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Virus entry into host, establishment of infection, spread in host, mechanisms of tissue damage.


Britt W.


Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis. Cambridge: Cambridge University Press; 2007. Chapter 41.


Cytomegaloviruses (CMV) were initially identified by distinct histopathological findings that were observed in tissue from a variety of infected mammals, including humans. Perhaps the most well-recognized finding were inclusion bearing cells in the salivary glands of infected animals (Jesionek and Kiolemenoglou, 1904; Ribbert, 1904; Goodpasture and Talbot, 1921; Cole and Kuttner, 1926). Similar histopathologic findings of intracellular inclusions were noted in tissues from infants dying as a result of severe congenital (present at birth) cytomegalovirus infection leading to the designation of this clinical syndrome as cytomegalic inclusion disease (Farber and Wolbach, 1932). Studies by several groups of investigators provided compelling evidence from natural history studies that HCMV was a relatively frequent cause of disease in infants infected in utero and, that this viral infection could result in neurologic impairment in infected infants (Hanshaw, 1971; Stagno et al., 1977; Pass et al., 1980; Williamson et al., 1982; Bale, 1984; Fowler et al., 1992). Importantly, these early studies demonstrated that even infants with subclinical or silent infections could develop neurological sequelae (Stagno et al., 1982, 1983; Williamson et al., 1992). In the late 1960s, HCMV was recognized as a significant cause of disease in allograft recipients and in the case of hematopoietic allograft recipients, HCMV infection became recognized as one of the most frequent causes of death in the post-transplant period (Rifkind, 1965; Myers et al., 1975; Ho, 1977; Rubin et al., 1979; Winston et al., 1979; Rubin et al., 1981; Rubin and Colvin, 1986; Rubin, 1990). Significant morbidity and mortality rates were reported in allograft recipients infected with HCMV until efficacious antiviral chemotherapy was developed for this agent (Emanuel et al., 1988; Schmidt et al., 1991; Goodrich et al., 1993; Winston et al., 1993). Similarly, HCMV rapidly emerged as a major opportunistic pathogen in patients with HIV infection, particularly those in the late stages of the retroviral infection (Klatt and Shibata, 1988; Gallant et al., 1992; Bowen et al., 1995; Selik et al., 1996; Spector et al., 1999). The spectrum of diseases associated with infection with HCMV has been well described in immunocompromised patients with acute infectious syndromes in which virus replication can be correlated with end-organ disease. Because immunocompromised patients often present with multi-organ dysfunction secondary to chronic underlying disease and in some cases the pharmacologic agents utilized to treat allograft rejection, it has been difficult to completely define the spectrum of clinical disease associated with HCMV infection. In contrast to findings in allograft recipients, the disease manifestations of congenitally (present at birth) infected infants can be related directly to HCMV infection. Yet even in this group of patients the contribution of organogenesis particularly that of the developing central nervous system, to the pathogenesis of disease in HCMV infected infants is not completely understood. As a result, it is sometimes difficult to directly translate the clinical features of congenital HCMV infections and end-organ disease to clinical syndromes observed in other patient populations such as allograft recipients. Lastly, it should be stressed that, in nearly all cases, symptomatic disease following acute HCMV infection is limited to patients with deficits in their immune system and clinical evidence of acute HCMV infection is rarely seen in normal hosts.

Copyright © Cambridge University Press 2007.

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