Institute for Life Sciences, Faculty of Medicine, University of Southampton, University Hospital Southampton NHS Foundation Trust, Southampton, United Kingdom.
Institute of Developmental Science, Human Development and Health, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
Front Immunol. 2018 Mar 2;9:328. doi: 10.3389/fimmu.2018.00328. eCollection 2018.
The success of prevention of mother to child transmission programs over the last two decades has led to an increasing number of infants who are exposed to human immunodeficiency virus (HIV), but who are not themselves infected (HIV-exposed, uninfected infants). Although the morbidity and mortality among HIV-exposed, uninfected infants is considerably lower than that among HIV-infected infants, they may remain at increased risk of infections in the first 2 years of life compared with their HIV-unexposed peers, especially in the absence of breastfeeding. There is some evidence of immunological differences in HIV-exposed, uninfected infants, which could play a role in susceptibility to infection. Cytomegalovirus (CMV) may contribute to the increased immune activation observed in HIV-exposed, uninfected infants. Infants born to HIV-infected women are at increased risk of congenital CMV infection, as well as early acquisition of postnatal CMV infection. In infants with HIV infection, CMV co-infection in early life is associated with higher morbidity and mortality. This review considers how HIV infection, HIV exposure, and CMV infection affect infant responses to vaccination, and explores possible immunological and other explanations for these findings. HIV-infected infants have lower vaccine-induced antibody concentrations following tetanus, diphtheria, pertussis, hepatitis B, and pneumococcal vaccination, although the clinical relevance of this difference is not known. Despite lower concentrations of maternal-specific antibody at birth, HIV-exposed, uninfected infants respond to vaccination at least as well as their HIV-unexposed uninfected peers. CMV infection leads to an increase in activation and differentiation of the whole T-cell population, but there is limited data on the effects of CMV infection on infant vaccine responses. In light of growing evidence of poor clinical outcomes associated with CMV infection in HIV-exposed, uninfected infants, further studies are particularly important in this group. A clearer understanding of the mechanisms by which maternal viral infections influence the developing infant immune system is critical to the success of maternal and infant vaccination strategies.
过去二十年，母婴传播预防项目的成功使得越来越多的婴儿暴露于人类免疫缺陷病毒（HIV）但并未感染（HIV 暴露但未感染婴儿）。尽管 HIV 暴露但未感染婴儿的发病率和死亡率明显低于 HIV 感染婴儿，但与未感染 HIV 的同龄人相比，他们在生命的头 2 年仍可能面临更高的感染风险，尤其是在没有母乳喂养的情况下。有一些证据表明，HIV 暴露但未感染婴儿的免疫存在差异，这可能会影响其对感染的易感性。巨细胞病毒（CMV）可能导致 HIV 暴露但未感染婴儿中观察到的免疫激活增加。HIV 感染母亲所生婴儿会增加先天性 CMV 感染以及产后早期获得 CMV 感染的风险。在 HIV 感染婴儿中，早期 CMV 合并感染与更高的发病率和死亡率相关。本文综述了 HIV 感染、HIV 暴露和 CMV 感染如何影响婴儿对疫苗的反应，并探讨了这些发现的可能免疫学和其他解释。与未感染 HIV 的婴儿相比，HIV 感染婴儿在接受破伤风、白喉、百日咳、乙肝和肺炎球菌疫苗接种后，其破伤风类毒素、白喉类毒素、无细胞百日咳、乙肝和肺炎球菌疫苗诱导的抗体浓度较低，但尚不清楚这种差异的临床意义。尽管出生时具有较低的母体特异性抗体浓度，但 HIV 暴露但未感染婴儿的疫苗接种反应至少与未感染 HIV 的未感染婴儿相当。CMV 感染会导致整个 T 细胞群体的激活和分化增加，但关于 CMV 感染对婴儿疫苗反应的影响的数据有限。鉴于越来越多的证据表明，CMV 感染与 HIV 暴露但未感染婴儿的不良临床结局相关，因此在该人群中进行进一步研究尤为重要。更清楚地了解母体病毒感染如何影响发育中婴儿的免疫系统，对于母婴疫苗接种策略的成功至关重要。
