Endothelial cells in human cytomegalovirus infection: one host cell out of many or a crucial target for virus spread?

@article{Adler2009EndothelialCI,
  title={Endothelial cells in human cytomegalovirus infection: one host cell out of many or a crucial target for virus spread?},
  author={Barbara Adler and Christian Sinzger},
  journal={Thrombosis and haemostasis},
  year={2009},
  volume={102 6},
  pages={
          1057-63
        }
}
Endothelial cells (EC) are assumed to play a central role in the spread of human cytomegalovirus (HCMV) throughout the body. Results from in-situ analyses of infected tissues and data from cell culture systems together strongly suggest that vascular EC can support productive replication of HCMV and thus contribute to its haematogeneous dissemination. By inducing an angiogenic response, HCMV may even promote growth of its own habitat. The particular role of EC is further supported by the fact… 
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Human cytomegalovirus productively infects lymphatic endothelial cells and induces a secretome that promotes angiogenesis and lymphangiogenesis through interleukin-6 and granulocyte-macrophage colony-stimulating factor.
TLDR
Evidence is provided that a clinical isolate of HCMV was able to productively infect purified lymph node-derived LECs and that it dysregulated the expression of several LEC genes involved in the inflammatory response to viral infection, suggesting that HCMVs induces haemangiogenesis and lymphangiogenic through an indirect mechanism that relies on the stimulation of IL-6 and GM-CSF secretion from infected cells.
A permanently growing human endothelial cell line supports productive infection with human cytomegalovirus under conditional cell growth arrest.
TLDR
The HEC-LTT cell line is a cell culture model representing the full viral replicative cycle of HCMV in ECs, and will facilitate long-term approaches that are not feasible in primary HUVECs.
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To the knowledge, the UL133-UL138 locus represents the first cell-type-dependent, postentry tropism determinant required for viral maturation.
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TLDR
Data contradict any privileged role of EC in CMV dissemination and challenge an indiscriminate applicability of the primary and secondary viremia concept of virus dissemination.
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Fibroblast populations derived from different tissues are uniformly permissive to CMV infection but retain phenotypic differences of potential importance for infection-induced cell–cell fusion, and ensuing viral spread and pathogenesis in different organs.
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TLDR
The tetraspanin CD151 was discovered as a previously unrecognized proviral host factor for HCMV and was found to support viral penetration into the target cells.
Developing a Human Cytomegalovirus strain for better in vitro research
TLDR
The greater fitness of viruses from these novel Merlin-BAC variants alleviated the selective pressures for the selection of de novo UL128L mutations in fibroblasts, and represent valuable reagents for future HCMV research.
The US16 Gene of Human Cytomegalovirus Is Required for Efficient Viral Infection of Endothelial and Epithelial Cells
TLDR
Data indicate that the US16 gene encodes a novel virus tropism factor that regulates, in a cell-specific manner, a pre-immediate-early phase of the HCMV replication cycle.
Human Cytomegalovirus UL135 and UL136 Genes Are Required for Postentry Tropism in Endothelial Cells
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Roles for the UL135 and UL136 proteins in commandeering host membrane-trafficking pathways for virus maturation are indicated, representing the first HCMV genes crucial for early- to late-stage tropism in ECs.
Toll-like receptor 4 is involved in the cell cycle modulation and required for effective human cytomegalovirus infection in THP-1 macrophages.
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