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Fig. 3
Hypothetical mechanism mediating interstrain differences in endothelial cell tropism.
While all HCMV strains can release their capsids into fibroblasts by direct fusion of their envelope
with the plasma membrane, cell type differences are assumed for viral entry into endothelial cells.
Both highly endotheliotropic and poorly endotheliotropic strains are internalized by endocytosis,
but only highly endotheliotropic can escape from endocytic vesicles and release their capsid into
the cytoplasm
endothelial cells, epithelial cells and macrophages. As the respective proteins are
structural components of the envelope of virion particles, it is not unexpected that
they exert their effects on the level of viral entry. The cellular counterparts mediat-
ing the cell-type-specificity of these virion components are to be defined.
Cell Tropism of Other Cytomegaloviruses
The tendency toward systemic dissemination resulting in infection of various
organs is not unique to human CMV but has also been reported for animal CMVs.
Apparently, a broad organ tropism is a hallmark of cytomegaloviruses, which is
based on a similarly broad cell tropism.
Under conditions of severe immunosuppression, murine CMV-infected cells
were found in lung, liver, spleen, kidneys, adrenals, gastrointestinal tract, brain,
salivary gland, and fibroblasts, epithelial cells, neuronal cells, glial cells, ependy-
mal cells hepatocytes and endothelial cells were identified as predominantly
infected cell types within these tissues (Reddehase et al. 1985; Podlech et al. 1998;
van Den Pol et al. 1999; Podlech et al. 2000). Likewise, a broad target cell range
including fibroblasts, SMC, EC, macrophages was found with rat CMV (Kloover
et al. 2000; van der Strate et al. 2003; Streblow et al. 2007).
While the histological distribution of HCMV and MCMV appears almost indistin-
guishable, the underlying mechanisms regulating cell tropism are apparently not
completely conserved between cytomegaloviruses from different species. Deletion of
the m45 gene abrogated replication of MCMV in endothelial cell cultures (Brune
et al. 2001) by sensitizing infected endothelial cells to apoptosis. In contrast,
deletion of UL45 did not influence the endothelial cell tropism of HCMV strain
