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Monday, 01/10/2022 6:46:00 PM

Monday, January 10, 2022 6:46:00 PM

Post# of 649
>>> Antibody-dependent enhancement


https://en.wikipedia.org/wiki/Antibody-dependent_enhancement


In antibody-dependent enhancement, sub-optimal antibodies (the blue Y-shaped structures in the graphic) bind to both viruses and Fc gamma receptors (labeled Fc?RII) expressed on immune cells promoting infection of these cells.

Antibody-dependent enhancement (ADE), sometimes less precisely called immune enhancement or disease enhancement, is a phenomenon in which binding of a virus to suboptimal antibodies enhances its entry into host cells, followed by its replication.[1][2] The suboptimal antibodies can result from natural infection or from vaccination. ADE may cause enhanced respiratory disease and acute lung injury after respiratory virus infection (ERD) with symptoms of monocytic infiltration and an excess of eosinophils in respiratory tract.[3] ADE along with type 2 T helper cell-dependent mechanisms may contribute to a development of the vaccine associated disease enhancement (VADE), which is not limited to respiratory disease.[3] Some vaccine candidates that targeted coronaviruses, RSV virus and Dengue virus elicited VADE, and were terminated from further development or became approved for use only for patients who had those viruses before.


Contents

1 Technical description
2 Coronavirus
2.1 COVID-19
3 Influenza
4 Dengue
5 HIV-1
6 Mechanism
6.1 Different virus serotypes
6.2 Conclusion
7 See also
8 References

Technical description

Antiviral antibodies promote viral infection of target immune cells by exploiting the phagocytic Fc?R or complement pathway.[4] After interaction with the virus the antibody binds Fc receptors (FcR) expressed on certain immune cells or some of the complement proteins. Fc?Rs bind antibodies via their fragment crystallizable region (Fc). Usually the process of phagocytosis is accompanied by virus degradation, however, if the virus is not neutralized (either due to low affinity binding or targeting to a non-neutralizing epitope), antibody binding might result in virus escape and therefore, enhanced infection. Thus, phagocytosis can cause viral replication, with the subsequent death of immune cells. The virus “deceives” the process of phagocytosis of immune cells and uses the host's antibodies as a Trojan horse. ADE may occur because of the non-neutralizing characteristic of the antibody, which binds viral epitopes other than those involved in host-cell attachment and entry. ADE may also happen because the antibodies are present at sub-neutralizing concentrations (yielding occupancies on viral epitopes below the threshold for neutralization).[5][6] In addition ADE can be induced when the strength of antibody-antigen interaction is below a certain threshold.[7][8] This phenomenon might lead to both increased virus infectivity and virulence. The viruses that can cause ADE frequently share some common features such as antigenic diversity, abilities to replicate and to establish persistence in immune cells.[1] ADE can occur during the development of a primary or secondary viral infection, as well as after vaccination with a subsequent virus challenge.[1][9][10] It has been observed mainly with positive-strand RNA viruses. Among them are Flaviviruses such as Dengue virus,[11] Yellow fever virus, Zika virus,[12][13] Coronaviruses, including alpha- and betacoronaviruses,[14] Orthomyxoviruses such as influenza,[15] Retroviruses such as HIV,[16][17][18] and Orthopneumoviruses such as RSV.[19][20][21]

The mechanism that involves phagocytosis of immune complexes via the Fc?RII / CD32 receptor is better understood compared to the complement receptor pathway.[22][23][24] Cells that express this receptor are represented by monocytes, macrophages, some categories of dendritic cells and B-cells. ADE is mainly mediated by IgG antibodies,[23] however, IgM along with complement,[25] and IgA antibodies[17][18] have also been shown to trigger ADE.

Coronavirus

COVID-19

Further information: COVID-19 vaccine misinformation and hesitancy § Antibody-dependent enhancement

ADE was a concern during late clinical stages of vaccine development against COVID-19.[26][27]


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