Hall Caroline Breese, Caserta Mary T, Schnabel Kenneth, Shelley Lynne M, Marino Andrea S, Carnahan Jennifer A, Yoo Christina, Lofthus Geraldine K, McDermott Michael P
Department of Pediatrics, University of Rochester School of Medicine and Dentistry, 601 Elmwood Ave, Box 689, Rochester, NY 14642, USA.
Pediatrics. 2008 Sep;122(3):513-20. doi: 10.1542/peds.2007-2838.
We examined the frequency and characteristics of chromosomally integrated human herpesvirus 6 among congenitally infected children.
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.
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 log(10) genomic copies per mug 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.
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.
我们研究了先天性感染儿童中染色体整合型人疱疹病毒6的频率和特征。
对有和没有先天性人疱疹病毒6感染的婴儿进行前瞻性监测。检测脐血单个核细胞、外周血单个核细胞、唾液、尿液和毛囊样本中的人疱疹病毒6 DNA。还评估了人疱疹病毒6 RNA、血清抗体和染色体整合型人疱疹病毒6水平。
85名婴儿中,43名有先天性感染,42名有产后感染。大多数先天性感染(86%)是由染色体整合型人疱疹病毒6引起的;6名婴儿(14%)有经胎盘感染。染色体整合型人疱疹病毒6感染的儿童在所有部位的病毒载量都很高(平均:每微克细胞DNA中5 - 6 log(10)基因组拷贝);在经胎盘感染或产后感染的儿童中,毛发样本中无人疱疹病毒6 DNA,其他样本中情况不一致,且病毒载量显著较低。对有染色体整合型人疱疹病毒6且检测了父母毛发样本的每个儿童的一位家长进行检测,发现其毛发中含有人类疱疹病毒6 DNA。A变体导致32%的染色体整合型人疱疹病毒6感染,而产后感染中这一比例为2%。仅在染色体整合型人疱疹病毒6样本中检测到复制型人疱疹病毒6(8%的脐血单个核细胞和外周血单个核细胞)。染色体整合型人疱疹病毒6感染的儿童、经胎盘感染的儿童和产后感染的儿童之间,以及母亲和父亲染色体整合型人疱疹病毒6传播的儿童之间,脐血人疱疹病毒6抗体水平相似。
人疱疹病毒6先天性感染主要由通过种系传递的染色体整合型病毒引起。染色体整合型人疱疹病毒6感染的婴儿在所有标本中病毒载量都很高,产生人疱疹病毒6抗体和mRNA。由于116名新生儿中可能有1名的血液标本存在染色体整合型人疱疹病毒6,其临床相关性有待研究。