Disease relevance of Antibody-Dependent Enhancement

• The results indicate that the FcRIII receptor on human macrophages and possibly another Fc receptor on human CD4+ lymphocytes mediate antibody-dependent enhancement of HIV infectivity and that this phenomenon proceeds through a mechanism independent of the CD4 protein [1].
• Based on these results we conclude that Fc gamma RII mediate antibody-dependent enhancement of dengue virus infection in addition to Fc gamma RI [2].
• Localization of antigenic sites of the S glycoprotein of feline infectious peritonitis virus involved in neutralization and antibody-dependent enhancement [3].
• Monoclonal antibodies to FcRI for immunoglobulin G substantially blocked antibody-dependent enhancement of HIV-1 infection [4].
• The S glycoprotein of feline infectious peritonitis virus (FIPV) has been shown to contain the antigenic sites responsible for eliciting both neutralization and antibody-dependent enhancement [3].

High impact information on Antibody-Dependent Enhancement

• The administration of a fourth dose resulted in homologous neutralizing activity in sera from 5 to 24 subjects (21%; CI, 7% to 37%) as well as in complement-mediated antibody-dependent enhancement in sera from 6 of 24 subjects (25%; CI, 10% to 42%) [5].
• Macrophages and monocytes have been associated with human RRV disease, and previous studies have shown that RRV is capable of infecting macrophages via both a natural virus receptor and by Fc receptor-mediated antibody-dependent enhancement (ADE) [6].
• Levels of B19-DNA and B19-NS1 mRNA transcription increased in the presence of anti-B19 IgG antibodies, but this effect decreased in the presence of anti-Fc receptor antibodies, showing antibody-dependent enhancement by B19 infection [7].
• This study is the first to suggest B19 infection of nonerythroid lineage cells with antibody-dependent enhancement [7].
• In this study it is demonstrated that complement-mediated antibody-dependent enhancement (C'-ADE) of HIV-1 infection in vitro is blocked by murine monoclonal antibodies to CD4 and complement receptor type 2 (CR2) while HIV-1 infection in the absence of C'-ADE is blocked by anti-CD4 but not anti-CR2 monoclonal antibodies [8].

Anatomical context of Antibody-Dependent Enhancement

• Human parvovirus B19 infection of monocytic cell line U937 and antibody-dependent enhancement [7].
• However, the results indicated a possible correlation between RSV infection of the infants and the occurrence of in vitro antibody-dependent enhancement of the cord blood sera at a serum dilution of 10(-2) [9].
• Considering that antibody dependent enhancement (ADE) plays an important role in the etiopathogenic mechanism of DHF/DSS, we decide to study the Dengue 2 virus (D2V) capability of replication in peripheral blood leukocytes (PBL) from asthmatic patients and healthy persons [10].

Gene context of Antibody-Dependent Enhancement

• The results do not support the hypothesis of the role of antibody-dependent enhancement giving rise to increased viremic titers and production of TNF alpha in patients [11].
• With the similarity in reactivity of 523, this antibody dependent enhancement was found in natural cytotoxicity to hu-H2 and MIA but not to CW3 [12].

References