新生儿免疫接种时母婴传播乙型肝炎病毒不一定是原发性疫

StephenW

新生儿免疫接种时母婴传播乙型肝炎病毒不一定是原发性疫苗失败 Get access Arrow
Samreen Ijaz, Jade Derrick, Justin Shute, Georgina Ireland, Iain Hayden, Siew Lin Ngui, Sema Mandal, Richard S Tedder
临床传染病，第 74 卷，第 7 期，2022 年 4 月 1 日，第 1151-1157 页，https://doi.org/10.1093/cid/ciab622
发表：
2021 年 7 月 12 日
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抽象的
背景

对携带乙型肝炎病毒 (HBV) 的母亲所生婴儿进行的监测项目为分析新生儿和婴儿早期的病毒学标志物提供了机会。这些数据提供了有关 HBV 传播机制的信息，以及如何更好地使用现有干预措施来控制在母婴界面发生的 HBV 感染。
方法

对从感染 HBV 的母亲所生婴儿采集的干血斑进行 HBV 血清学标志物的回顾性分析。此外，对出生后收集的新生儿血斑卡进行分子分析，这些血斑卡来自尽管接受了预防措施但仍被确定为感染 HBV 的婴儿。
结果

围产期暴露不能解释所有传播，至少有四分之一 (22%) 的婴儿已经在子宫内感染。所有人都携带野生型乙型肝炎表面抗原（HBsAg），在新生儿和婴儿早期样本中发现了相同的序列。相比之下，在围产期感染的婴儿（43%）中，选择具有 HBsAg 氨基酸变化的病毒很常见（80% 的序列），并且与相关的母体样本不同。
结论

目前被认为代表疫苗失败，很可能一部分 HBV 感染是由子宫内感染引起的。这些感染不太可能受到产后预防的影响，目前对母体抗病毒治疗的建议可能为时已晚，无法预防传播。应考虑在妊娠期间尽早使用抗病毒药物以降低宫内传播的风险，同时完成免疫计划也可降低围产期 HBV 传播的风险。
乙型肝炎病毒, 传播, 子宫内, 围产期, 疫苗

StephenW

Mother to Infant Transmission of Hepatitis B Virus in the Face of Neonatal Immunization Is Not Necessarily Primary Vaccine Failure Get access Arrow
Samreen Ijaz, Jade Derrick, Justin Shute, Georgina Ireland, Iain Hayden, Siew Lin Ngui, Sema Mandal, Richard S Tedder
Clinical Infectious Diseases, Volume 74, Issue 7, 1 April 2022, Pages 1151–1157, https://doi.org/10.1093/cid/ciab622
Published:
12 July 2021
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Abstract
Background

Surveillance programs undertaken in infants born to mothers with hepatitis B virus (HBV) provide an opportunity to analyze virological markers from the neonate and early infancy. These data inform on mechanisms of HBV transmission and how available interventions can be better used for control of HBV infections arising at the mother/child interface.
Methods

Retrospective analysis of HBV serological markers was undertaken in dried blood spots collected from infants born to mothers infected with HBV. In addition, molecular analysis was performed in newborn blood spot cards, collected after birth, from infants identified as infected with HBV despite receiving prophylaxis.
Results

Perinatal exposure could not account for all transmissions, with at least one-quarter (22%) of infants already infected in utero. All harbored a wild-type hepatitis B surface antigen (HBsAg), with identical sequences noted in the neonatal and early infancy samples. In contrast, in infants infected perinatally (43%), selection of viruses harboring amino acid changes in the HBsAg were common (80% of sequences) and divergent from the linked maternal sample.
Conclusion

Currently considered to represent vaccine failure, it is likely that a proportion of HBV infections result from in utero acquisition. These infections are unlikely to be susceptible to postnatal prophylaxis, and current recommendations for maternal antiviral treatment may be too late to prevent transmission. Consideration should be given to the earlier use of antivirals during gestation to reduce the risk of intrauterine transmission together with completion of the immunization schedule also to reduce the perinatal risk of HBV transmission.
hepatitis B virus, transmission, in utero, perinatal, vaccine