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Blood, 5 November 2009, Vol. 114, No. 19, pp. 4128-4137. Prepublished online as a Blood First Edition Paper on August 25, 2009; DOI 10.1182/blood-2008-12-197111. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2008-12-197111v1 114/19/4128    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 Google Scholar Articles by Cheung, A. K. L. Articles by Slobedman, B. PubMed PubMed Citation Articles by Cheung, A. K. L. Articles by Slobedman, B. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY The role of the human cytomegalovirus UL111A gene in down-regulating CD4+ T-cell recognition of latently infected cells: implications for virus elimination during latency Allen K. L. Cheung1, David J. Gottlieb2, Bodo Plachter3, Sandra Pepperl-Klindworth3, Selmir Avdic1, Anthony L. Cunningham1, Allison Abendroth1,4,*, and Barry Slobedman1,* 1 Centre for Virus Research and 2 Cellular Therapies Group, Westmead Millennium Institute and University of Sydney, Westmead, Australia; 3 Institute for Virology, University Medical Center of the University of Mainz, Mainz, Germany; and 4 Department of Infectious Diseases and Immunology, University of Sydney, Camperdown, Australia The capacity of human cytomegalovirus (HCMV) to establish and maintain a latent infection from which it can later reactivate ensures its widespread distribution in the population, but the mechanisms enabling maintenance of latency in the face of a robust immune system are poorly understood. We examined the role of the HCMV UL111A gene, which encodes homologs of the immunosuppressive cytokine interleukin-10 in the context of latent infection of myeloid progenitor cells. A UL111A deletion virus was able to establish, maintain, and reactivate from experimental latency in a manner comparable with parental virus, but major histocompatibility complex class II levels increased significantly on the surfaces of cells infected with the deletion virus. Importantly, there was an increase in both allogeneic and autologous peripheral blood mononuclear cells and CD4+ T-cell responses to UL111A deletion virus-infected myeloid progenitors, indicating that loss of the capacity to express viral interleukin-10 during latency results in latently infected cells becoming more readily recognizable by a critical arm of the immune response. The detection of a viral gene that suppresses CD4+ T-cell recognition of latently infected cells identifies an immune evasion strategy that probably enhances the capacity of HCMV to persist in a latent state within the human host. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: B. Slobedman, P. A. Barry, J. V. Spencer, S. Avdic, and A. Abendroth Virus-Encoded Homologs of Cellular Interleukin-10 and Their Control of Host Immune Function J. Virol., October 1, 2009; 83(19): 9618 - 9629. [Full Text] [PDF]

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