Antibody dependent enhancement

Antibody-dependent enhancement (ADE) occurs when non-neutralising antiviral proteins facilitate virus entry into host cells, leading to increased infectivity in the cells. Some cells do not have the usual receptors on their surfaces that viruses use to gain entry. The antiviral proteins (i.e., the antibodies) bind to antibody Fc receptors that some of these cells have in the plasma membrane. The viruses bind to the antigen binding site at the other end of the antibody. ADE is common in cells cultured in the laboratory, but rarely occurs in vivo except for dengue virus. This virus can use this mechanism to infect human macrophages, causing a normally mild viral infection to become life-threatening.

The most widely known example of ADE occurs in the setting of infection with the dengue virus (DENV). DENV is a single-stranded positive-polarity RNA virus of the Flaviviridae family. It causes a disease of varying severity in humans, from dengue fever (DF), which is usually self-limited, to dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS), either of which may be life-threatening. It is estimated that as many as 390 million individuals are infected with DENV annually.

The phenomenon of ADE may be observed when a person who has previously been infected with one serotype of DENV becomes infected many months or years later with a different serotype. In such cases, the clinical course of the disease is more severe, and these people have higher viremia compared with those in whom ADE has not occurred. This explains the observation that while primary (first) infections cause mostly minor disease (DF) in children, secondary infection (re-infection at a later date) is more likely to be associated with severe disease (DHF and/or DSS) in both children and adults.

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