Biology Reference
In-Depth Information
Conclusion
Fully understanding the establishment and maintenance of HCMV latent infection
as well as reactivation from latency remains a weighty problem. As molecular tech-
niques continue to progress, it is likely that global analyses of the effects of HCMV
infection on the cellular transcriptome and proteome will become even more possi-
ble. As our understanding of the functional heterogeneity of populations of CD34+
haematopoietic precursors increases, it may become possible to further clarify the
mechanisms which promote viral latency in only specific cell types. Why the main-
tenance of HCMV genomes occurs only in particular subsets of cells derived from
a common ancestor is unknown. As a consequence, what conditions in these cells
facilitate virus reactivation is also unknown.
Acknowledgements
We thank the many members of the laboratory, past and present, whose
work has contributed to the studies presented here. We also apologise to colleagues in the field
whose work has not been cited due to space limitations. Work from our laboratory which has con-
tributed to these studies was supported by the United Kingdom Medical Research Council and the
Wellcome Trust.
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