AI Article Synopsis

  • The study focused on congenital human herpesvirus 6 (HHV-6) infections in infants, examining how often and in what way HHV-6 is chromosomally integrated.
  • Among the 85 infants studied, 43 had congenital infections mostly due to chromosomal integration, while the remaining 42 had postnatal infections, with only 14% of congenital cases resulting from transplacental transmission.
  • The findings revealed that infants with chromosomally integrated HHV-6 had significantly higher viral loads across various biological samples compared to those with non-congenital infections, highlighting the importance of chromosomal integration in understanding HHV-6 transmission.

Article Abstract

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 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.

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.

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Source
http://dx.doi.org/10.1542/peds.2007-2838DOI Listing

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