在乙型肝炎病毒复制的急性期没有和以前接种细胞因子和趋

StephenW

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].

StephenW

在乙型肝炎病毒复制的急性期的幼稚和以前接种血液和血浆捐献者的细胞因子和趋化因子的响应

    希拉M. Keating1 ， 2 ，
    约翰·D Heitman1 ，
    十全武1 ，
    旭涛Deng1 ，2，
    苏珊L. Stramer4 ，
    玛丽三Kuhns5 ，
    卡罗琳Mullen5 ，
    菲利普·J Norris1 ，2,3和
    迈克尔P. Busch1 ， 2

+作者所属机构

    血魄系统研究所，旧金山，加利福尼亚州
    检验医学杂志2Departments
    3Medicine ，加州大学，旧金山，加利福尼亚州
    4American红十字会，马里兰州盖瑟斯堡
    5Abbott实验室，雅培公园，伊利诺伊州

    通讯：希拉M.基廷博士，血液系统研究所，旧金山和加利福尼亚州， 270共济大街，旧金山，CA 94118 （ [email protected] ）检验医学大学的院系。

    呈现部分：血库的美国协会，巴尔的摩，马里兰州2010年

摘要

背景。血液和血浆供体筛查乙型肝炎病毒（HBV ）的DNA ，乙肝病毒表面抗原（HBsAg ）和抗体表面（抗-HBs ）和核心（抗-HBc ）抗原可以识别谁收购了乙肝病毒，尽管以前乙肝疫苗接种的个人。

方法。 14乙肝病毒急性感染供体面板（ HBV-DNA-positive/anti-HBc-negative ）中， 6捐助者以前接种过疫苗（抗-HBs + ） 。我们调查的病毒动力学和免疫反应的差异在接种和未接种的个体。连续的标本进行了表征为HBV DNA和血清学标志物和39细胞因子。

结果。病毒负荷增加的速度减弱，而病毒在接种的个体（ P = 0.004 ）的清除速度更快。在未接种疫苗的个体，诱导蛋白10 （IP -10） ，白细胞介素-10（IL -10），巨噬细胞炎性蛋白1β（ MIP-1β ）和可溶性白细胞介素2Rα （中sIL -2Rα ）水平通常升高至峰值病毒血症的时间。与此相对，接种的个体中有IL-10和其在低得多的病毒负荷发生和正好与回忆抗乙肝表面（ HBs）中的反应和病毒血症的间隙中IP-10的反应早期峰值。

结论。有较早的感染者与以前的疫苗接种先天和适应性免疫的参与，可能解释在疫苗的突破感染抑制病毒血症。虽然突破感染发生在部分保护接种者，接种疫苗可能有助于早期控制的复制，限制了免疫激活和防止临床上显著急性和慢性HBV感染的发展。
关键词

    B型肝炎病毒
    接种疫苗
    细胞因子
    趋化因子
    急性感染
    免疫

    收到2013年6月19日。
    接受2013年9月6日。

    ©笔者2013年。发布时间由牛津大学出版社代表美国传染病学会。保留所有权利。对于权限，请发送电子邮件至： journals.permissions @ oup.com 。

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