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Viral Recombination

Viral Recombination

Cells are sometimes infected by more than one virus at once. When two viruses disassemble to expose their genomes for replication in the same cell, similar regions of their genomes can pair together and exchange sequences in a process called recombination. Alternatively, viruses with segmented genomes can swap segments in a process called reassortment.

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Related Experiment Video

Updated: Aug 3, 2025

Flow Virometry to Analyze Antigenic Spectra of Virions and Extracellular Vesicles

Flow Virometry to Analyze Antigenic Spectra of Virions and Extracellular Vesicles

Published on: January 25, 2017

Evolution of a Functionally Intact but Antigenically Distinct DENV Fusion Loop.

Rita M Meganck¹, Deanna Zhu², Stephanie Dong²

¹Department of Molecular Microbiology and Immunology, Saint Louis University.

Biorxiv : the Preprint Server for Biology

|April 10, 2023

Summary

Antibody-dependent enhancement (ADE) complicates Dengue virus (DENV) vaccines. This study engineered DENV variants (D2-FLM) that evade ADE-enhancing antibodies, offering a potential platform for safer DENV vaccines.

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Flow Virometry to Analyze Antigenic Spectra of Virions and Extracellular Vesicles

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Assessment of Immunologically Relevant Dynamic Tertiary Structural Features of the HIV-1 V3 Loop Crown R2 Sequence by ab initio Folding

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A Fluorogenic Peptide Cleavage Assay to Screen for Proteolytic Activity: Applications for coronavirus spike protein activation

A Fluorogenic Peptide Cleavage Assay to Screen for Proteolytic Activity: Applications for coronavirus spike protein activation

Published on: January 9, 2019

Area of Science:

Virology
Immunology
Vaccinology

Background:

Antibody-dependent enhancement (ADE) is a major challenge in Dengue virus (DENV) pathogenesis, complicating vaccine development and efficacy.
ADE is primarily mediated by antibodies targeting the conserved fusion loop (FL) of the DENV envelope protein, crucial for viral entry.
Existing DENV vaccines face safety concerns due to ADE, particularly in individuals with prior DENV exposure.

Approach:

Engineered a functional DENV variant (D2-FL) with mutations in the fusion loop (FL) to evade neutralization by FL-targeting antibodies.
Combined FL mutations with a modified prM cleavage site to create a mature DENV variant (D2-FLM) resistant to both prM- and FL-targeting antibodies.
Assessed the neutralization capacity of sera from Dengue virus-infected non-human primates (NHPs) against wildtype and engineered DENV strains.

Key Points:

The engineered D2-FL and D2-FLM variants demonstrate reduced neutralization by FL-targeting monoclonal antibodies.
D2-FLM evades both prM- and FL-binding antibodies but remains sensitive to other type-specific and cross-reactive antibodies.
Heterotypic (DENV4) immune NHP sera showed lower neutralization titers against D2-FLM compared to wildtype DENV2, while homotypic (DENV2) sera showed similar titers.

Conclusions:

D2-FL and D2-FLM are valuable tools for dissecting cross-reactive antibody subtypes in patient sera.
These engineered DENV variants represent a promising platform for developing safer live-attenuated DENV vaccines, potentially suitable for naive populations and children.