Biology Reference
In-Depth Information
55
Hearing Loss
Any sequela
IQ<70
45
35
25
15
5
-5
<100,000
>100,000
genome equivalents in peripheral blood
Fig. 2
Viral load and outcome of congenitally infected infants. DNA was extracted from 200 µl
of peripheral blood and analyzed for HCMV viral genomes (reported as genome equivalents/ml)
as described. Infants with congenital HCMV infection from a large natural history study of con-
genital HCMV infection were classified as having long-term neurologic sequelae, and more spe-
cifically hearing loss or diminished cognitive function (IQ<70). This study has been reported in
more detail (Boppana et al. 2005)
viral burden is less than those presenting with only hepatitis (Boppana et al. 2005).
This observation can be most readily explained by the duration of the congenital
infection such that a predominance of CNS disease can reflect an infection of longer
duration with resolution of the hepatic involvement.
Congenitally infected infants can excrete large amounts of virus, often reaching 4-5
logs of infectious virus per milliliter of urine, and can persistently excrete large
amounts of virus for years. These same infants can resolve clinical evidence of end-
organ disease within the first few months of life even with what is believed to be a
limited T lymphocyte response to HCMV (Gehrz et al. 1977; Starr et al. 1979; Pass
et al. 1983; Marchant et al. 2003; Gibson et al. 2004). It is of interest, however, that
contrary to this previous dogma, newborn infants and fetuses can mount CMV-specific
T cell responses, but whether these responses influence outcome of CMV infection in
these infants is unknown. Infected infants act as viral reservoirs in their families and
communities and serve as an important vector for spreading CMV in populations.
Allograft Recipients
The association of HCMV with disease in allograft recipients was described nearly
40 years ago (Rifkind 1965; Rubin et al. 1979). Current aggressive utilization of
antiviral agents both as treatment and prophylaxis, screening of blood products, and
whenever possible donor and recipient matching for CMV serological reactivity for
CMV have decreased the incidence of severe HCMV infections in allograft recipi-
ents. Early reports in bone marrow allograft recipients described mortality rates of
between 70% and 95% in patients with HCMV pneumonia (Meyers et al. 1982,
