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Cytokine and Chemokine Responses in the Acute Phase of Hepatitis B Virus Replication in Naive and Previously Vaccinated Blood and Plasma Donors
Sheila M. Keating1,2,
John D. Heitman1,
Shiquan Wu1,
Xutao Deng1,2,
Susan L. Stramer4,
Mary C. Kuhns5,
Carolyn Mullen5,
Philip J. Norris1,2,3 and
Michael P. Busch1,2
+ Author Affiliations
1Blood Systems Research Institute, San Francisco, California
2Departments of Laboratory Medicine
3Medicine, University of California, San Francisco, California
4American Red Cross, Gaithersburg, Maryland
5Abbott Laboratories, Abbott Park, Illinois
Correspondence: Sheila M. Keating, PhD, Blood Systems Research Institute, San Francisco, and Departments of Laboratory Medicine University of California, 270 Masonic Avenue, San Francisco, CA 94118 ([email protected]).
Presented in part: American Association of Blood Banks, Baltimore, Maryland 2010.
Abstract
Background. Blood and plasma donor screening for hepatitis B virus (HBV) DNA, HBV surface antigen (HBsAg), and antibodies to surface (anti-HBs) and core (anti-HBc) antigens allows identification of individuals who acquired HBV despite previous HBV vaccination.
Methods. Of 14 HBV acute infection donor panels (HBV-DNA-positive/anti-HBc-negative), 6 donors were previously vaccinated (anti-HBs+). We investigated the differences in viral kinetics and immune responses in vaccinated and nonvaccinated individuals. Serial specimens were characterized for HBV DNA and serological markers and 39 cytokines.
Results. The rate of viral load increase was blunted, and virus was cleared more rapidly in vaccinated individuals (P = .004). In unvaccinated individuals, induced protein 10 (IP-10), interleukin 10 (IL-10), macrophage inflammatory protein 1β (MIP-1β), and soluble interleukin 2Rα (sIL-2Rα) levels were commonly elevated at the time of peak viremia. In contrast, vaccinated individuals had earlier peaks in IL-10 and IP-10 responses that occurred at much lower viral loads and coincided with anamnestic anti-hepatitis B surface (HBs) responses and clearance of viremia.
Conclusion. There is earlier engagement of innate and adaptive immunity in infected subjects with previous vaccination, possibly explaining suppressed viremia in vaccine breakthrough infections. Although breakthrough infections occur in partially protected vaccine recipients, vaccination likely contributes to early control of replication, limiting immune activation and preventing development of clinically significant acute and chronic HBV infection.
Key words
hepatitis B virus
vaccination
cytokine
chemokine
acute infection
immunity
Received June 19, 2013.
Accepted September 6, 2013.
© The Author 2013. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: [email protected].
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