HCMV: persistence in the population: epidemiology and transmisson

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Abstract
Introduction Cytomegaloviruses (CMVs) are ubiquitous but highly species specific agents and are a common cause of infections in many animal species including humans (Weller, 1971). The characteristic cellular changes caused by CMV including cell enlargement with intranuclear inclusions were first reported in 1881 by Ribbert in the kidneys of a stillborn infant with congenital syphilis (Ribbert, 1904). Subsequent reports have described similar findings in the parotid glands of children and in the salivary glands from guinea pigs. It was initially thought that cytomegalic inclusion disease (CID) of the newborn was the sole manifestation of human CMV (HCMV) infection (Goodpasture and Talbot, 1921; Lipschutz, 1921; Cole and Kuttner, 1926; Lowenstein, 1907). Several groups of investigators have simultaneously isolated and propagated HCMV from infants and children with CID and from adenoidal tissue of children undergoing adenoidectomy (Rowe et al., 1956; Smith, 1956; Weller et al., 1957). As tissue culture isolation and serological assays became more widely available, HCMV was linked to a variety of illnesses, many of which have subsequently been shown to be unrelated to HCMV. A common characteristic of patients at risk for invasive HCMV infections is the suppression of host immune responsiveness. The onset of AIDS epidemic in the early 1980s has led to a dramatic expansion of the spectrum of HCMV disease. HCMV was the most common opportunistic infection in patients with AIDS and a major cause of morbidity and mortality in these patients until the introduction of highly active antiretroviral therapy (Jacobson et al., 1988; Gallant et al., 1992; Munoz et al., 1993; Spector et al., 1999).