Verhofstede Chris, Demecheleer Els, De Cabooter Nancy, Gaillard Philippe, Mwanyumba Fabian, Claeys Patricia, Chohan Varsha, Mandaliya Kishorchandra, Temmerman Marleen, Plum Jean
AIDS Reference Laboratory, Ghent University Hospital, Ghent, Belgium.
J Virol. 2003 Mar;77(5):3050-7. doi: 10.1128/jvi.77.5.3050-3057.2003.
Although several virologic and immunologic factors associated with an increased risk of perinatal human immunodeficiency virus type 1 (HIV-1) transmission have been described, the mechanism of mother-to-child transmission is still unclear. More specifically, the question of whether selective pressures influence the transmission remains unanswered. The aim of this study was to assess the genetic diversity of the transmitted virus after in utero transmission and after peripartum transmission and to compare the viral heterogeneity in the child with the viral heterogeneity in the mother. To allow a very accurate characterization of the viral heterogeneity in a single sample, limiting-dilution sequencing of a 1016-bp fragment of the env gene was performed. Thirteen children were tested, including 6 with in utero infections and 7 with peripartum infections. Samples were taken the day after birth and at the ages of 6 and 14 weeks. A homogeneous virus population was seen in six (46.2%) infants, of whom two were infected in utero and four were infected peripartum. A more heterogeneous virus population was detected in seven infants (53.8%), four infected in utero and three infected peripartum. The phylogenetic trees of the mother-child pairs presented a whole range of different tree topologies and showed infection of the child by one or more maternal variants. In conclusion, after HIV-1 transmission from mother to child a heterogeneous virus population was detected in approximately one-half of the children examined. Heterogeneous virus populations were found after peripartum infection as well as after in utero infection. Phylogenetic tree topologies argue against selection processes as the major mechanism driving mother-to-child transmission but support the hypothesis that virus variability is mainly driven by the inoculum level and/or exposure time.
虽然已经描述了几种与围产期1型人类免疫缺陷病毒(HIV-1)传播风险增加相关的病毒学和免疫学因素,但母婴传播的机制仍不清楚。更具体地说,选择性压力是否影响传播这一问题仍未得到解答。本研究的目的是评估子宫内传播和分娩时传播后所传播病毒的基因多样性,并比较儿童体内病毒的异质性与母亲体内病毒的异质性。为了能够非常准确地表征单个样本中的病毒异质性,对env基因的1016bp片段进行了有限稀释测序。对13名儿童进行了检测,其中6名儿童为子宫内感染,7名儿童为分娩时感染。在出生后第二天以及6周和14周龄时采集样本。在6名(46.2%)婴儿中观察到均匀的病毒群体,其中2名在子宫内感染,4名在分娩时感染。在7名婴儿(53.8%)中检测到更具异质性的病毒群体,4名在子宫内感染,3名在分娩时感染。母婴对的系统发育树呈现出一系列不同的树形拓扑结构,并显示儿童感染了一种或多种母体变异株。总之,在HIV-1从母亲传播给儿童后,在所检查的大约一半儿童中检测到异质性病毒群体。在分娩时感染以及子宫内感染后均发现了异质性病毒群体。系统发育树拓扑结构反对选择过程作为母婴传播的主要机制,但支持病毒变异性主要由接种物水平和/或暴露时间驱动这一假设。