John H. Beigel, MD


Crit Care Med. 2008;36(9):2660-2666. 

In This Article

Seasonal Influenza

Seasonal influenza, the influenza disease that occurs on a yearly basis, causes more than 200,000 hospitalizations and 41,000 deaths in the United States every year and is the seventh leading cause of death in the United States.[1] Despite this, 38% of unimmunized individuals feel they are not at risk for influenza and its related complications.[2] Although this may be easy to attribute to the per-ceptions of the lay public, physicians' attitudes are not much better; only 35% to 40% of healthcare workers are vaccinated annually; 40% of physicians believe that influenza is a benign disease that does not require treatment; and 29% believe that antiviral therapy decreases mortality, an efficacy that has never been shown in clinical trials.[3,4] Intensivists need to recognize the importance of seasonal influenza as a cause of severe morbidity and mortality, and be well versed on diagnosis, complications, therapy, and infection control measures associated with this disease.

Virus. Influenza viruses are members of Orthomyxoviridae family of viruses, and are negative strand RNA viruses.[5] Influenza viruses can be classified as A, B, or C. Influenza A is found in humans, other mammals, and birds, and is the only influenza virus which has historically caused pandemics. Types B and C, while previously thought found only in humans have been isolated from seals and pigs, respectively.[6,7,8] Influenza A and B are more common than type C, and cause more severe disease. Influenza C is a significant cause of respiratory infections in children younger than 6 yrs of age.[9] The majority of humans acquire protective antibodies to influenza C early in life and do not subsequently develop clinical disease.[10]

Influenza A can be further classified based on surface glycoproteins: hemagglutinin and neuraminidase. The viral hemagglutinin binds to host cell sialic acid conjugated glycoproteins.[11] This attachment is necessary for viral entry into the cell. The configuration of the sialic acid conjugated glycoproteins varies from species to species, and may serve to limit transfer of viruses across species.[12] Neuraminidase is important for viral release and propagation.[13] The naming convention signifies which of these proteins is on a given virus. Thus, the standard nomenclature is Influenza A HxNx (the x is the number corresponding to the specific type of hemagglutinin and neuraminidase). The nomenclature is relevant to clinicians because changes in hemagglutinin antigens, and to a lesser extent neuraminidase antigens, signal viruses that population may have little or no prior immunity to. When major antigenic shifts occur, patients unimmunized against the new strain may develop particularly severe disease.

Wild aquatic birds are the natural reservoir of influenza A viruses. There are 16 types of hemagglutinin (H1-H16) and nine types of neuraminidase (N1-N9) and all have been found circulating in wild and domestic birds.[14] Three types of hemagglutinin (H1-H3) and two neuraminidase (N1-N2) are known to have caused widespread disease in humans (H1N1, H2N2, H3N2). Only two of these viruses (H1N1 and H3N2) are currently circulating as seasonal influenza. H2N2 has not circulated in humans since 1968.


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