翻译完毕乙肝免疫策略资料，感谢大家

cici301

请斑竹分配,我也想尽一部分力

intoxication

pdf文件30页Postvaccination Testing for Serologic Response标题后
到31页References标题前

(非常抱歉，因为一点事情发上来发慢了，以下是我投的翻译内容）不好意思，发不去油箱，只好帖出来了

接种后对血清反应所做的测试

由HBsAg阳性妇女所生婴儿需接受接种后测试的建议由以下报告所提供。

（参阅HBsAg阳性妇女所生婴儿管理办法）。这里提供其他人接种后进行测试的建议。

1对于婴儿，小孩或者青少年，在其接受了常规接踵疫苗后不需要进行免疫性的血清测试。

2接种后的测试只推荐于以下随后临床管理依靠于其自身免疫状况知识之上的人群。

----卫生保健工作者

----慢性血液透析患者，HIV感染者和其他免疫受损人群。（例如，接受造血干细胞移植者或接受化疗者）

3在免疫程序完成最后一针后，通过允许抗HBs保护水平(≥10mIU/mL)的确定方法来进行持续1-2个月的测试。

4首个接种程序被认为产生免疫性后，抗HBs水平10mIU/mL的人。

----有长期保护的有免疫能力的人不需要做定期的进一步抗HBs水平测试

----有抑制免疫的人可能需要做每年的抗HBs水平测试。（参阅加强针剂）

5参加首个接种程序后抗HBs水平少于10mIU/mL的人需要从新接种。按照适当的时间表完成三针疫苗的接种
 
 后做一个为期1--2个月的抗HBs测试通常比在完成一针或更多针疫苗接种后做的血清测试来得更加实用。

6对于再次接种疫苗后无反应的人需进行HBsAg测试。

----假如HBsAg测试结果为阳性的人，则需要接受适当的管理（参阅附件B），任何家庭接触，性接触，

或共用针头都应该被区分开，并且进行预防接种。（参阅附件A）

----检测结果为阴性的人容易被感染HBV，所以这部分人被建议进行HBV的预防，并且需要获得HBIG作为

暴露后的预防，以防止任何已知的或可能的非肠道HBsAg阳性血液的暴露。（参阅附件C）

加强针剂

1对于接受过免疫，正处于正常免疫状况的婴儿，小孩或青少年，并不推荐他们进行加强针剂的注射。

 除非特殊情况（参阅接种后对血清反应所做的测试），否则对于任何年龄层的人，都不推荐通过血

 清测试来评定抗体水平。

2对于血液透析患者，是否需要进行加强针剂的注射由每年的乙肝表面抗原抗体（抗HBs)测试来确定。

 当抗HBs水平下降到少于10mIU/mL，就有必要进行一针加强针剂的注射了。

3对于其他的免疫力受损的人（例如爱滋病感染者，接受造血干细胞移植者或接受化疗者），是否需要为

 其进行加强针剂的注射到目前为止还没有定论。当抗HBs水平下降到少于10mIU/mL而进行抗HBs测试和注

 射加强针剂的人，被视为正处于高危暴露当中。

intoxication

以上是我的粗略翻译，翻译不好请多多包涵。

要是最后那段多的没有人认投，我也可以帮忙翻译的。

能为论坛和战友做事是我的荣幸。

欢迎大家多到论坛的英语版灌水~~~呵呵~~~~~~

mstzh

楼主：

    你好，我是一名在读的学生，想帮忙翻译一部分，一定会尽力。

    邮箱：[email protected]。

    

yyy777

我可以翻译一些，[email protected]

草样年华谁精彩

还有未翻译的英文部分吗？我也来帮忙。

[email protected]

chuck

刚刚才看到，

我的油箱[email protected]

翻译技术还可以，大家都来努力

八年抗战

我的部分如下，水平有限。

附录B

免疫疗法问题

乙型肝炎疫苗剂量和给药

Recommended vaccine doses vary by product, age of
recipient, and needs of special populations (see Table 2).
Administration of single-antigen or combination vaccine
simultaneously with other childhood vaccines produces
no clinically significant interference in antibody responses
(1–13). Although the antigen contents of vaccines differ,
vaccines made by different manufacturers are interchangeable,
except for the 2-dose schedule used for adolescents
aged 11–15 years, for which only Recombivax HB is
approved. Combination vaccines are not approved for use
as a birth dose because of potential suppression of the
immune response to subsequent doses of the Haemophilus
influenzae type b (Hib) component in Comvax (14) and
possible decreased immunogenicity of the diphtheria component
of Pediarix when administered at birth.

推荐的疫苗剂量因为产品、接受者年龄和特殊的群体（见表2）需要而不同。
单抗原的或复合的疫苗与其它儿童期的疫苗同时使用在抗体反应方面没有产生显著的临床干扰。（1-13）
尽管疫苗中抗原的内容不同，但除了计划2针剂量的用于11-15岁的青少年的疫苗外（只有 Recombivax HB被批准用于此阶段），
各厂商生产的疫苗是可交替使用的。复合疫苗不允许作为刚出生的第一针（birth dose)使用，因为其作为出生第一针使用时，
对以后的COMVAX(注：一种疫苗）中乙型流感嗜血杆菌(Hib)成分的免疫反应有潜在的抑制作用，
并有可能减少Pediarix中白喉成分的致免疫性。

Hepatitis B vaccine should be administered by intramuscular
injection. Injection into the buttock is associated
with decreased immunogenicity (15–18). Intradermal
administration can result in a lower seroconversion rate
and final concentration of antibody to hepatitis B surface
antigen compared with intramuscular administration; limited
data are available to assess long-term protection from
this route of administration (19,20).
乙型肝炎疫苗应该被用于肌肉注射，注射进臀部与致免疫性的降低有联系(15-18).
与肌肉用药相比,真皮层用药导致更低的血清转换率和最终更低的hbsag抗体(hbsab)浓度;
无足够的数据确认这种给药方式的长期保护作用.

The anterolateral thigh muscle is the recommended site
of administration for neonates (aged <1 month) and
infants (aged 1–12 months). For toddlers (aged 1–2 years)
and older children, either the anterolateral thigh or the
deltoid muscle may be used if the muscle mass is adequate.
The deltoid muscle is the preferred site of administration
for adolescents.
对新生儿（小于一个月)和婴儿(年龄在1-12个月之间)
，推荐注射点为大腿前外侧肌肉.对刚学会走路的孩子(年龄在1-2岁之间)或更大的孩子,
只要足够大,大腿前外侧肌和三角肌都是合适的注射点.
对青春期的孩子,三角肌是更应选择的注射点.

 For intramuscular injection, the needle should be long
enough to reach the muscle mass and prevent vaccine from
seeping into subcutaneous tissue, but not so long as to
involve underlying nerves and blood vessels or bone (21).
The appropriate needle length is usually 5/8” for neonates,
7/8”–1” for infants, and 7/8”–11/4” for toddlers, older children,
and adolescents. A 22- to 25-gauge needle should
be used.
对于肌肉注射来说,针应该够长能到达肌肉块中,以避免疫苗漏到皮下组织中.
但不要太长到达底层神经和血管或骨头.通常合适的长度是,对于新生儿,5/8",婴儿7/8"-1",
刚学会走路的孩子和更大一点的孩子,青春期的孩子7/8"-11/4".
应该使用22-到25-标准的针头.

Hepatitis B vaccine administered by any route or site other
than intramuscularly in the anterolateral thigh or deltoid
muscle should not be counted as valid and should be
repeated unless serologic testing indicates that an adequate
response has been achieved (see Postvaccination Testing
for Serologic Response).

乙肝疫苗注射在除大腿前外侧肌肉和三角肌以外的任何地方都不应作为有效注射，应该再次注射除非
血清检测证实已经获得有足够的（免疫）反应（见血清反应注射后测试Postvaccination Testing for Serologic Response)

Hepatitis B vaccine and other vaccines administered during
the same visit should be administered in different
injection sites. When more than one injection must be
administered in the same limb, the anterolateral thigh is
usually the preferred site, with injections separated by
1”–2” to avoid overlap in local reactions.

乙肝疫苗和其他疫苗在同一次注射时应该被注射在不同的注射点.
当必须在同一肢体上有多次注射的时候,通常选择大腿前外侧肌肉.各次注射应该隔开1"-2"以避免不良反应重叠.

For persons at risk for hemorrhage (e.g., persons with
hemophilia), the risk of bleeding after intramuscular
injection can be minimized by use of a 23-gauge (or
smaller) needle, application of direct pressure to the
injection site for >2 minutes, and administration of vaccine
immediately after infusion of coagulation factor. Subcutaneous
administration of vaccine can be considered
for these persons but might result in lower response and
an increased local reaction.

对有出血危险的人(如:血友病患者）。使用23-（或更小的）针，在注射点直接压大于两分钟，
在凝血因子输液后立刻使用疫苗可以最小化肌肉注射后的流血危险。对这些人可以考虑皮下注射
但是可能导致更低的免疫反应和更多的不良反应

Hepatitis B vaccine should be stored at 35°–46° F (2°–8° C)
and should not be frozen.

乙肝疫苗应该保存在华氏35°–46°(摄氏2°–8°),不应该冷冻.

 A vaccine information statement (VIS) must be provided
to recipients of hepatitis B vaccine. The National Childhood
Vaccine Injury Act of 1986 (42 U.S.C. § 300aa-26)
requires vaccine providers to give a copy of the most current
vaccine-specific VIS to all recipients (children or their
guardians) of vaccines that are included on the National
Vaccine Injury Compensation Program table maintained
by the Health Resources and Services Administration
(available at http://www. hrsa.gov). Hepatitis B vaccine is
included on this table. The most current VIS for
hepatitis B vaccine is available at http://www.cdc.gov/nip/
publications/vis. Statements in languages other than
English are available from the Immunization Action
Coalition at http://www.immunize.org.
必须提供疫苗信息审核(VIS)给乙肝疫苗的接受者.1986年国家儿童期疫苗注射法案(42 U.S.C § 300aa-26)
要求疫苗提供者提供一份最新的特定疫苗VIS给所有已经包含在健康资源服务部国家疫苗注射赔偿程序表中的疫苗(
见http://www.hrsa.gov)的接受者(儿童和他们的监护人).
乙肝疫苗也包含在这张表中.乙肝疫苗最新的VIS在http://www.cdc.gov/nip/publications/vis上
非英语的审核在http://www.immunize.org上的联合免疫行动中可以找到

Hepatitis B Immune Globulin (HBIG)
Dose and Administration

乙肝免疫球蛋白(HBIG)剂量和用法

 The standard dose of HBIG is 0.5 mL for postexposure
prophylaxis of infants born to hepatitis B surface antigen
(HBsAg)–positive women and 0.06 mL/kg for all other
applications.
用于乙肝表面抗原(HBsAg)阳性妇女生下的婴儿的暴露后预防,HBIG标准剂量为0.5mL.其他所有情况是0.06mL/kg

 HBIG may be administered simultaneously with hepatitis
B vaccine but in a different injection site.
HBIG可以与乙肝疫苗同时使用但应注射在不同点.

 HBIG is administered by intramuscular injection. For
infants, HBIG should be administered intramuscularly
in the anterolateral thigh using a 22–25-gauge needle that
is 7/8”–1” in length. For older children and adolescents,
an appropriate muscle mass (i.e., deltoid or gluteal) should
be chosen in which to deliver the larger volumes of HBIG
required for these age groups by using a needle length
appropriate for the person’s age and size (21).
HBIG应该用于肌肉注射,对于婴儿,HBIG应该使用22-25号针(7/8"-1")肌注于大腿前外侧肌肉.
对于更大一些的儿童和青春期孩子,应该选择合适的肌肉块(即三角肌或臀部),使能传送更大量的对这些年龄人群所需的HBIG.
针的长度应该与这个人的年龄和身材适应.

Vaccination with certain live-virus vaccines (measles,
mumps, rubella, and varicella) should be deferred for at
least 3 months after administration of HBIG because
HBIG can inhibit the response to these vaccines (21).
带有某些活病毒的疫苗(麻疹,腮腺炎,德国麻疹,水痘)应该在HBIG注射后至少3个月使用,因为HBIG能抑制对这些疫苗的反应.

 HBIG should be stored at 35°–46° F (2°–8° C) and should
not be frozen.
HBIG应该保存在华氏35°–46°(摄氏2°–8°),不应该冷冻.
.

IC

A Comprehensive Immunization Strategy to Eliminate Transmission of Hepatitis B Virus Infection in the United States

Recommendations of the Advisory Committee on Immunization Practices (ACIP) Part 1: Immunization of Infants, Children, and Adolescents

Please note: An erratum has been published for this article. To view the erratum, please click here.

Prepared by
Eric E. Mast, MD¹, Harold S. Margolis, MD,¹ Anthony E. Fiore, MD,¹ Edward W. Brink, MD,² Susan T. Goldstein, MD,¹ Susan A. Wang, MD,¹ Linda A. Moyer,¹ Beth P. Bell, MD,¹ Miriam J. Alter, PhD^1
1Division of Viral Hepatitis, National Center for Infectious Diseases, ²Immunization Services Division, National Immunization Program

The material in this report originated in the National Center for Infectious Diseases, Rima F. Khabbaz, MD, Director, Division of Viral Hepatitis, John W. Ward, MD, Director; and the National Immunization Program, Anne Schuchat, MD, Director, Immunization Services Division, Lance E. Rodewald, MD, Director.

Corresponding preparer: Eric E. Mast, MD, Division of Viral Hepatitis, National Center for Infectious Diseases, 1600 Clifton Road, NE, MS G-37, Atlanta, GA 30333. Telephone: 404-371-5460; Fax: 404-371-5221; E-mail: [email protected].

Summary

This report is the first of a two-part statement from the Advisory Committee on Immunization Practices (ACIP) that updates the strategy to eliminate hepatitis B virus (HBV) transmission in the United States. The report provides updated recommendations to improve prevention of perinatal and early childhood HBV transmission, including implementation of universal infant vaccination beginning at birth, and to increase vaccine coverage among previously unvaccinated children and adolescents. Strategies to enhance implementation of the recommendations include 1) establishing standing orders for administration of hepatitis B vaccination beginning at birth; 2) instituting delivery hospital policies and procedures and case management programs to improve identification of and administration of immunoprophylaxis to infants born to mothers who are hepatitis B surface antigen (HBsAg) positive and to mothers with unknown HBsAg status at the time of delivery; and 3) implementing vaccination record reviews for all children aged 11--12 years and children and adolescents aged <19 years who were born in countries with intermediate and high levels of HBV endemicity, adopting hepatitis B vaccine requirements for school entry, and integrating hepatitis B vaccination services into settings that serve adolescents. The second part of the ACIP statement, which will include updated recommendations and strategies to increase hepatitis B vaccination of adults, will be published separately.

Strategy to Eliminate Hepatitis B Virus Transmission

Hepatitis B virus (HBV) is a bloodborne and sexually transmitted virus. Rates of new infection and acute disease are highest among adults, but chronic infection is more likely to occur in persons infected as infants or young children. Before hepatitis B vaccination programs became routine in the United States, an estimated 30%--40% of chronic infections are believed to have resulted from perinatal or early childhood transmission, even though <10% of reported cases of hepatitis B occurred in children aged <10 years (1). Chronically infected persons are at increased lifetime risk for cirrhosis and hepatocellular carcinoma (HCC) and also serve as the main reservoir for continued HBV transmission.

Hepatitis B vaccination is the most effective measure to prevent HBV infection and its consequences. Since they were first issued in 1982, recommendations for hepatitis B vaccination have evolved into a comprehensive strategy to eliminate HBV transmission in the United States (2--6) (Box 1). A primary focus of this strategy is universal vaccination of infants to prevent early childhood HBV infection and to eventually protect adolescents and adults from infection. Other components include routine screening of all pregnant women for hepatitis B surface antigen (HBsAg) and postexposure immunoprophylaxis of infants born to HBsAg-positive women, vaccination of children and adolescents who were not previously vaccinated, and vaccination of unvaccinated adults at increased risk for infection.

To date, the immunization strategy has been implemented with considerable success. Recent estimates indicate that >95% of pregnant women are tested for HBsAg, and case management has been effective in ensuring high levels of initiation and

completion of postexposure immunoprophylaxis among identified infants born to HBsAg-positive women (7). Hepatitis B vaccine has been successfully integrated into the childhood vaccine schedule, and infant vaccine coverage levels are now equivalent to those of other vaccines in the childhood schedule. During 1990--2004, incidence of acute hepatitis B in the United States declined 75%. The greatest decline (94%) occurred among children and adolescents, coincident with an increase in hepatitis B vaccine coverage. As of 2004, among U.S. children aged 19--35 months, >92% had been fully vaccinated with 3 doses of hepatitis B vaccine (8). This success can be attributed in part to the established infrastructure for vaccine delivery to children and to federal support for perinatal hepatitis B prevention programs.

Vaccine coverage among adolescents has also increased substantially. Preliminary data demonstrate that 50%--60% of adolescents aged 13--15 years have records indicating vaccination (with 3 doses) against hepatitis B (CDC, unpublished data, 2003). As of November 2005, a total of 34 states require vaccination for middle-school entry (9). Certain programs provide hepatitis B vaccine to youth who engage in behaviors that place them at high risk for HBV infection (i.e., injection-drug use, having more than one sex partner, and male sexual activity with other males), and adolescent hepatitis B vaccination is included as a Health Plan Employer Data Information Set (HEDIS) measure (10).

Despite these successes, challenges remain. Even with improvements in the management of pregnant women, only approximately 50% of expected births to HBsAg-positive women are identified (on the basis of application of racial/ethnic-specific HBsAg prevalence estimates to U.S. natality data) for case management, which maximizes timely delivery of postexposure immunoprophylaxis (11; CDC, unpublished data, 2004). The need for proper management of women without prenatal care, including HBsAg testing at the time of admission for delivery and administration of the first dose of vaccine to infants <12 hours of birth, is underscored by the higher prevalence of HBsAg seropositivity among these women than among women who are screened prenatally (12). Even when maternal HBsAg testing does occur, certain infants of HBsAg-positive mothers do not receive postexposure immunoprophylaxis because of testing errors and lapses in reporting of test results (13), and infants of women with unknown HBsAg status at the time of delivery often do not receive a birth dose of vaccine (14). Birth dose coverage in 2004 was only 46% (National Immunization Survey, unpublished data, 2004), and coverage has not returned to levels from before July 1999 (54%), when recommendations were made to temporarily suspend administration of hepatitis B vaccines at birth until vaccines that do not contain thimerosal as a preservative became available (15). Among adolescents, efforts to prevent HBV transmission are hampered by the low rate of health-care visits in this age group compared with that of young children and the frequency of initiation of high-risk behaviors.

To address these remaining challenges and accelerate progress toward elimination of HBV transmission in the United States, the ACIP has updated the hepatitis B immunization recommendations for infants, children, and adolescents and supplemented the recommendations with strategies for implementation. The recommendations and implementation strategies address prevention of perinatal and early childhood transmission and routine vaccination of children and adolescents. A main focus is on universal infant vaccination beginning at birth, which provides a "safety net" for prevention of perinatal infection, prevents early childhood infections, facilitates implementation of universal vaccination recommendations, and prevents infections in adolescents and adults. The second part of the ACIP statement, which includes updated recommendations and implementation strategies to increase hepatitis B vaccination among unvaccinated adults, will be published separately (16).

Major Updates to the Recommendations

This report provides updated recommendations and approaches to address challenges in implementing the strategy to eliminate HBV transmission in the United States. These include the following measures:

• Improve prevention of perinatal and early childhood HBV transmission. Implement delivery hospital policies and procedures, case-management programs, and laws and regulations to improve identification of infants born to HBsAg-positive mothers and to mothers with unknown HBsAg status at the time of delivery, ensure administration of appropriate postexposure immunoprophylaxis to these infants beginning at birth, and administer a birth dose of hepatitis B vaccine to medically stable infants who weigh >2,000 g and who are born to HBsAg-negative mothers.
• Improve vaccine coverage of children and adolescents who were not previously vaccinated. Implement immunization record reviews for all children aged 11--12 years and children and adolescents aged <19 years who were born in countries in which HBV endemicity is high or intermediate (Figure 1 and Box 2); adopt hepatitis B vaccine requirements for school entry; and vaccinate all unvaccinated adolescents in settings that provide health-care services to persons in this age group.

IC

Background

Clinical Features and Natural History of HBV Infection

HBV is a 42-nm DNA virus classified in the Hepadnaviridae family. The liver is the primary site of HBV replication. After a susceptible person is exposed, the virus enters the liver via the bloodstream; no evidence exists indicating that the virus replicates at mucosal surfaces. HBV infection can produce either asymptomatic or symptomatic infection. The average incubation period is 90 days (range: 60--150 days) from exposure to onset of jaundice and 60 days (range: 40--90 days) from exposure to onset of abnormal serum alanine aminotransferase (ALT) levels (17,18).

The onset of acute disease is usually insidious. Infants and young children (aged <10 years) are typically asymptomatic (19). When present, clinical symptoms and signs might include anorexia, malaise, nausea, vomiting, abdominal pain, and jaundice. Extrahepatic manifestations of disease (e.g., skin rashes, arthralgias, and arthritis) also can occur (20). The fatality rate among persons with reported acute hepatitis B is 0.5%--1.5%, with highest rates in adults aged >60 years (21).

Although the consequences of acute hepatitis B can be severe, the majority of serious sequelae associated with HBV disease occur in persons who are chronically infected. Persons with chronic infection also serve as the major reservoir for continued HBV transmission. Chronic infection occurs in approximately 90% of infected infants, 30% of infected children aged <5 years, and <5% of infected persons aged >5 years, with continuing viral replication in the liver and persistent viremia (19,22--24). Primary infections also become chronic more frequently in immunosuppressed persons (e.g., hemodialysis patients and persons with human immunodeficiency virus [HIV] infection) (23,25,26). On the basis of data from follow-up studies of persons infected with HBV as infants or young children, approximately 25% of those with chronic infection die prematurely from cirrhosis or liver cancer; the majority remain asymptomatic until onset of cirrhosis or end-stage liver disease (27--29).

No specific treatment exists for acute hepatitis B. Persons who have chronic HBV infection require medical evaluation and regular monitoring (30,31). Therapeutic agents approved by the Food and Drug Administration (FDA) for treatment of chronic hepatitis B can achieve sustained suppression of HBV replication and remission of liver disease in certain persons (31). Periodic screening with alfa fetoprotein or imaging studies has been demonstrated to enhance early detection of HCC (31). Chronically infected persons with HCC have been reported to have experienced long-term survival after resection or ablation of small HCCs, and persons who were screened had a substantial survival advantage compared with historic controls (31).

Reinfection or reactivation of latent HBV infection has been reported among certain groups of immunosuppressed persons, including renal transplant recipients, HIV-infected patients, bone marrow transplant recipients, and patients receiving chemotherapy (32--35). The frequency with which this phenomenon occurs is unknown.

Interpretation of Serologic Markers of HBV Infection

The antigens and antibodies associated with HBV infection include HBsAg and antibody to HBsAg (anti-HBs), hepatitis B core antigen (HBcAg) and antibody to HBcAg (anti-HBc), and hepatitis B e antigen (HBeAg) and antibody to HBeAg (anti-HBe). At least one serologic marker is present during the different phases of HBV infection (Table 1) (18,36). Serologic assays are commercially available for all markers except HBcAg because no free HBcAg circulates in blood.

The presence of a confirmed HBsAg result is indicative of ongoing HBV infection. All HBsAg-positive persons should be considered infectious. In newly infected persons, HBsAg is the only serologic marker detected during the first 3--5 weeks after infection, and it persists for variable periods at very low levels. The average time from exposure to detection of HBsAg is 30 days (range: 6--60 days) (17,18). Highly sensitive single-sample nucleic acid tests can detect HBV DNA in the serum of an infected person 10--20 days before detection of HBsAg (37). Transient HBsAg positivity has been reported for up to 18 days after vaccination and is clinically insignificant (38,39).

Anti-HBc appears at the onset of symptoms or liver test abnormalities in acute HBV infection and persists for life. Acute or recently acquired infection can be distinguished by the presence of the IgM class of anti-HBc, which is detected at the onset of acute hepatitis B and persists for up to 6 months if the disease resolves. In patients who develop chronic hepatitis B, IgM anti-HBc can persist at low levels during viral replication and can result in positive tests for IgM anti-HBc (40). In addition, false-positive IgM anti-HBc test results can occur. Because the positive predictive value is low in asymptomatic persons, for diagnosis of acute hepatitis B, testing for IgM anti-HBc should be limited to persons with clinical evidence of acute hepatitis or an epidemiologic link to a case.

In persons who recover from HBV infection, HBsAg is eliminated from the blood, usually within 3--4 months, and anti-HBs develops during convalescence. The presence of anti-HBs typically indicates immunity from HBV infection. Infection or immunization with one genotype of HBV confers immunity to all genotypes. In addition, anti-HBs can be detected for several months after hepatitis B immune globulin (HBIG) administration. The majority of persons who recover from natural infection will be positive for both anti-HBs and anti-HBc, whereas persons who respond to hepatitis B vaccine have only anti-HBs. In persons who become chronically infected, HBsAg and anti-HBc persist, typically for life. HBsAg will become undetectable in approximately 0.5%--2% of chronically infected persons yearly, and anti-HBs will occur in the majority of these persons (41--44).

In certain persons, the only HBV serologic marker detected in serum is anti-HBc. Isolated anti-HBc can occur after HBV infection among persons who have recovered but whose anti-HBs levels have waned or among persons in whom anti-HBs failed to occur. Persons in the latter category include those with circulating HBsAg levels not detectable by commercial assays. These persons are unlikely to be infectious except under circumstances in which they are the source for direct percutaneous exposure of susceptible recipients to substantial quantities of virus (e.g., through blood transfusion or following liver transplantation) (45). HBV DNA has been detected in the blood of <5% of persons with isolated anti-HBc (46). Typically, the frequency of isolated anti-HBc relates directly to the prevalence of HBV infection in the population. In populations with a high prevalence of HBV infection, isolated anti-HBc likely indicates previous infection, with loss of anti-HBs. For persons in populations with a low prevalence of HBV infection, an isolated anti-HBc result often represents a false-positive reaction. The majority of these persons have a primary anti-HBs response after a 3-dose series of hepatitis B vaccine (47,48). Infants who are born to HBsAg-positive mothers and who do not become infected might have detectable anti-HBc for <24 months after birth from passively transferred maternal antibody.

HBeAg can be detected in the serum of persons with acute or chronic HBV infection. The presence of HBeAg correlates with viral replication and high levels of virus (i.e., high infectivity) (49,50). Anti-HBe correlates with the loss of replicating virus and with lower levels of virus, although reversion to HBeAg positivity has been observed (44).

Epidemiology of HBV Infection

Transmission

HBV is transmitted by percutaneous (i.e., puncture through the skin) or mucosal (i.e., direct contact with mucous membranes) exposure to infectious blood or to body fluids that contain blood. All HBsAg-positive persons are infectious, but those who are also HBeAg positive are more infectious because their blood contains high titers of HBV (typically 10⁷--10⁹ virions/mL) (49,50). Although HBsAg has been detected in multiple body fluids, only serum, semen, and saliva have been demonstrated to be infectious (51,52). HBV is comparatively stable in the environment and remains viable for >7 days on environmental surfaces at room temperature (53). HBV at concentrations of 10^2--3 virions/mL can be present on environmental surfaces in the absence of any visible blood and still cause transmission (53,54).

For infants and children, the two primary sources of HBV infection are perinatal transmission from infected mothers and horizontal transmission from infected household contacts. Adolescents are at risk for HBV infection primarily through high-risk sexual activity (i.e., sex with more than one partner and male sexual activity with other males) and injection-drug use (21). Transmission of HBV via transfusion of blood and plasma-derived products is rare because of donor screening for HBsAg and viral inactivation procedures.

For a newborn infant whose mother is positive for both HBsAg and HBeAg, the risk for chronic HBV infection is 70%--90% by age 6 months in the absence of postexposure immunoprophylaxis (55--57). For infants of women who are HBsAg positive but HBeAg negative, the risk for chronic infection is <10% in the absence of postexposure immunoprophylaxis (58--60). Rare cases of fulminant hepatitis B among perinatally infected infants also have been reported (61,62). Studies suggest that breastfeeding by an HBsAg-positive mother does not increase the risk for acquisition of HBV infection in the infant (63).

Children who are not infected at birth remain at risk from long-term interpersonal contact with their infected mothers. In one study, 38% of infants who were born to HBsAg-positive mothers and who were not infected perinatally became infected by age 4 years (64). In addition, children living with any chronically infected persons are at risk for becoming infected through percutaneous or mucosal exposures to blood or infectious body fluids (e.g., sharing a toothbrush, contact with exudates from dermatologic lesions, contact with HBsAg-contaminated surfaces). HBV transmission rates to susceptible household contacts of chronically infected persons have varied (range: 14%--60%) (65,66). High rates of infection also have been reported among unvaccinated long-term residents of institutions for the mentally handicapped (67,68), and, in rare instances, person-to-person transmission has been reported in child care settings (69,70).

Incidence

During 1990--2004, overall incidence of reported acute hepatitis B declined 75%, from 8.5 to 2.1 per 100,000 population. The most dramatic declines occurred in the cohort of children to whom recommendations for routine infant and adolescent vaccination have applied. Incidence among children aged <12 years and adolescents aged 12--19 years declined 94%, from 1.1 to 0.36 and 6.1 to 2.8 per 100,000 population, respectively (Figure 2). Since implementation of routine childhood immunization, an estimated 6,800 perinatal infections and an additional 18,700 infections during the first 10 years of life have been prevented annually in the United States (71).

Although infections in infants and children aged <10 years represented <10% of all HBV infections before implementation of childhood immunization programs, childhood infections resulted in an estimated 30%--40% of the chronic HBV infections among persons who acquired their infections in the United States (1). In two population-based studies conducted among Asian/Pacific Islander children who were born in the United States before perinatal hepatitis B prevention programs were widely implemented, 61%--66% of the chronic HBV infections occurred in children born to HBsAg-negative mothers (72,73). A substantial proportion of these chronic infections would not have been prevented by a selective program of identification and immunization of only infants born to HBsAg-positive mothers.

In addition to declines in incidence among all age groups, racial disparities in hepatitis B incidence among children have been substantially reduced (Figure 3). The reduction of the disparity between Asian/Pacific Islander and other children is consistent with recent observations noting a decline in seroprevalence of HBV infection after successful implementation of routine hepatitis B vaccination among Asians who have recently immigrated to the United States (74,75). However, as hepatitis B incidence has declined among U.S.-born children, unvaccinated foreign-born children account for a high proportion of infections. During 2001--2002, of 19 children born after 1991 in whom acute hepatitis B had been verified, eight (42%) were foreign born (76).

Prevalence

In the U.S. population, the overall age-adjusted prevalence of HBV infection (including persons with chronic infection and those with previous infection) was 4.9% in the third National Health and Nutrition Examination Survey (NHANES III, 1988--1994) (77). Foreign-born persons (particularly Asian/Pacific Islanders) who have emigrated from countries in which HBV is endemic (Figure 1 and Box 2) contribute disproportionately to the burden of chronic HBV infection in the United States. The prevalence of chronic HBV infection among foreign-born persons immigrating to the United States from Central and Southeast Asia, the Middle East, and Africa varies (range: 5%--15%) and reflects the patterns of HBV infection in the countries and regions of origin for these persons. During 1994--2003, approximately 40,000 immigrants with chronic HBV infection were admitted annually to the United States for permanent residence (78; CDC, unpublished data, 2005).