Etiology

Seasonal influenza virus is a member of the orthomyxovirus family. It has a segmented, single-stranded RNA genome that can be classified into influenza A, B, and C based on antigenic differences. The RNA codes for five structural proteins and three nonstructural proteins. Protein M and nucleoprotein NP elements are used to classify the virus into the types A, B, and C. Other elements of the virus structure, hemagglutinin (H antigen) and neuraminidase (N antigen), are important in the pathogenesis of the disease. The H antigen is required for binding and entry of the virus into the cell. The N antigen helps the mature virus escape from the cell.

Seasonal influenza virus types A and B are also divided into a number of subtypes. These subtypes are defined by the H and N antigens present on the virus. There are three antigenic subtypes of H antigen (H1, H2, and H3) and two antigenic subtypes of N antigen (N1 and N2), allowing for a number of different combinations. Antibodies to one subtype of H or N antigen do not react with another type of the H or N antigen.

Seasonal influenza C is not associated with epidemics or pandemics and causes mild disease. Influenza A is responsible for frequent (usually annual) local outbreaks or larger epidemics of varying intensity every 2-3 years, or occasional pandemics. Influenza B causes outbreaks approximately every 4 years, with usually milder disease than influenza A.[9] Epidemics usually occur from late autumn to early spring.

Small point mutations in the proteins that make up the seasonal influenza virus cause antigenic drift, and this is the reason new vaccines are required each influenza season. Larger changes that result in new hemagglutinin or neuraminidase proteins cause antigenic shifts and may result in pandemics. Special terminology used when discussing an influenza virus includes the type of influenza virus, the place it was first located, and the year it was first discovered.

Pathophysiology

Seasonal influenza virus is transmitted through infected respiratory droplets that are aerosolized by coughing, sneezing, or talking. Less commonly, contact with fomites may cause transmission.[5]

The virus binds to and enters the tracheobronchial ciliated epithelium by utilizing the viral surface hemagglutinin (H antigen). Viral replication then occurs. Peak viral shedding occurs in the first 48 to 72 hours of exposure to the virus, then declines and becomes undetectable within 10 days. Children and immunocompromised people may shed virus for several weeks.[10]

Classification

Influenza virus types

Seasonal influenza virus is classified into influenza A, B, and C based on antigenic differences. Other elements of the virus structure are hemagglutinin (H antigen) and neuraminidase (N antigen).

Seasonal influenza virus types A and B are divided into several subtypes. These subtypes are defined by the H and N antigens present on the virus. There are three antigenic subtypes of H antigen (H1, H2, and H3) and two antigenic subtypes of N antigen (N1 and N2), allowing for several different combinations.

Seasonal influenza C is not associated with epidemics or pandemics and causes mild disease.

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