Influenza viruses are enveloped, negative-sense, single-stranded RNA viruses belonging to the family Orthomyxoviridae. They are classified into four main types: influenza A, B, C, and D. Influenza A and B viruses are responsible for the majority of seasonal human influenza infections; influenza C is generally associated with milder illness and influenza D primarily infects cattle and is not known to cause disease in humans.

Influenza viruses enter host cells mainly through receptor-mediated endocytosis, with micropinocytosis also involved in the entry of elongated viral particles. Following entry, the viral envelope fuses with the endosomal membrane, allowing release of the viral ribonucleoprotein complexes into the cytoplasm. These complexes are then transported to the nucleus, where viral RNA replication and transcription occur. Newly synthesised viral components are transported to the plasma membrane, where progeny virions assemble and are released by budding. This release process is facilitated by the viral neuraminidase protein, which helps cleave sialic acid residues and prevents newly formed virions from remaining attached to the host-cell surface.

Influenza A and B viruses have segmented genomes composed of eight RNA segments, which encode multiple proteins involved in viral replication, structural assembly, host-cell interaction, and immune evasion. Two major surface glycoproteins, haemagglutinin and neuraminidase, play central roles in the viral life cycle. Haemagglutinin mediates attachment to sialic acid receptors on host cells and promotes membrane fusion, while neuraminidase supports viral release and spread. Influenza A viruses are further divided into subtypes based on the antigenic properties of their haemagglutinin and neuraminidase proteins. Currently circulating seasonal human influenza A viruses include A(H1N1) and A(H3N2).

A defining feature of influenza viruses is their capacity for rapid genetic and antigenic change. Antigenic drift occurs through the gradual accumulation of mutations, particularly in the genes encoding haemagglutinin and neuraminidase. This process enables influenza viruses to partially evade pre-existing immunity and contributes to recurrent seasonal epidemics. Influenza A viruses can also undergo antigenic shift, in which reassortment of genome segments between different influenza viruses generates novel strains. When such strains acquire the ability to infect and transmit efficiently among humans, they may have pandemic potential. These evolutionary mechanisms make continuous surveillance and regular updating of seasonal influenza vaccines essential.

Influenza viruses are transmitted primarily through respiratory droplets and aerosols produced when infected individuals cough, sneeze, talk, or breathe. Infection causes seasonal respiratory disease worldwide, with clinical outcomes ranging from mild upper respiratory tract illness to severe pneumonia and systemic complications. Common symptoms include fever, cough, sore throat, headache, myalgia, and fatigue. Severe disease is more likely to occur in older adults, young children, pregnant women, and people with underlying medical conditions or weakened immune systems.

Seasonal influenza is estimated to cause approximately 1 billion infections globally each year, including 3-5 million cases of severe disease and up to 650,000 respiratory deaths annually. In addition to its direct health impact, influenza places a substantial burden on healthcare systems and contributes to significant economic losses through medical costs, absenteeism, and reduced productivity.

Vaccination remains the primary strategy for preventing influenza infection and reducing the risk of severe disease. However, vaccine effectiveness varies between seasons due to ongoing viral evolution and the difficulty of predicting which strains will circulate. Antiviral therapies are also available, including neuraminidase inhibitors such as oseltamivir and zanamivir, as well as the polymerase acidic protein inhibitor baloxavir marboxil. These treatments can reduce disease severity and duration when administered early, although antiviral resistance may emerge. Amantadine, an inhibitor of the influenza A M2 ion channel, is no longer used for flu treatment due to the widespread development of viral resistance. The continuing evolution of influenza viruses, together with the persistent risk of future pandemics, highlights the need for improved vaccines, broader antiviral options, and sustained global surveillance.

Overall, influenza viruses are highly adaptable respiratory pathogens with major clinical and public health importance. Their ability to evolve rapidly, cause annual epidemics, and occasionally give rise to pandemic strains makes them a continuing priority for virology research, vaccine development, and antiviral discovery.