Hepatitis C Virus–Escape Studies for Human Monoclonal Antibody AR4A Reveal Isolate-Specific Resistance and a High Barrier to Resistance

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

Hepatitis C Virus–Escape Studies for Human Monoclonal Antibody AR4A Reveal Isolate-Specific Resistance and a High Barrier to Resistance. / Velázquez-moctezuma, Rodrigo; Galli, Andrea; Law, Mansun; Bukh, Jens; Prentoe, Jannick.

In: The Journal of Infectious Diseases, Vol. 219, No. 1, 2019, p. 68-79.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Velázquez-moctezuma, R, Galli, A, Law, M, Bukh, J & Prentoe, J 2019, 'Hepatitis C Virus–Escape Studies for Human Monoclonal Antibody AR4A Reveal Isolate-Specific Resistance and a High Barrier to Resistance', The Journal of Infectious Diseases, vol. 219, no. 1, pp. 68-79. https://doi.org/10.1093/infdis/jiy481

APA

Velázquez-moctezuma, R., Galli, A., Law, M., Bukh, J., & Prentoe, J. (2019). Hepatitis C Virus–Escape Studies for Human Monoclonal Antibody AR4A Reveal Isolate-Specific Resistance and a High Barrier to Resistance. The Journal of Infectious Diseases, 219(1), 68-79. https://doi.org/10.1093/infdis/jiy481

Vancouver

Velázquez-moctezuma R, Galli A, Law M, Bukh J, Prentoe J. Hepatitis C Virus–Escape Studies for Human Monoclonal Antibody AR4A Reveal Isolate-Specific Resistance and a High Barrier to Resistance. The Journal of Infectious Diseases. 2019;219(1):68-79. https://doi.org/10.1093/infdis/jiy481

Author

Velázquez-moctezuma, Rodrigo ; Galli, Andrea ; Law, Mansun ; Bukh, Jens ; Prentoe, Jannick. / Hepatitis C Virus–Escape Studies for Human Monoclonal Antibody AR4A Reveal Isolate-Specific Resistance and a High Barrier to Resistance. In: The Journal of Infectious Diseases. 2019 ; Vol. 219, No. 1. pp. 68-79.

Bibtex

@article{bb36771ee49146ef868a4b91e968bb86,
title = "Hepatitis C Virus–Escape Studies for Human Monoclonal Antibody AR4A Reveal Isolate-Specific Resistance and a High Barrier to Resistance",
abstract = "Global control of hepatitis C virus (HCV) depends on development of a prophylactic vaccine. We studied escape for cross-genotype-reactive neutralizing antibody AR4A, providing valuable information for HCV vaccine design. We cultured HCV Core-NS2 recombinants H77(genotype 1a)/JFH1 or the highly-antibody-sensitive hypervariable region 1 (HVR1)-deleted variants H77/JFH1∆HVR1 and J6(genotype 2a)/JFH1∆HVR1 in Huh7.5 cells with AR4A. Long-term AR4A exposure of H77/JFH1 and H77/JFH1∆HVR1 did not yield resistance. However, J6/JFH1∆HVR1 developed the envelope-E2 substitutions I696T or I696N, which reduced AR4A binding (I696N>I696T). I696N conferred greater AR4A-resistance than I696T in J6/JFH1∆HVR1, whereas the reverse was observed in J6/JFH1. This was because I696N, but not I696T, conferred broadly increased antibody neutralization sensitivity to J6/JFH1. I696N and I696T abrogated infectivity of H77/JFH1 and broadly increased neutralization sensitivity of S52(genotype 3a)/JFH1. In conclusion, I696 is in the AR4A epitope, which has a high barrier to resistance, thus strengthening the rationale for its inclusion in rational HCV vaccine designs.",
author = "Rodrigo Vel{\'a}zquez-moctezuma and Andrea Galli and Mansun Law and Jens Bukh and Jannick Prentoe",
year = "2019",
doi = "10.1093/infdis/jiy481",
language = "English",
volume = "219",
pages = "68--79",
journal = "Journal of Infectious Diseases",
issn = "0022-1899",
publisher = "Oxford University Press",
number = "1",

}

RIS

TY - JOUR

T1 - Hepatitis C Virus–Escape Studies for Human Monoclonal Antibody AR4A Reveal Isolate-Specific Resistance and a High Barrier to Resistance

AU - Velázquez-moctezuma, Rodrigo

AU - Galli, Andrea

AU - Law, Mansun

AU - Bukh, Jens

AU - Prentoe, Jannick

PY - 2019

Y1 - 2019

N2 - Global control of hepatitis C virus (HCV) depends on development of a prophylactic vaccine. We studied escape for cross-genotype-reactive neutralizing antibody AR4A, providing valuable information for HCV vaccine design. We cultured HCV Core-NS2 recombinants H77(genotype 1a)/JFH1 or the highly-antibody-sensitive hypervariable region 1 (HVR1)-deleted variants H77/JFH1∆HVR1 and J6(genotype 2a)/JFH1∆HVR1 in Huh7.5 cells with AR4A. Long-term AR4A exposure of H77/JFH1 and H77/JFH1∆HVR1 did not yield resistance. However, J6/JFH1∆HVR1 developed the envelope-E2 substitutions I696T or I696N, which reduced AR4A binding (I696N>I696T). I696N conferred greater AR4A-resistance than I696T in J6/JFH1∆HVR1, whereas the reverse was observed in J6/JFH1. This was because I696N, but not I696T, conferred broadly increased antibody neutralization sensitivity to J6/JFH1. I696N and I696T abrogated infectivity of H77/JFH1 and broadly increased neutralization sensitivity of S52(genotype 3a)/JFH1. In conclusion, I696 is in the AR4A epitope, which has a high barrier to resistance, thus strengthening the rationale for its inclusion in rational HCV vaccine designs.

AB - Global control of hepatitis C virus (HCV) depends on development of a prophylactic vaccine. We studied escape for cross-genotype-reactive neutralizing antibody AR4A, providing valuable information for HCV vaccine design. We cultured HCV Core-NS2 recombinants H77(genotype 1a)/JFH1 or the highly-antibody-sensitive hypervariable region 1 (HVR1)-deleted variants H77/JFH1∆HVR1 and J6(genotype 2a)/JFH1∆HVR1 in Huh7.5 cells with AR4A. Long-term AR4A exposure of H77/JFH1 and H77/JFH1∆HVR1 did not yield resistance. However, J6/JFH1∆HVR1 developed the envelope-E2 substitutions I696T or I696N, which reduced AR4A binding (I696N>I696T). I696N conferred greater AR4A-resistance than I696T in J6/JFH1∆HVR1, whereas the reverse was observed in J6/JFH1. This was because I696N, but not I696T, conferred broadly increased antibody neutralization sensitivity to J6/JFH1. I696N and I696T abrogated infectivity of H77/JFH1 and broadly increased neutralization sensitivity of S52(genotype 3a)/JFH1. In conclusion, I696 is in the AR4A epitope, which has a high barrier to resistance, thus strengthening the rationale for its inclusion in rational HCV vaccine designs.

U2 - 10.1093/infdis/jiy481

DO - 10.1093/infdis/jiy481

M3 - Journal article

C2 - 30102355

VL - 219

SP - 68

EP - 79

JO - Journal of Infectious Diseases

JF - Journal of Infectious Diseases

SN - 0022-1899

IS - 1

ER -

ID: 208888915