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首页> 外文期刊>Pediatrics: Official Publication of the American Academy of Pediatrics >Chromosomal Integration of Human Herpesvirus 6 Is the Major Mode of Congenital Human Herpesvirus 6 Infection
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Chromosomal Integration of Human Herpesvirus 6 Is the Major Mode of Congenital Human Herpesvirus 6 Infection

机译:人类疱疹病毒6的染色体整合是先天性人类疱疹病毒6感染的主要模式。

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OBJECTIVE. We examined the frequency and characteristics of chromosomally integrated human herpesvirus 6 among congenitally infected children.METHODS. Infants with and without congenital human herpesvirus 6 infection were prospectively monitored. Cord blood mononuclear cell, peripheral blood mononuclear cell, saliva, urine, and hair follicle samples were examined for human herpesvirus 6 DNA. Human herpesvirus 6 RNA, serum antibody, and chromosomally integrated human herpesvirus 6 levels were also assessed.RESULTS. Among 85 infants, 43 had congenital infections and 42 had postnatal infections. Most congenital infections (86%) resulted from chromosomally integrated human herpesvirus 6; 6 infants (14%) had transplacental infections. Children with chromosomally integrated human herpesvirus 6 had high viral loads in all sites (mean: 5–6 log10 genomic copies per μg of cellular DNA); among children with transplacental infection or postnatal infection, human herpesvirus 6 DNA was absent in hair samples and inconsistent in other samples, and viral loads were significantly lower. One parent of each child with chromosomally integrated human herpesvirus 6 who had parental hair samples tested had hair containing human herpesvirus 6 DNA. Variant A caused 32% of chromosomally integrated human herpesvirus 6 infections, compared with 2% of postnatal infections. Replicating human herpesvirus 6 was detected only among chromosomally integrated human herpesvirus 6 samples (8% of cord blood mononuclear cells and peripheral blood mononuclear cells). Cord blood human herpesvirus 6 antibody levels were similar among children with chromosomally integrated human herpesvirus 6, transplacental infection, and postnatal infection and between children with maternal and paternal chromosomally integrated human herpesvirus 6 transmission.CONCLUSIONS. Human herpesvirus 6 congenital infection results primarily from chromosomally integrated virus which is passed through the germ-line. Infants with chromosomally integrated human herpesvirus 6 had high viral loads in all specimens, produced human herpesvirus 6 antibody, and mRNA. The clinical relevance needs study as 1 of 116 newborns may have chromosomally integrated human herpesvirus 6 blood specimens.
机译:目的。我们检查了先天感染儿童中染色体整合的人类疱疹病毒6的频率和特征。前瞻性监测有无先天性人类疱疹病毒6感染的婴儿。检查脐带血单核细胞,外周血单核细胞,唾液,尿液和毛囊样品中的人类疱疹病毒6 DNA。还评估了人类疱疹病毒6 RNA,血清抗体和染色体整合的人类疱疹病毒6水平。在85名婴儿中,有43名患有先天性感染,有42名患有产后感染。大多数先天性感染(86%)是由染色体整合的人类疱疹病毒引起的[6]。 6例婴儿(14%)患有胎盘感染。携带人类染色体疱疹病毒6型染色体的儿童在所有位​​点都有很高的病毒载量(平均:每微克细胞DNA 5-6 log10基因组拷贝);在经胎盘感染或产后感染的儿童中,头发样本中不存在人类疱疹病毒6 DNA,其他样本中不一致,病毒载量显着降低。每个患有染色体整合的人类疱疹病毒6的孩子的一名父母,其父母头发样本均经过测试,其头发中含有人类疱疹病毒6 DNA。变体A导致32%的染色体整合人类疱疹病毒6感染,而出生后感染的感染率为2%。仅在染色体整合的人疱疹病毒6样本(脐血单核细胞和外周血单核细胞的8%)中检测到复制型人疱疹病毒6。结论脐带血人疱疹病毒6抗体水平在染色体整合的人类疱疹病毒6患儿,经胎盘感染和产后感染以及母体和父亲的染色体整合的人类疱疹病毒6患儿之间相似。人疱疹病毒6先天性感染主要是由通过种系传递的染色体整合病毒引起的。具有染色体整合的人类疱疹病毒6的婴儿在所有标本中均具有高病毒载量,并产生人类疱疹病毒6抗体和mRNA。临床相关性需要研究,因为116名新生儿中有1名可能具有染色体整合的人类疱疹病毒6份血液标本。
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