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- W2767221489 abstract "By the end of 2015, 185 countries had implemented universal vaccination against hepatitis B in all newborn infants to prevent hepatitis B virus (HBV) infection. Whether a booster dose of hepatitis B vaccine is required in adolescence or young adulthood remains controversial, although booster vaccination is generally considered unnecessary, even when hepatitis B surface antibody (anti-HBs) levels decline to <10 mIU/ml (Gara et al., 2015Gara N. Abdalla A. Rivera E. Zhao X. Werner J.M. Liang T.J. et al.Durability of antibody response against hepatitis B virus in healthcare workers vaccinated as adults.Clin Infect Dis. 2015; 60: 505-513Crossref PubMed Scopus (36) Google Scholar, Bruce et al., 2016Bruce M.G. Bruden D. Hurlburt D. Zanis C. Thompson G. Rea L. et al.Antibody levels and protection after hepatitis B vaccine: results of a 30-year follow-up study and response to a booster dose.J Infect Dis. 2016; 214: 16-22Crossref PubMed Scopus (171) Google Scholar). A recent editorial in the International Journal of Infectious Diseases (Carmody, 2017Carmody E. Time to re-evaluate the effect of the adolescent booster of hepatitis B vaccine.Int J Infect Dis. 2017; 60: 88-90Abstract Full Text Full Text PDF PubMed Scopus (8) Google Scholar) referred to an article by Wang et al. published in Vaccine (Wang et al., 2017Wang Y. Chen T. Lu L.L. Wang M. Wang D. Yao H. et al.Adolescent booster with hepatitis B virus vaccines decreases HBV infection in high-risk adults.Vaccine. 2017; 35: 1064-1070Crossref PubMed Scopus (26) Google Scholar), and pointed out that it is time to re-evaluate the effect of the adolescent booster of hepatitis B vaccine. The author of the editorial considered that children of hepatitis B surface antigen (HBsAg)-positive mothers are less protected from HBV infection in young adulthood with the neonatal three-dose series of hepatitis B vaccine, and that a booster dose in early adolescence would be beneficial for these children. Indeed, based only on the data presented in the article by Wang et al., 2017Wang Y. Chen T. Lu L.L. Wang M. Wang D. Yao H. et al.Adolescent booster with hepatitis B virus vaccines decreases HBV infection in high-risk adults.Vaccine. 2017; 35: 1064-1070Crossref PubMed Scopus (26) Google Scholar, booster vaccination does appear to be required. Wang et al. reported that, of 9786 participants who received neonatal vaccination and were HBsAg-negative in childhood (10–11 years old, 1996–2000), 50 (0.51%) were identified with chronic HBV infection in young adulthood (23–28 years old, 2010–2014). Based on the mother’s HBsAg status, 28 (2.99%) of 936 uninfected children born to HBsAg-positive mothers and 22 (0.25%) of 8850 uninfected children born to HBsAg-negative mothers became HBV carriers in young adulthood. Among these 936 uninfected children born to HBsAg-positive mothers, 12 (2.12%) of 566 children with positive anti-HBs and 16 (4.32%) of 370 children with negative anti-HBs became carriers in young adulthood. Furthermore, the authors assessed the effect of booster vaccination at 10–11 years old on HBV infection status at 23–28 years old. The results showed that the HBsAg prevalence in young adults born to HBsAg-negative mothers had no significant difference in the following four subgroups: anti-HBs-positive with a booster (9/3965, 0.23%), anti-HBs-positive without a booster (1/1012, 0.10%), anti-HBs-negative with a booster (7/2736, 0.26%), anti-HBs-negative without a booster (5/1138, 0.44%). Among young adults born to HBsAg-positive mothers, the HBsAg prevalence in the above four subgroups was 2.01% (9/447), 2.52% (3/119), 3.09% (8/259), and 7.21% (8/111), respectively; the prevalence in adults who were anti-HBs-negative and did not receive a booster in childhood was significantly higher than that in any other subgroup. However, because several critical issues in the study by Wang et al., 2017Wang Y. Chen T. Lu L.L. Wang M. Wang D. Yao H. et al.Adolescent booster with hepatitis B virus vaccines decreases HBV infection in high-risk adults.Vaccine. 2017; 35: 1064-1070Crossref PubMed Scopus (26) Google Scholar are not clearly described and some results are obviously exceptional, I consider that the clinical implications of this study are obscure in the assessment of the effect of the adolescent hepatitis B booster vaccine. First, whether the two surveys (2010–2014 and 1996–2000, respectively) included the same participants is questionable. The authors mentioned that 9786 vaccinated individuals were tested both in childhood (10–11 years old, 1996–2000) and young adulthood (23–28 years old, 2010–2014), but the statement that “a total of 6132 and 6067 individuals had stored serum samples for 10–11 year time-point and 23–28 year time-point respectively” raises the question of whether these samples collected in the two surveys were from the same subjects. Only for those who were tested both in childhood and in adulthood may the hepatitis B serological marker results be reliably compared. Based on a closely related article by the same authors (Qu et al., 2014Qu C. Chen T. Fan C. Zhan Q. Wang Y. Lu J. et al.Efficacy of neonatal HBV vaccination on liver cancer and other liver diseases over 30-year follow-up of the Qidong hepatitis B intervention study: a cluster randomized controlled trial.PLoS Med. 2014; 11e1001774Crossref PubMed Scopus (91) Google Scholar), the study initially included a total of 38 366 vaccinated infants during 1985–1990, and two cross-sectional surveys were conducted in 1996–2000 and 2008–2012, respectively, which correspond to the same survey periods in the article by Wang et al., 2017Wang Y. Chen T. Lu L.L. Wang M. Wang D. Yao H. et al.Adolescent booster with hepatitis B virus vaccines decreases HBV infection in high-risk adults.Vaccine. 2017; 35: 1064-1070Crossref PubMed Scopus (26) Google Scholar. The HBsAg prevalence was 2.16% (470/21 770) in children during 1996–2000 and 1.83% (315/17 207) in young adults during 2008–2012. It is also unknown whether the two surveys included the same participants, since only 56.7% (21 770/38 366) and 50.7% (17 207/33 947) were tested in the first and second surveys, respectively. Based on the report of Wang et al., 2017Wang Y. Chen T. Lu L.L. Wang M. Wang D. Yao H. et al.Adolescent booster with hepatitis B virus vaccines decreases HBV infection in high-risk adults.Vaccine. 2017; 35: 1064-1070Crossref PubMed Scopus (26) Google Scholar, 0.51% (50/9786) of uninfected children in 1996–2000 caught a new infection and became carriers before the second survey. Logically, one may assume that the young adults would have a higher HBV prevalence due to the newly developed chronic infection after childhood, but the actual prevalence was reduced (from 2.16% to 1.83%); the authors attributed the lower prevalence in young adults to the natural clearance of HBsAg (Qu et al., 2014Qu C. Chen T. Fan C. Zhan Q. Wang Y. Lu J. et al.Efficacy of neonatal HBV vaccination on liver cancer and other liver diseases over 30-year follow-up of the Qidong hepatitis B intervention study: a cluster randomized controlled trial.PLoS Med. 2014; 11e1001774Crossref PubMed Scopus (91) Google Scholar). If the de novo HBsAg prevalence of 0.51% occurred after 2000 (Wang et al., 2017Wang Y. Chen T. Lu L.L. Wang M. Wang D. Yao H. et al.Adolescent booster with hepatitis B virus vaccines decreases HBV infection in high-risk adults.Vaccine. 2017; 35: 1064-1070Crossref PubMed Scopus (26) Google Scholar) and the HBsAg-positive rate of 1.83% in the young adults during 2008–2012 (Qu et al., 2014Qu C. Chen T. Fan C. Zhan Q. Wang Y. Lu J. et al.Efficacy of neonatal HBV vaccination on liver cancer and other liver diseases over 30-year follow-up of the Qidong hepatitis B intervention study: a cluster randomized controlled trial.PLoS Med. 2014; 11e1001774Crossref PubMed Scopus (91) Google Scholar) truly reflects the prevalence, it means that only 1.32% (1.83% minus 0.51%) HBsAg prevalence in the young adults (2008–2012) was derived from childhood (1996–2000). Based on these results, one may calculate the cumulated HBsAg clearance rate between childhood and young adulthood in this population: as high as 38.9% ((2.16%–1.32%)/2.16%) of chronic HBV infections spontaneously cleared HBsAg. This is an exceptionally high clearance rate (annual ∼2.6%) in adolescents and young adults. The clearance of HBsAg in childhood and adolescence seldom occurs. A Japanese study showed that none of 548 children diagnosed with chronic HBV infection under 15 years of age underwent HBsAg clearance during 7.8 years of follow-up (Takano et al., 2017Takano T. Tajiri H. Hosono S. Inui A. Murakami J. Ushijima K. et al.Natural history of chronic hepatitis B virus infection in children in Japan: a comparison of mother-to-child transmission with horizontal transmission.J Gastroenterol. 2017; ([Epub ahead of print])Crossref Scopus (17) Google Scholar). Of 349 HBV-infected children identified at a mean age of 8.4 years in Taiwan, only 12.0% spontaneously cleared HBsAg during 20.6 years of follow-up, with an annual rate of 0.58% and a cumulated HBsAg clearance rate of 7.62% between the ages of 10 and 25 years (Chiu et al., 2014Chiu Y.C. Liao S.F. Wu J.F. Lin C.Y. Lee W.C. Chen H.L. et al.Factors affecting the natural decay of hepatitis B surface antigen in children with chronic hepatitis B virus infection during long-term follow-up.J Pediatr. 2014; 165: 767-772.e1Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar). Therefore, without the guarantee of the same participants having been investigated in the two surveys, the HBsAg prevalence acquired in the two surveys just reflects the overall HBV carrier rates in this population, but cannot be used to calculate the clearance rate (Qu et al., 2014Qu C. Chen T. Fan C. Zhan Q. Wang Y. Lu J. et al.Efficacy of neonatal HBV vaccination on liver cancer and other liver diseases over 30-year follow-up of the Qidong hepatitis B intervention study: a cluster randomized controlled trial.PLoS Med. 2014; 11e1001774Crossref PubMed Scopus (91) Google Scholar), as well as the prevalence of newly developed chronic HBV infection (Wang et al., 2017Wang Y. Chen T. Lu L.L. Wang M. Wang D. Yao H. et al.Adolescent booster with hepatitis B virus vaccines decreases HBV infection in high-risk adults.Vaccine. 2017; 35: 1064-1070Crossref PubMed Scopus (26) Google Scholar). Second, Wang et al. reported that 2.12% (12/566) of uninfected children who were anti-HBs-positive were found to be HBV carriers in young adulthood, and even in anti-HBs-positive children who received a booster, 2.0% became carriers (Wang et al., 2017Wang Y. Chen T. Lu L.L. Wang M. Wang D. Yao H. et al.Adolescent booster with hepatitis B virus vaccines decreases HBV infection in high-risk adults.Vaccine. 2017; 35: 1064-1070Crossref PubMed Scopus (26) Google Scholar). These findings indicate that chronic breakthrough infection in the presence of anti-HBs occurred frequently, which is very unusual. Indeed, chronic HBV infection in the offspring of HBsAg-positive mothers, particularly those with high HBV DNA levels or positive for hepatitis B e antigen (HBeAg), may occur even after passive (hepatitis B immunoglobulin, HBIG) and active (hepatitis B vaccine) immunoprophylaxis; however, the infection usually occurs perinatally. Established chronic breakthrough infection in the presence of anti-HBs rarely occurs, except for infection with mutant virus. Lu et al., in a study from Taiwan, reported that during 15 years of observation, one (1.3%) of 78 vaccinated children of HBsAg- and HBeAg-positive mothers (genotype B) was diagnosed as an HBV carrier (mixed genotypes B and C, no mutation) at 15 years of age; the child was HBsAg-negative at 7 years old, indicating that infection occurred between the ages of 7 and 15 years. However, it is unknown whether the child was infected in the presence or absence of anti-HBs, since his anti-HBs was only 21 mIU/ml at 1.5 years old (Lu et al., 2004Lu C.Y. Chiang B.L. Chi W.K. Chang M.H. Ni Y.H. Hsu H.M. et al.Waning immunity to plasma-derived hepatitis B vaccine and the need for boosters 15 years after neonatal vaccination.Hepatology. 2004; 40: 1415-1420Crossref PubMed Scopus (150) Google Scholar). In Thailand, none of 87 vaccinated infants of HBsAg-positive mothers became HBV carriers during 20 years of follow-up (Poovorawan et al., 2011Poovorawan Y. Chongsrisawat V. Theamboonlers A. Leroux-Roels G. Kuriyakose S. Leyssen M. et al.Evidence of protection against clinical and chronic hepatitis B infection 20 years after infant vaccination in a high endemicity region.J Viral Hepat. 2011; 18: 369-375Crossref PubMed Scopus (81) Google Scholar). A 30-year prospective observational study performed in Hong Kong that initially enrolled 1086 infants born to HBsAg-positive mothers and vaccinated after birth, showed that none of the tested participants had a chronic infection after 3 years of age, although the proportion of anti-HBs ≥10 mIU/ml declined from 91.2% at year 1 to 37.4% at year 30 (Lin and Wong, 2013Lin A.W. Wong K.H. Long-term protection of neonatal hepatitis B vaccination in a 30-year cohort in Hong Kong.J Hepatol. 2013; 59: 1363-1364Abstract Full Text Full Text PDF PubMed Scopus (17) Google Scholar). Not until 2009 was a case of genuine acute hepatitis B reported; this occurred in a vaccinated homosexual man who was positive for anti-HBs (Boot et al., 2009Boot H.J. van der Waaij L.A. Schirm J. Kallenberg C.G. van Steenbergen J. Wolters B. Acute hepatitis B in a healthcare worker: a case report of genuine vaccination failure.J Hepatol. 2009; 50: 426-431Abstract Full Text Full Text PDF PubMed Scopus (31) Google Scholar). Third, the finding that as high as 10% (5/50) of children who were negative for HBsAg and positive for hepatitis B core antibody (anti-HBc) became HBsAg carriers in young adulthood is also exceptional. Whether these anti-HBc-positive children were also anti-HBs-positive is not known, as the authors did not mention this (Wang et al., 2017Wang Y. Chen T. Lu L.L. Wang M. Wang D. Yao H. et al.Adolescent booster with hepatitis B virus vaccines decreases HBV infection in high-risk adults.Vaccine. 2017; 35: 1064-1070Crossref PubMed Scopus (26) Google Scholar); if positive, it should be nearly impossible to acquire a novel HBV infection except mutant virus. The authors used occult HBV infection (OBI) to explain the result (Shahmoradi et al., 2012Shahmoradi S. Yahyapour Y. Mahmoodi M. Alavian S.M. Fazeli Z. Jazayeri S.M. High prevalence of occult hepatitis B virus infection in children born to HBsAg-positive mothers despite prophylaxis with hepatitis B vaccination and HBIG.J Hepatol. 2012; 57: 515-521Abstract Full Text Full Text PDF PubMed Scopus (91) Google Scholar), but OBI is extremely low in infants of HBsAg-positive mothers (Liu et al., 2014Liu Y. Wen J. Chen J. Xu C. Hu Y. Zhou Y.H. Rare detection of occult hepatitis B virus infection in children of mothers with positive hepatitis B surface antigen.PLoS One. 2014; 9e112803Crossref PubMed Scopus (13) Google Scholar), and most of the reported OBI cases in vaccinated infants or children result from occult cross-contamination (Zhou, 2016Zhou Y.H. Occult hepatitis B virus infection, or occult cross-contamination, in children of HBsAg positive mothers (correspondence).J Viral Hepat. 2016; 23: 830Crossref PubMed Scopus (6) Google Scholar). Actually, the same authors reported this high proportion of OBI in vaccinated children from the same area (Xu et al., 2010Xu L. Wei Y. Chen T. Lu J. Zhu C.L. Ni Z. et al.Occult HBV infection in anti-HBs-positive young adults after neonatal HB vaccination.Vaccine. 2010; 28: 5986-5992Crossref PubMed Scopus (49) Google Scholar), but more than half of the OBI was caused by cross-contamination, as evidenced by 51.2% of isolates with an identical HBV sequence; this is impossible in different individuals except if they were infected with the same virus. Additionally, anti-HBc positivity in the absence of HBsAg usually indicates a resolved infection, with or without the existence of virus in the liver. Reactivation of HBV in such subjects is rarely seen in those who are immunocompetent, especially in young subjects. Fourth, Wang et al. reported that only 82 (34.17%) of the 240 anti-HBc-positive children remained anti-HBc-positive in young adulthood (Wang et al., 2017Wang Y. Chen T. Lu L.L. Wang M. Wang D. Yao H. et al.Adolescent booster with hepatitis B virus vaccines decreases HBV infection in high-risk adults.Vaccine. 2017; 35: 1064-1070Crossref PubMed Scopus (26) Google Scholar), indicating that as high as 66% of anti-HBc positivity turned out to be negative during approximately 15 years. This is against the general notion that anti-HBc, once produced by natural HBV infection, is usually maintained for decades, and even life-long (Seeff et al., 1987Seeff L.B. Beebe G.W. Hoofnagle J.H. Norman J.E. Buskell-Bales Z. Waggoner J.G. et al.A serologic follow-up of the 1942 epidemic of post-vaccination hepatitis in the United States Army.N Engl J Med. 1987; 316: 965-970Crossref PubMed Scopus (193) Google Scholar). Although false-positive results may occur in the detection of anti-HBc, the reagents from Roche Diagnostics GmbH used in a Cobas e-601 system (Wang et al., 2017Wang Y. Chen T. Lu L.L. Wang M. Wang D. Yao H. et al.Adolescent booster with hepatitis B virus vaccines decreases HBV infection in high-risk adults.Vaccine. 2017; 35: 1064-1070Crossref PubMed Scopus (26) Google Scholar) would be unlikely to have so high a false-positive rate. Thus, one may raise the question of whether the samples were from the same subjects or the samples were mismatched in the two surveys. Fifth, close contact between mother and child usually occurs during infancy and young childhood and this contact decreases as the child grows up. More importantly, approximately 10% of the fathers of these children born to HBsAg-negative mothers were also HBsAg-positive, since the HBsAg prevalence in the mothers was approximately 9.6% (Wang et al., 2017Wang Y. Chen T. Lu L.L. Wang M. Wang D. Yao H. et al.Adolescent booster with hepatitis B virus vaccines decreases HBV infection in high-risk adults.Vaccine. 2017; 35: 1064-1070Crossref PubMed Scopus (26) Google Scholar) and Chinese males have a relatively higher HBsAg prevalence than Chinese females (Liang et al., 2009Liang X. Bi S. Yang W. Wang L. Cui G. Cui F. et al.Epidemiological serosurvey of hepatitis B in China–declining HBV prevalence due to hepatitis B vaccination.Vaccine. 2009; 27: 6550-6557Crossref PubMed Scopus (745) Google Scholar). Children at the age of 10–11 years and in adolescence actually have comparable contact with their mothers and fathers. However, the study by Wang et al., 2017Wang Y. Chen T. Lu L.L. Wang M. Wang D. Yao H. et al.Adolescent booster with hepatitis B virus vaccines decreases HBV infection in high-risk adults.Vaccine. 2017; 35: 1064-1070Crossref PubMed Scopus (26) Google Scholar showed that the adolescent booster vaccination appeared to be beneficial for children of HBsAg-positive mothers, but not for children of HBsAg-negative mothers. It is difficult to find an explanation for these results. Last, it should also be stressed that neonatal vaccination reported in the study by Wang et al., 2017Wang Y. Chen T. Lu L.L. Wang M. Wang D. Yao H. et al.Adolescent booster with hepatitis B virus vaccines decreases HBV infection in high-risk adults.Vaccine. 2017; 35: 1064-1070Crossref PubMed Scopus (26) Google Scholar was not verified based on the vaccination cards, but on whether the birth place was located in ‘vaccination towns’ (Qu et al., 2014Qu C. Chen T. Fan C. Zhan Q. Wang Y. Lu J. et al.Efficacy of neonatal HBV vaccination on liver cancer and other liver diseases over 30-year follow-up of the Qidong hepatitis B intervention study: a cluster randomized controlled trial.PLoS Med. 2014; 11e1001774Crossref PubMed Scopus (91) Google Scholar). In real-life practice, even though the ‘vaccination towns’ were assigned, it would still be difficult to vaccinate all infants in the towns because of preterm birth, neonatal illness, maternal fear of the adverse effects associated with the vaccine, and other factors. Indeed, the same authors reported an HBsAg prevalence of 2.16% in the vaccinated children from the same area during 1996–2000 (Qu et al., 2014Qu C. Chen T. Fan C. Zhan Q. Wang Y. Lu J. et al.Efficacy of neonatal HBV vaccination on liver cancer and other liver diseases over 30-year follow-up of the Qidong hepatitis B intervention study: a cluster randomized controlled trial.PLoS Med. 2014; 11e1001774Crossref PubMed Scopus (91) Google Scholar). However, recent surveys have shown that the HBsAg prevalence in children born after the implementation of universal hepatitis B vaccination in China is 0.35–1.0% (Liang et al., 2009Liang X. Bi S. Yang W. Wang L. Cui G. Cui F. et al.Epidemiological serosurvey of hepatitis B in China–declining HBV prevalence due to hepatitis B vaccination.Vaccine. 2009; 27: 6550-6557Crossref PubMed Scopus (745) Google Scholar, Yonghao et al., 2015Yonghao G. Jin X. Jun L. Pumei D. Ying Y. Xiuhong F. et al.An epidemiological serosurvey of hepatitis B virus shows evidence of declining prevalence due to hepatitis B vaccination in central China.Int J Infect Dis. 2015; 40: 75-80Abstract Full Text Full Text PDF PubMed Scopus (29) Google Scholar, Lin et al., 2016Lin X. Yang J. Lu H. Zhou Y. Zhou G. Wu H. et al.Minimization of hepatitis B infection among children in Jiangsu, China, 12 years after integration of hepatitis B vaccine into the expanded program on immunization.Vaccine. 2016; 34: 6458-6463Crossref PubMed Scopus (14) Google Scholar). Although the relatively higher HBsAg prevalence may be explained in part by the unavailability of HBIG for infants of HBsAg-positive mothers (Wang et al., 2017Wang Y. Chen T. Lu L.L. Wang M. Wang D. Yao H. et al.Adolescent booster with hepatitis B virus vaccines decreases HBV infection in high-risk adults.Vaccine. 2017; 35: 1064-1070Crossref PubMed Scopus (26) Google Scholar), studies have shown that the hepatitis B vaccine alone has comparable protective efficacy to the combination of HBIG and vaccine in infants born to HBsAg-positive but HBeAg-negative mothers (Yang et al., 2003Yang Y.J. Liu C.C. Chen T.J. Lee M.F. Chen S.H. Shih H.H. et al.Role of hepatitis B immunoglobulin in infants born to hepatitis B e antigen-negative carrier mothers in Taiwan.Pediatr Infect Dis J. 2003; 22: 584-588Crossref PubMed Google Scholar, Chen et al., 2012Chen H.L. Lin L.H. Hu F.C. Lee J.T. Lin W.T. Yang Y.J. et al.Effects of maternal screening and universal immunization to prevent mother-to-infant transmission of HBV.Gastroenterology. 2012; 142: 773-781.e2Abstract Full Text Full Text PDF PubMed Scopus (197) Google Scholar, Lu et al., 2017Lu Y. Liang X.F. Wang F.Z. Yan L. Li R.C. Li Y.P. et al.Hepatitis B vaccine alone may be enough for preventing hepatitis B virus transmission in neonates of HBsAg (+)/HBeAg (-) mothers.Vaccine. 2017; 35: 40-45Crossref PubMed Scopus (30) Google Scholar). Together, these results suggest that the vaccination might have been suboptimal in the study population. Additionally, the anti-HBs response after the primary vaccination was not presented, and the non-response to vaccination and loss of detectable anti-HBs in the children were not distinguished, which makes the interpretation of the results more complicated. In brief, numerous investigations have demonstrated that a full primary vaccination course with three doses of hepatitis B vaccine may provide long-term protection against chronic HBV infection (Gara et al., 2015Gara N. Abdalla A. Rivera E. Zhao X. Werner J.M. Liang T.J. et al.Durability of antibody response against hepatitis B virus in healthcare workers vaccinated as adults.Clin Infect Dis. 2015; 60: 505-513Crossref PubMed Scopus (36) Google Scholar, Bruce et al., 2016Bruce M.G. Bruden D. Hurlburt D. Zanis C. Thompson G. Rea L. et al.Antibody levels and protection after hepatitis B vaccine: results of a 30-year follow-up study and response to a booster dose.J Infect Dis. 2016; 214: 16-22Crossref PubMed Scopus (171) Google Scholar, FitzSimons et al., 2013FitzSimons D. Hendrickx G. Vorsters A. Van Damme P. Hepatitis B vaccination: a completed schedule enough to control HBV lifelong? Milan, Italy, 17-18 November 2011.Vaccine. 2013; 31: 584-590Crossref PubMed Scopus (60) Google Scholar, European Consensus Group on Hepatitis B Immunity, 2000European Consensus Group on Hepatitis B Immunity Are booster immunisations needed for lifelong hepatitis B immunity?.Lancet. 2000; 355: 561-565Abstract Full Text Full Text PDF PubMed Scopus (435) Google Scholar, Van Damme, 2016Van Damme P. Long-term protection after hepatitis B vaccine.J Infect Dis. 2016; 214: 1-3Crossref PubMed Scopus (43) Google Scholar). To date, no convincing data have been documented to support the necessity of a booster dose of hepatitis B vaccine in children or adolescents vaccinated successfully. Care should be taken when interpreting exceptional data, such as those found in the article by Wang et al., which are difficult to explain logically. Whether a booster dose of hepatitis B vaccine in adolescents is necessary for those high-risk individuals with anti-HBs <10 mIU/ml requires further investigation." @default.
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- W2767221489 title "Be cautious for exceptional results in evaluating the effect of adolescent booster of hepatitis B vaccine" @default.
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- W2767221489 cites W2032254038 @default.
- W2767221489 cites W2034561831 @default.
- W2767221489 cites W2075136594 @default.
- W2767221489 cites W2089145440 @default.
- W2767221489 cites W2116757586 @default.
- W2767221489 cites W2126893086 @default.
- W2767221489 cites W2130279349 @default.
- W2767221489 cites W2139424610 @default.
- W2767221489 cites W2171741586 @default.
- W2767221489 cites W2315040777 @default.
- W2767221489 cites W2317048712 @default.
- W2767221489 cites W2471883653 @default.
- W2767221489 cites W2553138088 @default.
- W2767221489 cites W2555762646 @default.
- W2767221489 cites W2571521813 @default.
- W2767221489 cites W2587612472 @default.
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- W2767221489 cites W2917871838 @default.
- W2767221489 cites W4244536823 @default.
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