Influenza virus is transmitted from person to person primarily in droplets released by sneezing and coughing.
Inhaled influenza viruses reach lower respiratory tract, tra-cheobronchial tree, the primary site of the disease. They attach to sialic acid receptors on epithelial cells by HA pres-ent on the viral envelope. Relatively few viruses are needed to infect lower respiratory tract than the upper respiratory tract.
Neuraminidase of the viral envelope may act on the N-acetyl neuraminic acid residues in mucus to produce liq-uefaction. In concert with mucociliary transport, this lique-fied mucus may help spread the virus through the respiratory tract. Infection of mucosal cells results in cellular destruction and desquamation of the superficial mucosa. The resulting edema and mononuclear cell infiltration of the involved areas are accompanied by symptoms including nonproductive cough, sore throat, and nasal discharge. Although the cough may be striking, the most prominent symptoms of influenza are systemic: fever, muscle aches, and general prostration. The virus remains localized to the respiratory tract; hence viremia does not occur.
In an uncomplicated case, virus can be recovered from respi-ratory secretions for 3–8 days. Peak quantities of 104–107 infec-tious units/mL are detected at the time of maximal illness. After 1–4 days of peak shedding, the titer begins to drop, in concert with the progressive abatement of disease.
Occasionally, in patients with underlying heart or lung dis-ease, the infection may extensively involve the alveoli, resulting in interstitial pneumonia, sometimes with marked accumula-tion of edema and lung hemorrhage. Pure viral pneumonia of this type is a severe illness with a high mortality. Virus titers in secretions are high, and viral shedding is prolonged. In most cases, however, pneumonia associated with influenza is caused by bacteria, principally pneumococci, staphylococci, and Gram-negative bacteria. These bacteria can invade and cause disease, because the preceding viral infection damages the normal defenses of the lung.
Antibody is the primary defense in immunity to reinfection. IgA antibody, which predominates in upper respiratory secretions, is less persistent than secretory IgG, but contributes to con-fer immunity. Secretory IgG antibody, which predominates in lower respiratory secretions, appears to be the most important.
Antibodies provide long-lasting immunity against the infecting influenza strain. Only antibodies directed against HA is able to prevent infection. Antibodies against HA neu-tralizes the infectivity of the virus, thereby preventing the dis-ease. Antibodies against NA do not neutralize infectivity but reduce severity of the disease. They act presumably by impair-ing the action of NA against N-acetyl neuraminic acid residues in the virion envelope and thus promoting virus aggregation. The antibodies against the internal ribonucleoprotein group-specific antigen do not confer any immunity.
Immunity to influenza virus is strain-specific and lasts for many years. Recurrent cases of influenza are caused primarily by antigenically different strains. The role of cell-mediated immu-nity in conferring protection against influenza is not clear.