Influenza is an acute respiratory infection caused by influenza viruses, primarily influenza A and influenza B in humans. It commonly affects the nose, throat, bronchi and sometimes the lungs, and typically produces a relatively abrupt illness characterised by fever, chills, headache, marked tiredness, muscle aches, cough and sore throat.
Influenza A viruses are classified by surface proteins called haemagglutinin and neuraminidase, producing designations such as H1N1 and H3N2, whereas human influenza B viruses belong to distinct lineages rather than receiving the same H and N subtype nomenclature. Influenza differs from the Common Cold because systemic symptoms such as fever, myalgia and profound fatigue are often more prominent, although clinical features overlap and symptoms alone cannot always establish the cause.
Influenza viruses are enveloped viruses with a segmented, single-stranded RNA genome. Their segmented genome contributes to genetic variation because exchange of genome segments can occur when different influenza A viruses infect the same host cell, a process known as reassortment. Smaller genetic changes arise through mutation and selection, allowing viruses to evolve progressively and sometimes evade existing population immunity.
Antigenic drift describes ongoing incremental changes in viral antigens, whereas antigenic shift generally refers to a major reassortment event that can create an influenza A virus with substantially different antigenic properties and potentially pandemic significance. Influenza A has a broad animal reservoir, particularly among birds and pigs, and this ecological diversity contributes to its evolutionary potential. Influenza B circulates mainly among humans and generally undergoes evolutionary change without the same extensive animal-host diversity associated with influenza A.
Transmission occurs predominantly through respiratory particles and aerosols produced when infected people breathe, talk, cough or sneeze, with transmission also possible when contaminated hands or surfaces contribute to contact with the mouth, nose or eyes. Viral replication in respiratory epithelial cells produces local inflammation and contributes to systemic immune responses responsible for many symptoms.
The incubation period is commonly around one to four days, and infected people can transmit virus before symptoms become obvious and for several days afterwards, with children and people with weakened immune systems sometimes remaining infectious for longer. Seasonal influenza activity varies geographically and temporally, generally increasing during colder months in temperate regions. Crowded indoor environments, close contact and limited ventilation can facilitate spread, while population immunity, vaccination coverage, viral evolution and environmental conditions all influence the scale of seasonal outbreaks.
Most otherwise healthy people recover from influenza without specific medical treatment, but the illness can cause substantial morbidity and occasionally severe complications. Viral pneumonia may occur, and influenza can also predispose people to secondary bacterial pneumonia. Other recognised complications include worsening of asthma or chronic lung disease, dehydration, sinus or ear complications, inflammation affecting the heart or brain in uncommon circumstances, and severe systemic illness requiring hospital care.
Risk is higher in older adults, very young children, pregnant people and people with certain chronic medical conditions or weakened immune systems. Severe disease can involve respiratory failure, sepsis-like systemic deterioration and multi-organ complications. Importantly, the absence of a high fever does not exclude influenza, particularly in older adults or people whose immune response is altered, and uncomplicated influenza cannot reliably be distinguished from other respiratory infections solely from symptom patterns.
Diagnosis can be based on clinical assessment when influenza is circulating and the presentation is characteristic, but laboratory testing can identify influenza virus when confirmation is clinically useful. Rapid molecular assays generally provide greater sensitivity than older rapid antigen tests, while more comprehensive molecular methods can distinguish influenza A and B and sometimes provide additional information. Testing is particularly relevant in hospital settings, outbreaks, high-risk patients and situations where the result could alter treatment or infection-control decisions.
Antiviral medicines can reduce illness duration and may reduce complications when appropriately prescribed, with greatest benefit when treatment begins early, although treatment may still be appropriate later for people with severe disease or increased risk of complications. Antibiotics do not treat influenza itself because influenza is viral, although antibiotics may be required when a separate or secondary bacterial infection is diagnosed.
Vaccination is the principal population-level method for reducing influenza morbidity and transmission-related burden. Seasonal vaccines are updated because circulating viruses evolve, and formulations are selected to provide protection against strains expected to circulate during the relevant season. Vaccine effectiveness varies between seasons and populations because it depends on the match between vaccine and circulating viruses, the recipient's age and immune response, and other factors, but vaccination can still reduce the likelihood of severe disease even when infection occurs.
Vaccination strategies often prioritise groups at increased risk of complications and people whose work brings them into contact with vulnerable populations. Public-health measures such as staying home when acutely ill, improving ventilation, hand hygiene and appropriate respiratory etiquette can complement vaccination, particularly during periods of high transmission.
Influenza has considerable historical and public-health significance because influenza A viruses have caused major pandemics when viruses with novel antigenic characteristics acquired the capacity for efficient human transmission. The 1918 pandemic caused extraordinarily high mortality worldwide, while later pandemics included those associated with influenza A viruses in 1957, 1968 and 2009. These events illustrate the distinction between seasonal epidemics caused by established lineages and pandemics involving sustained global spread of a virus with substantially different antigenic characteristics. Influenza surveillance therefore extends beyond clinical medicine and includes monitoring viruses in humans and relevant animal populations, sequencing viral genomes, analysing epidemiological patterns and evaluating antiviral resistance. Pandemic preparedness depends on rapid detection, laboratory capacity, vaccine development, health-system planning and international information sharing.
A common misconception is that every episode of influenza produces dramatic fever and body aches, or that every severe respiratory illness during winter is influenza. In reality, influenza has a broad clinical spectrum, ranging from mild illness to life-threatening disease, and several other viruses can produce similar symptoms. Another misconception is that vaccination causes influenza; properly formulated non-live influenza vaccines cannot cause influenza infection, although temporary soreness, fatigue or other immune-response symptoms can occur after vaccination.
Influenza also should not be confused with stomach illnesses that are colloquially called “flu” in some settings. For accurate interpretation, the term refers specifically to infection with influenza viruses. Its significance extends beyond individual symptoms because influenza affects absenteeism, healthcare demand, vulnerable populations and seasonal mortality, making surveillance, vaccination, appropriate antiviral use and infection-control practices important components of respiratory-health management.
