The broad target cell range provides the basis for a highly complex interaction between HCMV and the human host, which can be adapted to many different situations during their lifelong relationship. It should always be kept in mind that HCMV can successfully enter its host, spread within the body, establish latency, reactivate frequently throughout life and be transmitted to other individuals mostly without ever causing clinically apparent disease (for aspects of latency, see the chapters by M. Reeves and J. Sinclair, this volume and M.J. Reddehase et al., this volume). Many of these aspects of HCMV's silent life are still a matter of speculation. More robust information is available on the contribution of certain cell types to viral dissemination and organ infection under conditions when insufficient immune control allows virus replication to exceed the threshold of clinical manifestation (see also the chapter by W. Britt, this volume). Conclusions from analyses of severely ill patients on the behavior of HCMV in the normal host (Fig. 2) are therefore made, with the provision that an intact immune control may modify the apparent cell and organ tropism.
blood vessel lung
Fig. 2 Hypothetical contribution of various cell types to hematogenous dissemination and organ manifestation as deduced from immunohistochemical findings and cell culture data. Black dots represent virus intestine
Fig. 2 Hypothetical contribution of various cell types to hematogenous dissemination and organ manifestation as deduced from immunohistochemical findings and cell culture data. Black dots represent virus
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