| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
,¶,||,#
* Department of Microbiology and Immunology, University of Western Ontario, London, Ontario, Canada;
Division of Experimental Therapeutics, Toronto General Research Institute, University Health Network, Toronto, Ontario, Canada;
Division of Hematology and Immunodeficiency Service, Royal Victoria Hospital, McGill University Health Centre, Montreal, Quebec, Canada;
Animal Resources Division, Heath Canada, Ottawa, Ontario, Canada;
¶ National Laboratory for HIV Pathogenesis, Heath Canada, Ottawa, Ontario, Canada;
|| McGill AIDS Center, McGill University, Montreal, Quebec, Canada; and
# Department of Immunology, University of Toronto, Toronto, Ontario, Canada
HIV infection is characterized by a host response composed of adaptive and innate immunity that partially limits viral replication; however, it ultimately fails in eradicating the virus. To model host gene expression during acute HIV infection, we infected cynomolgus macaques with the SIV/HIV-1 chimeric virus, SHIV89.6P, and profiled gene expression in peripheral blood over a 5-wk period using a high density cDNA microarray. We demonstrate that viral challenge induced a widespread suppression of genes regulating innate immunity, including the LPS receptors, CD14 and TLR4. An overexpression of 16 IFN-stimulated genes was also observed in response to infection; however, it did not correlate with control over viral titers. A statistical analysis of the dataset identified 10 genes regulating apoptosis with differential expression during the first 2 wk of infection (p < 0.004). Quantitative real-time PCR verified transcriptional increases in IFN-
-inducible genes and decreases in genes regulating innate immunity. Therefore, the persistence of high viral loads despite an extensive IFN response suggests that HIV can resist in vivo IFN treatment despite published reports of in vitro efficacy. The transcriptional suppression of genes regulating innate immunity may allow HIV to evade acute host responses and establish a chronic infection and may reduce innate host defense against opportunistic infections.
This article has been cited by other articles:
|
|
 |
|
  M. M. Nelson, A. R. Jones, J. C. Carmen, A. P. Sinai, R. Burchmore, and J. M. Wastling Modulation of the Host Cell Proteome by the Intracellular Apicomplexan Parasite Toxoplasma gondii Infect. Immun., February 1, 2008; 76(2): 828 - 844. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. D. Hyrcza, C. Kovacs, M. Loutfy, R. Halpenny, L. Heisler, S. Yang, O. Wilkins, M. Ostrowski, and S. D. Der Distinct Transcriptional Profiles in Ex Vivo CD4+ and CD8+ T Cells Are Established Early in Human Immunodeficiency Virus Type 1 Infection and Are Characterized by a Chronic Interferon Response as Well as Extensive Transcriptional Changes in CD8+ T Cells J. Virol., April 1, 2007; 81(7): 3477 - 3486. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Audige, M. Urosevic, E. Schlaepfer, R. Walker, D. Powell, S. Hallenberger, H. Joller, H.-U. Simon, R. Dummer, and R. F. Speck Anti-HIV State but Not Apoptosis Depends on IFN Signature in CD4+ T Cells J. Immunol., November 1, 2006; 177(9): 6227 - 6237. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. M. Murray, L. J. Picker, M. K. Axthelm, and M. L. Linial Expanded Tissue Targets for Foamy Virus Replication with Simian Immunodeficiency Virus-Induced Immunosuppression J. Virol., January 15, 2006; 80(2): 663 - 670. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
