{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T06:24:54Z","timestamp":1789712694808,"version":"4.0.1"},"reference-count":37,"publisher":"American Academy of Pediatrics (AAP)","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2008,9,1]]},"abstract":"<jats:p>OBJECTIVE. We examined the frequency and characteristics of chromosomally integrated human herpesvirus 6 among congenitally infected children.<\/jats:p>\n               <jats:p>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.<\/jats:p>\n               <jats:p>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\u20136 log10 genomic copies per \u03bcg 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.<\/jats:p>\n               <jats:p>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.<\/jats:p>","DOI":"10.1542\/peds.2007-2838","type":"journal-article","created":{"date-parts":[[2008,9,1]],"date-time":"2008-09-01T13:27:57Z","timestamp":1220275677000},"page":"513-520","source":"Crossref","is-referenced-by-count":181,"title":["Chromosomal Integration of Human Herpesvirus 6 Is the Major Mode of Congenital Human Herpesvirus 6 Infection"],"prefix":"10.1542","volume":"122","author":[{"given":"Caroline Breese","family":"Hall","sequence":"first","affiliation":[{"name":"Departments of Pediatrics"},{"name":"Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mary T.","family":"Caserta","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kenneth","family":"Schnabel","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lynne M.","family":"Shelley","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrea S.","family":"Marino","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jennifer A.","family":"Carnahan","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christina","family":"Yoo","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Geraldine K.","family":"Lofthus","sequence":"additional","affiliation":[{"name":"Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael P.","family":"McDermott","sequence":"additional","affiliation":[{"name":"Biostatistics and Computational Biology, University of Rochester School of Medicine and Dentistry, Rochester, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"417","published-online":{"date-parts":[[2008,9,1]]},"reference":[{"key":"2021120905241308600_R1","doi-asserted-by":"crossref","unstructured":"Hall CB, Long CE, Schnabel KC, et al. 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