One in twenty people exposed to the virus will not become infected in spite of the lack of prior exposure, a testament to the effectiveness of these passive immune measures. Interferon produced by a cell initially infected with a virus binds to and triggers responses in neighboring uninfected cells that enable them to resist infection by degrading viral mRNA and inhibiting protein synthesis. As the immune system processes viral antigens, the adaptive immune mechanisms begin to impact the course of the infection. Cytotoxic T cells and helper T cells begin to appear, and antibodies are produced specific for viral proteins. IgA becomes highly concentrated in upper respiratory mucosae to become the primary defense against reinfection.
Antibodies facilitate the antiviral effort in a number of ways.
They can act directly on free viruses, either alone or in conjunction with complement activation. Antibodies can attach to free viruses to block binding to or entry into healthy cells, or to prevent viral uncoating. Antibodies plus complement can either block viral receptors or damage the viral envelope. And they can act on infected cells, also either alone or with complement activation. Antibodies plus complement can lyse infected cells directly and opsonize infected cells to facilitate phagocytosis.