Biology Reference
In-Depth Information
followed by prolonged excretion of infectious virus, often persisting for several
years, transmission is commonplace during childhood in human societies in which
crowding and group care of children take place. In the developed world, this has
been observed in children from lower socioeconomic groups and children attending
group care centers (Adler 1989; de Mello et al. 1996; Bale et al. 1999). In that latter
setting, infection may be acquired by over 50% of attendees and infections with
multiple viral strains have been observed, presumably through exposure to virus
containing saliva and urine (Hutto et al. 1986; Pass et al. 1987; Adler 1991; Bale
et al. 1996). In older children and sexually active adolescents and adults, infection
is presumed to follow sexual exposure as cervical secretions and semen are rich
sources of virus (Lang and Kummer 1975; Pass et al. 1982; Drew et al. 1984;
Rinaldo et al. 1992; Collier et al. 1995). Sexual transmission of HCMV is consistent
with the extremely high rates of serological reactivity in sexually active populations
such as gay men and individuals attending sexually transmitted disease clinics
(Drew et al. 1981; Chandler et al. 1985, 1987; Handsfield et al. 1985; Berry et al.
1988; Collier et al. 1989; Fowler and Pass 1991; Sohn et al. 1991; Shen et al. 1994;
Ross et al. 2005). Contact with young children excreting infectious virus represents
another mode of acquisition of HCMV by adults. Reinfections with new strains of
virus appears commonplace in normal hosts and in immunocompromised hosts
(Drew and Mintz 1984; Chou 1986, 1987; Bale et al. 1996; Boppana et al. 2001).
In the normal host, reinfections are more common in populations with increased
risks of exposure such as children attending group care centers or sexually active
populations. Whether the full pathogenic potential of HCMV can follow a reinfec-
tion in a normal host remains an important question; however, reinfections can lead
to serologic reactivity specific for the new viral strain and in pregnant women,
transmission to the fetus and fetal disease, indicating that the disease-inducing
potential of reinfection is similar to that associated with primary infection in normal
hosts and can be associated with significant morbidity in immunocompromised
patients such as transplant recipients (Boppana et al. 2001). Reinfection has also
been documented in previously infected and seroreactive laboratory rodents and
nonhuman primates (J. Nelson, personal communication) (Gorman et al. 2006).
Lastly, non-community-acquired HCMV infections are associated with exposure to
blood and blood products from infected donors, transplantation of allografts from
infected donors, and in the past by exposure of newborn infants to banked human
breast milk (Chou 1986; Bowden 1995; Vochem et al. 1998; Lawrence and
Lawrence 2004).
Disease associated with acute infections in the normal host is infrequent but
when present is limited to nonspecific viral syndromes that are characterized by
low-grade fevers, fatigue, evidence of mild hepatocellular damage, and occasionally
transient bone marrow suppression (Cohen and Corey 1985; Pannuti et al. 1985;
Horwitz et al. 1986; Porath et al. 1987). These clinical manifestations of end-organ
disease are consistent with a disseminated infection and are mirrored by experimental
infection of the mouse, rat, guinea pig and rhesus macaque by their respective
CMVs (Griffith et al. 1981; Bia et al. 1983; Stals et al. 1990; Kern 1999; Lockridge
