ArticlePLoS pathogens2017
A novel mechanism of antibody-mediated enhancement of flavivirus infection.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed.
- Omsk Hemorrhagic Fever Virus and Powassan Virus Infections at Different Times After Immunization with the TBE Vaccine in In Vivo Experiments.International journal of molecular sciences · 2026Article
- Conserved histidine residues and the control of tick-borne encephalitis virus maturation.The Journal of general virology · 2026Article
- Neutralizing and enhancing monoclonal antibodies in SARS-CoV-2 convalescent patients: lessons from early variant infection and impact on shaping emerging variants.Emerging microbes & infections · 2024Article
- The Flavivirus Non-Structural Protein 5 (NS5): Structure, Functions, and Targeting for Development of Vaccines and Therapeutics.Vaccines · 2024Review
- Characterization of Two Highly Specific Monoclonal Antibodies Targeting the Glycan Loop of the Zika Virus Envelope Protein.Viral immunology · 2024Article
- EDIII-Fc induces protective immune responses against the Zika virus in mice and rhesus macaque.PLoS neglected tropical diseases · 2023Article
- A Prototype-Pathogen Approach for the Development of Flavivirus Countermeasures.The Journal of infectious diseases · 2023Review
- Antibodies Capable of Enhancing SARS-CoV-2 Infection Can Circulate in Patients with Severe COVID-19.International journal of molecular sciences · 2023Article
- New Neutralizing Epitope Exposed on the Domain II of Tick-Borne Encephalitis Virus Envelope Glycoprotein E.Viruses · 2023Article
- Impact of structural dynamics on biological functions of flaviviruses.The FEBS journal · 2023Review
- Induction of humoral and cell-mediated immunity to the NS1 protein of TBEV with recombinant Influenza virus and MVA affords partial protection against lethal TBEV infection in mice.Frontiers in immunology · 2023Article
- A recombinant Modified Vaccinia virus Ankara expressing prME of tick-borne encephalitis virus affords mice full protection against TBEV infection.Frontiers in immunology · 2023Article
- Highly pathogenic coronaviruses and the kidney.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Review
- Review
- New Anti-Flavivirus Fusion Loop Human Antibodies with Zika Virus-Neutralizing Potential.International journal of molecular sciences · 2022Article
- Article
- COVID-19: inflammatory responses, structure-based drug design and potential therapeutics.Molecular diversity · 2022Review
- The Immunopathobiology of SARS-CoV-2 Infection.FEMS microbiology reviews · 2021Article
- Article
- Antibody-Dependent Enhancement of Bacterial Disease: Prevalence, Mechanisms, and Treatment.Infection and immunity · 2021Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Antibody-dependent enhancement of viral infection is a well-described phenomenon that is based on the cellular uptake of infectious virus-antibody complexes following their interaction with Fcγ receptors expressed on myeloid cells. Here we describe a novel mechanism of antibody-mediated enhancement of infection by a flavivirus (tick-borne encephalitis virus) in transformed and primary human cells, which is independent of the presence of Fcγ receptors. Using chemical cross-linking and immunoassays, we demonstrate that the monoclonal antibody (mab) A5, recognizing an epitope at the interface of the dimeric envelope protein E, causes dimer dissociation and leads to the exposure of the fusion loop (FL). Under normal conditions of infection, this process is triggered only after virus uptake by the acidic pH in endosomes, resulting in the initiation of membrane fusion through the interaction of the FL with the endosomal membrane. Analysis of virus binding and cellular infection, together with inhibition by the FL-specific mab 4G2, indicated that the FL, exposed after mab A5- induced dimer-dissociation, mediated attachment of the virus to the plasma membrane also at neutral pH, thereby increasing viral infectivity. Since antibody-induced enhancement of binding was not only observed with cells but also with liposomes, it is likely that increased infection was due to FL-lipid interactions and not to interactions with cellular plasma membrane proteins. The novel mechanism of antibody-induced infection enhancement adds a new facet to the complexity of antibody interactions with flaviviruses and may have implications for yet unresolved effects of polyclonal antibody responses on biological properties of these viruses.
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