Influenza is an infectious respiratory disease caused by influenza A and B viruses in humans. It is characterized by annual seasonal epidemics and sporadic pandemic outbreaks involving influenza A viruses of zoonotic origin. The World Health Organization estimates that annual influenza epidemics result in approximately 1 billion infections, 3–5 million cases of severe illness, and 300,000–500,000 deaths. The severity of pandemic influenza depends on factors such as the virulence of the virus strain and pre-existing immunity. The most severe pandemic, in 1918, resulted in over 40 million deaths worldwide. Influenza vaccines are formulated annually to match circulating strains, but vaccine efficacy is not optimal, especially in cases of antigenic mismatch. Antiviral agents targeting the enzyme neuraminidase have been developed but are limited in use. Emerging approaches include the development of universal influenza vaccines that provide protection against antigenically distant viruses, though these need further clinical testing. Influenza viruses are enveloped negative-sense single-stranded RNA viruses with segmented genomes. Influenza A and B viruses contain eight RNA segments encoding various viral proteins, including HA and NA, which are the most antigenically variable. Influenza A viruses circulate in humans and animals, while influenza B viruses are restricted to humans. The segmented nature of the viral genome enables reassortment, leading to increased virus diversity. Pandemic influenza occurs every 10–50 years, with the 2009 pandemic caused by a novel H1N1 influenza A virus reassortant previously circulating in pigs. The major burden of influenza in humans is from seasonal epidemics, with most infections occurring in children. Seasonal influenza A H1N1 and H3N2 currently circulate, but influenza A H2N2 viruses were the only human circulating strains from 1957 to 1968. Pandemic influenza viruses spread rapidly due to the lack of pre-existing immunity, leading to increased virulence. Influenza viruses are transmitted through the respiratory route, with avian influenza viruses in wild birds transmitted through fecal-oral or fecal-respiratory routes. Influenza viruses replicate in epithelial cells of the respiratory or intestinal tract, causing severe inflammation and immune cell infiltration. Influenza viruses can evolve through antigenic drift, where small mutations accumulate in HA and NA, necessitating frequent vaccine updates. Antigenic shift refers to drastic changes in HA, associated with pandemics. Influenza viruses adapt to new hosts through genetic changes, often involving reassortment, to optimize receptor binding and other functions. Host innate and adaptive immune responses play crucial roles in controlling viral replication and clearance, with T cell and B cell immunity contributing to protection against infection.Influenza is an infectious respiratory disease caused by influenza A and B viruses in humans. It is characterized by annual seasonal epidemics and sporadic pandemic outbreaks involving influenza A viruses of zoonotic origin. The World Health Organization estimates that annual influenza epidemics result in approximately 1 billion infections, 3–5 million cases of severe illness, and 300,000–500,000 deaths. The severity of pandemic influenza depends on factors such as the virulence of the virus strain and pre-existing immunity. The most severe pandemic, in 1918, resulted in over 40 million deaths worldwide. Influenza vaccines are formulated annually to match circulating strains, but vaccine efficacy is not optimal, especially in cases of antigenic mismatch. Antiviral agents targeting the enzyme neuraminidase have been developed but are limited in use. Emerging approaches include the development of universal influenza vaccines that provide protection against antigenically distant viruses, though these need further clinical testing. Influenza viruses are enveloped negative-sense single-stranded RNA viruses with segmented genomes. Influenza A and B viruses contain eight RNA segments encoding various viral proteins, including HA and NA, which are the most antigenically variable. Influenza A viruses circulate in humans and animals, while influenza B viruses are restricted to humans. The segmented nature of the viral genome enables reassortment, leading to increased virus diversity. Pandemic influenza occurs every 10–50 years, with the 2009 pandemic caused by a novel H1N1 influenza A virus reassortant previously circulating in pigs. The major burden of influenza in humans is from seasonal epidemics, with most infections occurring in children. Seasonal influenza A H1N1 and H3N2 currently circulate, but influenza A H2N2 viruses were the only human circulating strains from 1957 to 1968. Pandemic influenza viruses spread rapidly due to the lack of pre-existing immunity, leading to increased virulence. Influenza viruses are transmitted through the respiratory route, with avian influenza viruses in wild birds transmitted through fecal-oral or fecal-respiratory routes. Influenza viruses replicate in epithelial cells of the respiratory or intestinal tract, causing severe inflammation and immune cell infiltration. Influenza viruses can evolve through antigenic drift, where small mutations accumulate in HA and NA, necessitating frequent vaccine updates. Antigenic shift refers to drastic changes in HA, associated with pandemics. Influenza viruses adapt to new hosts through genetic changes, often involving reassortment, to optimize receptor binding and other functions. Host innate and adaptive immune responses play crucial roles in controlling viral replication and clearance, with T cell and B cell immunity contributing to protection against infection.