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Original Article
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Volume 344:1366-1371 May 3, 2001 Number 18
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Intrauterine Transmission of Cytomegalovirus to Infants of Women with Preconceptional Immunity
Suresh B. Boppana, M.D., Lisa B. Rivera, M.P.H., M.B.A., Karen B. Fowler, Dr.P.H., Michael Mach, Ph.D., and William J. Britt, M.D.

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ABSTRACT

Background Preconceptional immunity against cytomegalovirus (CMV) provides only partial protection against intrauterine transmission of the virus. Whether congenital CMV infection in the offspring of women who are seropositive for CMV can occur after maternal reinfection with a different strain of CMV is unknown.

Methods Serum specimens from 46 women with preconceptional immunity against CMV that were obtained during the previous pregnancy and the current pregnancy were analyzed for antibodies against the strain-specific epitopes of CMV glycoprotein H. Virus-neutralizing activity in maternal serum samples was measured against the AD169 laboratory strain of CMV and the CMV isolates available from seven infected infants. In addition, the nucleotide sequences of the glycoprotein H gene from the seven CMV isolates were determined.

Results Eleven of the 16 mothers with infected infants (69 percent) had antibodies against the glycoprotein H epitopes present on two laboratory strains of CMV, AD169 and Towne. Ten of the 16 mothers with infected children (62 percent) acquired new antibody specificities against glycoprotein H, as compared with only 4 of the 30 mothers of uninfected infants (13 percent, P<0.001). The samples obtained at the time of the current delivery from four of the seven mothers contained at least twice as many neutralizing antibodies against the CMV isolated from their infants as were present in the samples obtained at the previous delivery. The specificity of the newly acquired maternal antibodies reflected the amino acid sequence of the glycoprotein H epitope of CMV from these four infants.

Conclusions In women who are seropositive for CMV, reinfection with a different strain of CMV can lead to intrauterine transmission and symptomatic congenital infection.


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From the Departments of Pediatrics (S.B.B., L.B.R., K.B.F., W.J.B.), Epidemiology (K.B.F.), and Microbiology (S.B.B., W.J.B.), University of Alabama at Birmingham, Birmingham; and the Institute for Clinical and Molecular Virology, University of Erlangen-Nürnberg, Erlangen, Germany (M.M.).

Address reprint requests to Dr. Boppana at the Department of Pediatrics, University of Alabama at Birmingham, 1600 7th Ave. S., Suite 752, Birmingham, AL 35233, or at sboppana{at}peds.uab.edu.

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