what the virus does and what the vaccine anticipates.

The takeaway

Influenza persists not because it is the deadliest virus, but because its biology exploits the gap between what our immune systems remember and what the virus now looks like. A sloppy polymerase produces constant small changes (drift), and a split genome allows rare but dramatic swaps (shift). Public health has built a global system of surveillance and twice-yearly vaccine selection to chase that moving target, and the results are imperfect: CDC's effectiveness estimates range from 10% to 60% across seasons, with a median of 40%.

Understanding that variability is the practical payoff. A bad season usually means a mismatch between vaccine and virus, a subtype that has not circulated recently, or too many respiratory pathogens at once, not a failure of the idea behind vaccination. For decisions about your own health, a clinician or local health agency can say what is recommended for you this season.

Frequently Asked Questions

Q: Can you get flu from the flu shot? A: No. Inactivated flu vaccines contain killed virus or purified viral proteins, so there is no functioning virus that can cause influenza. Mild fever or aches after vaccination reflect the immune system responding to the shot. The nasal spray contains live but weakened virus and is a different product from the injection.

Q: Why does flu peak in winter? A: No single factor explains it. Indoor crowding, school schedules, cold and dry air that may help droplets and virus particles persist, and seasonal changes in the airway and immune response probably all contribute. Tropical regions often show a less pronounced pattern, so seasonality varies by climate.

Q: What is the difference between a cold and the flu? A: They are caused by different viruses. According to CDC, flu typically begins abruptly with common fever lasting three to four days, frequent headache, and often severe body aches, while colds begin gradually and commonly involve a stuffy nose and sore throat. Flu also carries a higher risk of complications such as pneumonia.

Q: Why do antivirals work best when started early? A: Viral replication in the airway grows quickly after infection. CDC says antivirals work best when started within one to two days of symptom onset, because blocking the virus while it is still multiplying has the biggest effect. Later treatment can still help people who are very sick or at high risk.

Q: Can you get flu twice in one season? A: It is possible. Several subtypes and lineages can circulate at the same time, and immunity to one does not reliably protect against another. Drift also means that earlier infections protect less well against newer variants.

Q: Why do flu pandemics happen only every few decades? A: A pandemic requires a virus with surface proteins that most people have never encountered, plus the ability to spread efficiently between humans. CDC counts four flu pandemics in the past 100 years. That combination arises rarely, often through reassortment involving animal viruses, but when it does the population has little immunity.

Q: Is there a universal flu vaccine? A: Not yet. Researchers are pursuing vaccines that target parts of the virus that change less than the head of hemagglutinin, but none is licensed for general use. Current seasonal vaccines are re-formulated annually and target three viruses: one A(H1N1), one A(H3N2), and one B/Victoria.

Q: How long am I contagious with flu? A: CDC says flu can be detected in most infected people starting about one day before symptoms develop and for up to five to seven days after becoming sick, with peak contagiousness during the first three days of illness. Young children and people with weakened immune systems may be contagious longer.

Sources

• World Health Organization. Influenza (seasonal) fact sheet (burden, types, high-risk groups, antivirals).
• WHO. Global Influenza Programme: recommendations on vaccine composition (February and September meetings).
• CDC. Types of influenza viruses (types, 18 H and 11 N subtypes, B/Yamagata, trivalent composition).
• CDC. Influenza virus changes: drift and shift.
• CDC. Flu vaccine effectiveness studies (VE by season).
• CDC. How flu vaccines are made.
• CDC. Flu burden (2010 to 2025 US estimates).
• CDC. Flu symptoms and antiviral drugs.
• CDC. H5 bird flu: current situation (updated October 15, 2026).
• Wikipedia. Influenza A virus, Hemagglutinin (influenza), and Influenza pandemic (mechanism details and pandemic death-estimate ranges).

For related virus deep-dives, see our guides to how the immune system recognizes threats, the complement system, and T-cell receptors.

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