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J Virol, June 1998, p. 4970-4979, Vol. 72, No. 6
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Permissive Cytomegalovirus Infection of Primary
Villous Term and First Trimester Trophoblasts
D. G.
Hemmings,
R.
Kilani,
C.
Nykiforuk,
J.
Preiksaitis, and
L. J.
Guilbert*
Department of Medical Microbiology and
Immunology, University of Alberta, Edmonton, Alberta, Canada T6G 2H7
Received 4 December 1997/Accepted 2 March 1998
Forty percent of women with primary cytomegalovirus (CMV)
infections during pregnancy infect their fetuses with complications for
the baby varying from mild to severe. How CMV crosses the syncytiotrophoblast, the barrier between maternal blood and fetal tissue in the villous placenta, is unknown. Virus may cross by infection of maternal cells that pass through physical breaches in the
syncytiotrophoblast or by direct infection of the syncytiotrophoblast, with subsequent transmission to underlying fetal placental cells. In
this study, we show that pure (>99.99%), long-term and healthy (>3
weeks) cultures of syncytiotrophoblasts are permissively infected with
CMV. Greater than 99% of infectious progeny virus remained cell
associated throughout culture periods up to 3 weeks. Infection of term
trophoblasts required a higher virus inoculum, was less efficient, and
progressed more slowly than parallel infections of placental and human
embryonic lung fibroblasts. Three laboratory strains (AD169, Towne, and
Davis) and a clinical isolate from a congenitally infected infant all
permissively infected trophoblasts, although infection efficiencies
varied. The infection of first trimester syncytiotrophoblasts with
strain AD169 occurred at higher frequency and progressed more rapidly
than infection of term cells but less efficiently and rapidly than
infection of fibroblasts. These results show that villous
syncytiotrophoblasts can be permissively infected by CMV but that the
infection requires high virus titers and proceeds slowly and that
progeny virus remains predominantly cell associated.
*
Corresponding author. Mailing address: HMRC 6-25, University of Alberta, Edmonton, Alberta, Canada T6G 2H7. Phone: (403)
492-4910. Fax: (403) 492-0368. E-mail:
larry.guilbert{at}ualberta.ca.
J Virol, June 1998, p. 4970-4979, Vol. 72, No. 6
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
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