Modeling Infectious Bursal Disease Virus (IBDV) Antigenic Drift In Vitro
Infectious bursal disease virus (IBDV) vaccines do not induce sterilizing immunity, and vaccinated birds can become infected with field strains. Vaccine-induced immune selection pressure drives the evolution of antigenic drift variants that accumulate amino acid changes in the hypervariable region (...
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MDPI AG
2022-12-01
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Online Access: | https://www.mdpi.com/1999-4915/15/1/130 |
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author | Amin S. Asfor Vishwanatha R. A. P. Reddy Salik Nazki Joanna Urbaniec Andrew J. Brodrick Andrew J. Broadbent |
author_facet | Amin S. Asfor Vishwanatha R. A. P. Reddy Salik Nazki Joanna Urbaniec Andrew J. Brodrick Andrew J. Broadbent |
author_sort | Amin S. Asfor |
collection | DOAJ |
description | Infectious bursal disease virus (IBDV) vaccines do not induce sterilizing immunity, and vaccinated birds can become infected with field strains. Vaccine-induced immune selection pressure drives the evolution of antigenic drift variants that accumulate amino acid changes in the hypervariable region (HVR) of the VP2 capsid, which may lead to vaccine failures. However, there is a lack of information regarding how quickly mutations arise, and the relative contribution different residues make to immune escape. To model IBDV antigenic drift in vitro, we serially passaged a classical field strain belonging to genogroup A1 (F52/70) ten times, in triplicate, in the immortalized chicken B cell line, DT40, in the presence of sub-neutralizing concentrations of sera from birds inoculated with IBDV vaccine strain 2512, to generate escape mutants. This assay simulated a situation where classical strains may infect birds that have suboptimal vaccine-induced antibody responses. We then sequenced the HVR of the VP2 capsid at passage (P) 5 and 10 and compared the sequences to the parental virus (P0), and to the virus passaged in the presence of negative control chicken serum that lacked IBDV antibodies. Two escape mutants at P10 had the same mutations, D279Y and G281R, and a third had mutations S251I and D279N. Furthermore, at P5, the D279Y mutation was detectable, but the G281R mutation was not, indicating the mutations arose with different kinetics. |
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issn | 1999-4915 |
language | English |
last_indexed | 2024-03-09T11:02:35Z |
publishDate | 2022-12-01 |
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spelling | doaj.art-d0f5f339d2f14d77a3a98f8e9241bdbb2023-12-01T01:10:47ZengMDPI AGViruses1999-49152022-12-0115113010.3390/v15010130Modeling Infectious Bursal Disease Virus (IBDV) Antigenic Drift In VitroAmin S. Asfor0Vishwanatha R. A. P. Reddy1Salik Nazki2Joanna Urbaniec3Andrew J. Brodrick4Andrew J. Broadbent5Birnaviruses Group, The Pirbright Institute, Ash Road, Woking GU24 0NF, UKBirnaviruses Group, The Pirbright Institute, Ash Road, Woking GU24 0NF, UKBirnaviruses Group, The Pirbright Institute, Ash Road, Woking GU24 0NF, UKBirnaviruses Group, The Pirbright Institute, Ash Road, Woking GU24 0NF, UKDepartment of Animal and Avian Sciences, College of Agriculture and Natural Resources, University of Maryland, College Park, MD 20742, USABirnaviruses Group, The Pirbright Institute, Ash Road, Woking GU24 0NF, UKInfectious bursal disease virus (IBDV) vaccines do not induce sterilizing immunity, and vaccinated birds can become infected with field strains. Vaccine-induced immune selection pressure drives the evolution of antigenic drift variants that accumulate amino acid changes in the hypervariable region (HVR) of the VP2 capsid, which may lead to vaccine failures. However, there is a lack of information regarding how quickly mutations arise, and the relative contribution different residues make to immune escape. To model IBDV antigenic drift in vitro, we serially passaged a classical field strain belonging to genogroup A1 (F52/70) ten times, in triplicate, in the immortalized chicken B cell line, DT40, in the presence of sub-neutralizing concentrations of sera from birds inoculated with IBDV vaccine strain 2512, to generate escape mutants. This assay simulated a situation where classical strains may infect birds that have suboptimal vaccine-induced antibody responses. We then sequenced the HVR of the VP2 capsid at passage (P) 5 and 10 and compared the sequences to the parental virus (P0), and to the virus passaged in the presence of negative control chicken serum that lacked IBDV antibodies. Two escape mutants at P10 had the same mutations, D279Y and G281R, and a third had mutations S251I and D279N. Furthermore, at P5, the D279Y mutation was detectable, but the G281R mutation was not, indicating the mutations arose with different kinetics.https://www.mdpi.com/1999-4915/15/1/130infectious bursal disease virus (IBDV)antigenic driftimmune escapeescape mutanthypervariable regionHVR |
spellingShingle | Amin S. Asfor Vishwanatha R. A. P. Reddy Salik Nazki Joanna Urbaniec Andrew J. Brodrick Andrew J. Broadbent Modeling Infectious Bursal Disease Virus (IBDV) Antigenic Drift In Vitro Viruses infectious bursal disease virus (IBDV) antigenic drift immune escape escape mutant hypervariable region HVR |
title | Modeling Infectious Bursal Disease Virus (IBDV) Antigenic Drift In Vitro |
title_full | Modeling Infectious Bursal Disease Virus (IBDV) Antigenic Drift In Vitro |
title_fullStr | Modeling Infectious Bursal Disease Virus (IBDV) Antigenic Drift In Vitro |
title_full_unstemmed | Modeling Infectious Bursal Disease Virus (IBDV) Antigenic Drift In Vitro |
title_short | Modeling Infectious Bursal Disease Virus (IBDV) Antigenic Drift In Vitro |
title_sort | modeling infectious bursal disease virus ibdv antigenic drift in vitro |
topic | infectious bursal disease virus (IBDV) antigenic drift immune escape escape mutant hypervariable region HVR |
url | https://www.mdpi.com/1999-4915/15/1/130 |
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