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Commentary 10.1172/JCI128370

Are we there yet? The never-ending quest for an Epstein-Barr virus vaccine

Sandhya Sharma and Rayne H. Rouce

Center for Cell and Gene Therapy, Baylor College of Medicine, Houston Methodist Hospital and Texas Children’s Hospital, Houston, Texas, USA. Texas Children’s Cancer and Hematology Centers, Baylor College of Medicine, Houston, Texas, USA.

Address correspondence to: Rayne H. Rouce, 1102 Bates Street, Suite 1770, Houston, Texas 77030, USA. Phone: 832.824.4723; Email: rhrouce@txch.org.

Find articles by Sharma, S. in: JCI | PubMed | Google Scholar |

Center for Cell and Gene Therapy, Baylor College of Medicine, Houston Methodist Hospital and Texas Children’s Hospital, Houston, Texas, USA. Texas Children’s Cancer and Hematology Centers, Baylor College of Medicine, Houston, Texas, USA.

Address correspondence to: Rayne H. Rouce, 1102 Bates Street, Suite 1770, Houston, Texas 77030, USA. Phone: 832.824.4723; Email: rhrouce@txch.org.

Find articles by Rouce, R. in: JCI | PubMed | Google Scholar

First published April 15, 2019 - More info

Published in Volume 129, Issue 5 on May 1, 2019
J Clin Invest. 2019;129(5):1836–1838. https://doi.org/10.1172/JCI128370.
© 2019 American Society for Clinical Investigation
First published April 15, 2019 - Version history

The Epstein-Barr virus (EBV) is estimated to infect a large part of the population and is associated with a variety of human tumors; therefore, EBV is an important target for vaccine development. In this issue of the JCI, Rühl et al. developed a promising heterologous prime-boost vaccination strategy for EBV-associated malignancies and symptomatic primary infection. The authors show that two prime-boost regimens, using either dendritic cells or an adenovirus approach targeting nuclear antigen EBNA1 followed by a modified vaccinia virus Ankara (MVA) booster, induced significant T cell–mediated, EBV-specific immune control and Ab production. These findings suggest that administration of heterologous prime-boost vaccinations targeting EBNA1 may result in potent CD4+ and CD8+ T cell–mediated EBV immune control and may be a promising clinical approach.

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