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Delayed antibody dependent enhancement of low passage dengue virus 4 isolates.

ABSTRACT: The concept of antibody dependent enhancement (ADE) of dengue virus (DENV) infection is a cornerstone of our current understanding of dengue pathogenesis, although some questions as to the mechanism remain, particularly in regards to the behavior of low and high passage virus isolates. This study utilized two low passage DENV 4 isolates and a laboratory adapted DENV 4 isolate to investigate the potential of low passage isolates to undergo ADE.Little or no ADE of infection was observed on day 2 post infection with low passage isolates, while high enhancement of infection was seen with the laboratory adapted virus. However, both of the low passage isolates showed high levels of infection (60-100%) by day 5 post infection.These results show that low passage DENV 4 viruses undergo ADE mediated infection, but that the process is significantly temporally delayed as compared to laboratory adapted DENV 4.

SUBMITTER: Wikan N

PROVIDER: S-EPMC4556410 | biostudies-literature | 2015

REPOSITORIES: biostudies-literature

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Delayed antibody dependent enhancement of low passage dengue virus 4 isolates.

Wikan Nitwara N Libsittikul Sirikwan S Yoksan Sutee S Auewarakul Prasert P Smith Duncan R DR

BMC research notes 20150902

<h4>Background</h4>The concept of antibody dependent enhancement (ADE) of dengue virus (DENV) infection is a cornerstone of our current understanding of dengue pathogenesis, although some questions as to the mechanism remain, particularly in regards to the behavior of low and high passage virus isolates. This study utilized two low passage DENV 4 isolates and a laboratory adapted DENV 4 isolate to investigate the potential of low passage isolates to undergo ADE.<h4>Results</h4>Little or no ADE o ...[more]

PMID: 26328895

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Project description:BackgroundThe majority of dengue patients infected with any serotype of dengue virus (DENV) are asymptomatic, but the remainder may develop a wide spectrum of clinical symptoms, ranging from mild dengue fever (DF) to severe dengue hemorrhagic fever (DHF). Severe cases occur more often in patients who experience a secondary infection with a different virus serotype. A phenomenon called antibody-dependent enhancement (ADE) has been proposed to explain the onset of these severe cases, but the exact mechanism of ADE remains unclear.Methodology/principal findingVirus neutralization and ADE assays were performed using ultracentrifugation supernatants of acute-phase sera from patients with secondary infections or human monoclonal antibodies (HuMAbs) as anti-DENV antibodies. Virus sources included infectious serum-derived viruses from the ultracentrifugation precipitates, laboratory-culture adapted DENV, or recombinant DENVs derived from patient sera. In contrast to the high levels of ADE observed with laboratory virus strains, low ADE was observed with autologous patient-derived viruses, when patient sera were used to provide the antibody component in the ADE assays. Similar results were obtained using samples from DF and DHF patients. Recombinant-viruses derived from DHF patients showed only minor differences in neutralization and ADE activity in the presence of HuMAbs or plasma derived from the same DHF patient.Conclusion/significanceSerum or plasma taken from patients during the acute phase of a secondary infection showed high levels of ADE, but no neutralization activity, when assayed in the presence of laboratory-adapted virus strains. By contrast, serum or plasma from the same patient showed high levels of neutralization activity but failed to induce significant ADE when the assays were performed with autologous virus. These results demonstrate the significance of the virus source when measuring ADE. They also suggest that repeated passage of DENV in cell culture has endowed it with the capacity to induce high levels of ADE.

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Delayed antibody dependent enhancement of low passage dengue virus 4 isolates.

Publications

Delayed antibody dependent enhancement of low passage dengue virus 4 isolates.

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