Tulane National Primate Research Center, Covington, Louisiana, United States of America.
Molecular and Cellular Biology PhD Program, University of Washington, Seattle, Washington, United States of America.
PLoS One. 2018 Oct 24;13(10):e0206330. doi: 10.1371/journal.pone.0206330. eCollection 2018.
Human infants frequently acquire human cytomegalovirus (HCMV) through breastfeeding, resulting in persistent high-level viral shedding in saliva and urine and infectivity to others, including pregnant women. Thus, vaccination to interrupt postnatal HCMV transmission is an attractive strategy to prevent HCMV spread and congenital infection. Rhesus CMV (RhCMV) in nonhuman primates is a valuable model for the study of immune strategies to prevent CMV transmission. Although rhesus monkeys typically acquire RhCMV before 1 year of age, the timing and mode of natural infant RhCMV transmission remain unknown.
We followed 5 RhCMV-seropositive dams and their infants from birth until weaning, approximately 6 months later. RhCMV DNA levels in plasma, breast milk, saliva, and urine were measured every 2 weeks by quantitative PCR. RhCMV-specific T cell responses in peripheral blood and breast milk were measured by interferon gamma ELISpot assays. Serum IgG antibody levels were measured by ELISA.
Four of five postpartum RhCMV-seropositive mothers had intermittent, low-level RhCMV shedding in breast milk, whereas all had high-magnitude RhCMV shedding in saliva and urine. The kinetics of maternal blood RhCMV-specific T cell responses and viral shedding in urine and saliva did not strongly associate, though dams with consistently high systemic RhCMV-specific T cell responses tended to have undetectable RhCMV shedding in breast milk. All RhCMV-exposed infants had intermittent, low-level RhCMV shedding in saliva during the lactation period, with minimal systemic RhCMV-specific T cell responses.
Despite exposure to RhCMV shedding in breast milk and other maternal fluids, postnatal mother-to-child RhCMV transmission appears to be less efficient than that of HCMV. A greater understanding of the determinants of RhCMV transmission and its usefulness as a model of HCMV mucosal acquisition may provide insight into strategies to prevent HCMV infections in humans.
人类婴儿通过母乳喂养经常感染人巨细胞病毒(HCMV),导致唾液和尿液中持续高水平的病毒脱落,并具有感染他人的能力,包括孕妇。因此,接种疫苗以阻断产后 HCMV 传播是预防 HCMV 传播和先天性感染的一种有吸引力的策略。非人类灵长类动物中的恒河猴巨细胞病毒(RhCMV)是研究预防 CMV 传播的免疫策略的有价值模型。尽管恒河猴通常在 1 岁之前获得 RhCMV,但自然婴儿 RhCMV 传播的时间和方式仍不清楚。
我们从出生开始跟踪 5 只 RhCMV 血清阳性的母猴及其幼崽,直到大约 6 个月后断奶。通过定量 PCR 每两周测量一次血浆、母乳、唾液和尿液中的 RhCMV DNA 水平。通过干扰素 γ ELISpot 测定法测量外周血和母乳中的 RhCMV 特异性 T 细胞反应。通过 ELISA 测量血清 IgG 抗体水平。
5 只产后 RhCMV 血清阳性的母亲中有 4 只间歇性、低水平的 RhCMV 从母乳中脱落,而所有母亲的唾液和尿液中均有高幅度的 RhCMV 脱落。母体血液 RhCMV 特异性 T 细胞反应和尿液及唾液中病毒脱落的动力学没有很强的关联,尽管始终具有高全身性 RhCMV 特异性 T 细胞反应的母猴倾向于母乳中 RhCMV 脱落无法检测到。所有 RhCMV 暴露的婴儿在哺乳期均有唾液中间歇性、低水平的 RhCMV 脱落,全身 RhCMV 特异性 T 细胞反应最小。
尽管接触了母乳和其他母源液体中的 RhCMV 脱落,但产后母婴 RhCMV 传播的效率似乎低于 HCMV。对 RhCMV 传播的决定因素及其作为 HCMV 黏膜获得模型的有用性的更深入了解,可能为预防人类 HCMV 感染提供策略。