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Blood, 15 August 2005, Vol. 106, No. 4, pp. 1305-1313. Prepublished online as a Blood First Edition Paper on April 21, 2005; DOI 10.1182/blood-2004-12-4899. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-12-4899v1 106/4/1305    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 Peretti, S. Articles by Pope, M. Search for Related Content PubMed PubMed Citation Articles by Peretti, S. Articles by Pope, M. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Immunomodulatory effects of HSV-2 infection on immature macaque dendritic cells modify innate and adaptive responses Silvia Peretti, Andrew Shaw, James Blanchard, Rudolf Bohm, Gavin Morrow, Jeffrey D. Lifson, Agegnehu Gettie, and Melissa Pope From the Center for Biomedical Research, Population Council, New York, NY; Tulane National Primate Research Center, Tulane University, Covington, LA; AIDS Vaccine Program, Science Applications International Corporation (SAIC)–Frederick, National Cancer Institute at Frederick, MD; and Aaron Diamond AIDS Research Center, New York, NY. Herpes simplex viruses (HSV) infect human and murine dendritic cells (DCs) and interfere with their immunostimulatory functions in culture. HSV-2 infection increases human immunodeficiency virus (HIV) spread in patients, and DCs also promote HIV infection. We have studied these topics in rhesus macaque monocyte-derived DCs (moDCs) to set the stage for future studies of these issues in animals. We provide the first evidence that macaque DCs become infected by HSV-2. Structural viral proteins (ICP5 [infected cell protein 5], glycoprotein D [gD], envelope) were detected in the cell periphery, and a functional protein (infected cell protein 8 [ICP8]) was predominantly found in the nucleus after infection. Infectious HSV-2 induced apoptotic death, decreased expression of HLA-DR, CD40, CD80, CD83, and CD86, and increased release of interleukin-6 (IL-6), tumor necrosis factor- (TNF-), macrophage inflammatory protein-1 (MIP-1) (CCL3), and RANTES (regulated on activation normal T cells expressed and secreted) (CCL5) but not IL-12 or interferon- (IFN-) by macaque DCs. This coincided with HSV-2–infected DCs stimulating weak T-cell responses, including impaired SIV-specific responses. Comparable HSV-2 protein expression, DC apoptosis, as well as membrane immunophenotype and functional modifications were observed in HSV-2–exposed human moDCs. Such HSV-2–induced modifications of macaque and human DCs could augment DC-driven immunodeficiency virus infection. This work affords the basis for future macaque studies to explore how HSV-2 impacts the efficacy of strategies being developed to prevent HIV transmission. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. D. Sloan and K. R. Jerome Herpes Simplex Virus Remodels T-Cell Receptor Signaling, Resulting in p38-Dependent Selective Synthesis of Interleukin-10 J. Virol., November 15, 2007; 81(22): 12504 - 12514. [Abstract] [Full Text] [PDF] M. Thapa, W. A. Kuziel, and D. J. J. Carr Susceptibility of CCR5-Deficient Mice to Genital Herpes Simplex Virus Type 2 Is Linked to NK Cell Mobilization J. Virol., April 15, 2007; 81(8): 3704 - 3713. [Abstract] [Full Text] [PDF]

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