Mothers with ciHHV-6 can produce active virus, transmit HHV-6 infection to children transplacentally
Dr. Louis Flamand’s laboratory at Laval University, Quebec, has sequenced parts of the HHV-6 gB gene found in the cord blood (CB) of infants with transplacentally-acquired HHV-6. These sequences were found to be identical to those of their mothers with chromosomally integrated HHV-6 (ciHHV-6), and divergent from the sequences of other known HHV-6 strains. These findings suggest that ciHHV-6 can become reactivated and then acquired transplacentally.
HHV-6 has only been recently identified as an agent able to cause congenital infection, and the mechanism of this event has been the subject of much speculation. Dr. Caroline B. Hall and associates at the University of Rochester reported in 2008 that the primary mode (86%) of transmission of congenital HHV-6 was ciHHV-6 being acquired via germline transmission, with transplacental transmission accounting for the remaining cases (14%) (Hall 2008). Hall investigated further and found that 100% of all of the infants with transplacentally acquired HHV-6 had mothers with chromosomally integrated HHV-6 (Hall 2010). Furthermore, the HHV-6 species of the mother matched the species of the infant. Flamand’s sequencing study suggests that a mother’s integrated virus can indeed infect her non-ciHHV-6 infant. Children born with closely related CMV (HHV-5) often develop developmental delays, mental retardation and a loss of hearing and vision. Hall initiated a study to determine the consequences of congenital HHV-6 infection before she passed away earlier this year. This study will be continued by her associate at the University of Rochester, Pediatric Infectious Diseases specialist Dr. Mary Caserta.
Since chromosomal integration of HHV-6 was first discovered by Italian researchers in 1993, the question of whether ciHHV-6 might reactivate from its integrated state and generate infectious virions has been a source of debate among experts in the field (Pellett 2011). For years it was assumed that the integrated virus was stable and inconsequential. Then in 2010, Arbuckle et al demonstrated that the virus could be activated in vitro by chemical stimulation (Arbuckle 2010). Flamand’s sequencing study represents the best evidence to date that the virus can activate in vivo. Further study is required as the authors could not rule out the possibility that cells laden with integrated virus from the mother were transmitted to the infant via maternal microchimerism, a condition in which cells from the mother cross the placenta and circulate in the fetus.
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