A Review: Understanding Molecular Mechanisms of Antibody-Dependent Enhancement in Viral Infections

Antibody Dependent Enhancement (ADE) of an infection has been of interest in the investigation of many viruses. It is associated with the severity of the infection. ADE is mediated by non-neutralizing antibodies, antibodies at sub-neutralizing concentrations, or cross-reactive non-neutralizing antib...

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Bibliographic Details
Published in:Vaccines (Basel) 2023-07, Vol.11 (7), p.1240
Main Authors: Sawant, Jyoti, Patil, Ajit, Kurle, Swarali
Format: Article
Language:English
Subjects:
Analysis
Antibodies
Antibody Dependent Enhancement (ADE)
Antigens
Complement
Complement component C1q
complement protein C1q
Complement system
Cytotoxicity
Dengue fever
Development and progression
Ebola virus
Fc receptor
Fc receptors
Health aspects
HIV
Human immunodeficiency virus
Immunomodulation
Immunotherapy
Infections
Kinases
Lysis
mechanism of ADE
Methods
Middle East respiratory syndrome
Molecular mechanics
Molecular modelling
Neutralizing
Pathogens
Proteins
Receptors
Replication
Respiratory diseases
Review
Severe acute respiratory syndrome
Severe acute respiratory syndrome coronavirus 2
severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
Vaccine development
Vaccines
Vector-borne diseases
Viral antibodies
Viral diseases
Viral infections
Virus diseases
Viruses
West Nile virus
Zika virus
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Description
Summary:Antibody Dependent Enhancement (ADE) of an infection has been of interest in the investigation of many viruses. It is associated with the severity of the infection. ADE is mediated by non-neutralizing antibodies, antibodies at sub-neutralizing concentrations, or cross-reactive non-neutralizing antibodies. Treatments like plasma therapy, B cell immunizations, and antibody therapies may trigger ADE. It is seen as an impediment to vaccine development as well. In viruses including the Dengue virus (DENV), severe acute respiratory syndrome (SARS) virus, Middle East respiratory syndrome (MERS) virus, human immunodeficiency virus (HIV), Ebola virus, Zika virus, and influenza virus, the likely mechanisms of ADE are postulated and described. ADE improves the likelihood of productively infecting cells that are expressing the complement receptor or the Fc receptor (FcR) rather than the viral receptors. ADE occurs when the FcR, particularly the Fc gamma receptor, and/or complement system, particularly Complement 1q (C1q), allow the entry of the virus-antibody complex into the cell. Moreover, ADE alters the innate immune pathways to escape from lysis, promoting viral replication inside the cell that produces viral particles. This review discusses the involvement of FcR and the downstream immunomodulatory pathways in ADE, the complement system, and innate antiviral signaling pathways modification in ADE and its impact on facilitating viral replication. Additionally, we have outlined the modes of ADE in the cases of different viruses reported until now.
ISSN:2076-393X
2076-393X
DOI:10.3390/vaccines11071240