Serum neutralization activity declines but memory B cells persist after cure of chronic hepatitis C

Akira Nishio, Sharika Hasan, Heiyoung Park, Nana Park, Jordan H. Salas, Eduardo Salinas, Lela Kardava, Paul Juneau, Nicole Frumento, Guido Massaccesi, Susan Moir, Justin R. Bailey, Arash Grakoui, Marc G. Ghany and Barbara Rehermann ()
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Akira Nishio: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, DHHS
Sharika Hasan: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, DHHS
Heiyoung Park: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, DHHS
Nana Park: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, DHHS
Jordan H. Salas: Johns Hopkins University School of Medicine
Eduardo Salinas: Emory University School of Medicine
Lela Kardava: National Institutes of Health, DHHS
Paul Juneau: Office of Research Services, National Institutes of Health
Nicole Frumento: Johns Hopkins University School of Medicine
Guido Massaccesi: Johns Hopkins University School of Medicine
Susan Moir: National Institutes of Health, DHHS
Justin R. Bailey: Johns Hopkins University School of Medicine
Arash Grakoui: Emory University School of Medicine
Marc G. Ghany: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, DHHS
Barbara Rehermann: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, DHHS

Nature Communications, 2022, vol. 13, issue 1, 1-16

Abstract: Abstract The increasing incidence of hepatitis C virus (HCV) infections underscores the need for an effective vaccine. Successful vaccines to other viruses generally depend on a long-lasting humoral response. However, data on the half-life of HCV-specific responses are lacking. Here we study archived sera and mononuclear cells that were prospectively collected up to 18 years after cure of chronic HCV infection to determine the role of HCV antigen in maintaining neutralizing antibody and B cell responses. We show that HCV-neutralizing activity decreases rapidly in potency and breadth after curative treatment. In contrast, HCV-specific memory B cells persist, and display a restored resting phenotype, normalized chemokine receptor expression and preserved ability to differentiate into antibody-secreting cells. The short half-life of HCV-neutralizing activity is consistent with a lack of long-lived plasma cells. The persistence of HCV-specific memory B cells and the reduced inflammation after cure provide an opportunity for vaccination to induce protective immunity against re-infection.

Date: 2022
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DOI: 10.1038/s41467-022-33035-z

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