Biology Reference
In-Depth Information
follows primary maternal rubella virus infection during pregnancy and transmis-
sion to the fetus. In the case of rubella infections, once the prevalence of maternal
seroimmunity to rubella virus exceeds approximately 85%, the incidence of
congenital rubella infection falls dramatically (Preblud and Alford 1990; MMWR
1997). Thus, the parameters of protective maternal immune responses to viruses
such as rubella that do not establish persistent infections in the host or remain
endemic in the population appear to differ substantially from those that are necessary
to limit congenital CMV infections. It is of interest that aspects of the epidemi-
ology of CMV mirror those seen in congenital syphilis infections, a sexually
acquired infection that does not appear to induce protective immunity and whose
incidence increases as the prevalence of the infection increases in the population
(Anonymous 1999).
Transmission of HCMV to the developing fetus following maternal primary infec-
tion occurs in between 20% and 50% of cases (Stagno et al. 1982b; Griffiths and
Baboonian 1984; Yow et al. 1988; Stagno and Britt 2006). Because fetal infection
occurs in 0.1%-2.0% of women with preconceptional immunity to HCMV, it is clear
that maternal immunity plays a major role in protecting the fetus from virus infection
(Table 2 ). However, at what level this host response modulates intrauterine transmis-
sion of HCMV and fetal disease is not understood. Recent studies of parameters of
HCMV infection and host immunity during primary HCMV infections in pregnancy
have described increased levels of viremia and delayed development of CD4
+
and
CD8
+
responses to HCMV that can be correlated with increased rates of fetal infection
(Gibson et al. 2007). Although consistent with previous observations that the develop-
ment of specific adaptive immune responses appeared delayed in primary HCMV
infections, the interval between virus acquisition and the development of adaptive
immunity in these women cannot be precisely determined (Gibson et al. 2007).
Table 2
Nonprimary maternal HCMV infection and outcome of
congenital HCMV infection
Type of maternal infection
Primary
Non-Primary
Incidence of congenital infection
13%
a
87%
Transmission rate to fetus
20%-40%
0.1%-2.0%
b
Incidence of congenitally
24%
c
5%-8%
infected infants
with sequelae
Infants with sequelae
31.2
43.5%-69.5
following congenital
HCMV infection
d
a
Stagno et al. 1982
b
Transmission rates following nonprimary infection varying depend-
ing on age and socioeconomic status of population
c
Fowler et al. 1992
d
Rate calculated per 1,000 infants with congenital HCMV infection
following primary (130) and nonprimary infection (870)
