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Blood, 1 December 2006, Vol. 108, No. 12, pp. 3691-3699. Prepublished online as a Blood First Edition Paper on August 24, 2006; DOI 10.1182/blood-2005-12-026682. This Article Full Text Full Text (PDF) Supplemental Table All Versions of this Article: blood-2005-12-026682v1 108/12/3691    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Cheung, A. K. L. Articles by Slobedman, B. Search for Related Content PubMed PubMed Citation Articles by Cheung, A. K. L. Articles by Slobedman, B. Related Collections Hematopoiesis and Stem Cells Gene Expression Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS Viral gene expression during the establishment of human cytomegalovirus latent infection in myeloid progenitor cells Allen K. L. Cheung, Allison Abendroth, Anthony L. Cunningham, and Barry Slobedman From the Centre for Virus Research, Westmead Millennium Institute and University of Sydney, Westmead, New South Wales, Australia; and the Department of Infectious Diseases and Immunology, University of Sydney, Australia. Human cytomegalovirus (HCMV) establishes and maintains a latent infection in myeloid cells and can reactivate to cause serious disease in allograft recipients. To better understand the molecular events associated with the establishment of latency, we tracked the virus following infection of primary human myeloid progenitor cells at days 1, 2, 3, 5, and 11. At all time points, the viral genome was maintained in most cells at approximately 10 copies. Infectious virus was not detected, but virus could be reactivated by extended fibroblast coculture. In contrast to wild-type HCMV, the viral genome was rapidly lost from myeloid progenitors infected with ultraviolet (UV)–inactivated virus, suggesting viral gene expression was required for efficient establishment of latency. To identify viral genes associated with the establishment phase, RNA from each time point was interrogated using custom-made HCMV gene microarrays. Using this approach, we detected expression of viral RNAs at all time points. The pattern of expression differed from that which occurs during productive infection, and decreased over time. This study provides evidence that a molecular pathway into latency is associated with expression of a unique subset of viral transcripts. Viral genes expressed during the establishment phase may serve as targets for therapies to interrupt this process. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. L. Stern and B. Slobedman Human Cytomegalovirus Latent Infection of Myeloid Cells Directs Monocyte Migration by Up-Regulating Monocyte Chemotactic Protein-1 J. Immunol., May 15, 2008; 180(10): 6577 - 6585. [Abstract] [Full Text] [PDF] R. T. Saffert and R. F. Kalejta Human Cytomegalovirus Gene Expression Is Silenced by Daxx-Mediated Intrinsic Immune Defense in Model Latent Infections Established In Vitro J. Virol., September 1, 2007; 81(17): 9109 - 9120. [Abstract] [Full Text] [PDF] F. Goodrum, M. Reeves, J. Sinclair, K. High, and T. Shenk Human cytomegalovirus sequences expressed in latently infected individuals promote a latent infection in vitro Blood, August 1, 2007; 110(3): 937 - 945. [Abstract] [Full Text] [PDF]

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