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Title: Gene expression profiling of the host response to HIV-1 B, C, or A/E infection in monocyte-derived dendritic cells

Journal Article · · Virology
 [1];  [1];  [1];  [1];  [1];  [1]
  1. McGill AIDS Center, Lady Davis Institute for Medical Research, Jewish General Hospital, Departments of Microbiology and Immunology and Medicine, McGill University, 3755 Cote Ste. Catherine, Montreal, Quebec, H3T1E2 (Canada)

Dendritic cells (DC) are among the first targets of human immunodeficiency virus type-1 (HIV-1) infection and in turn play a crucial role in viral transmission to T cells and in the regulation of the immune response. The major group of HIV-1 has diversified genetically based on variation in env sequences and comprise at least 11 subtypes. Because little is known about the host response elicited against different HIV-1 clade isolates in vivo, we sought to use gene expression profiling to identify genes regulated by HIV-1 subtypes B, C, and A/E upon de novo infection of primary immature monocyte-derived DC (iMDDCs). A total of 3700 immune-related genes were subjected to a significance analysis of microarrays (SAM); 656 genes were selected as significant and were further divided into 8 functional categories. Regardless of the time of infection, 20% of the genes affected by HIV-1 were involved in signal transduction, followed by 14% of the genes identified as transcription-related genes, and 7% were classified as playing a role in cell proliferation and cell cycle. Furthermore, 7% of the genes were immune response genes. By 72 h postinfection, genes upregulated by subtype B included the inhibitor of the matrix metalloproteinase TIMP2 and the heat shock protein 40 homolog (Hsp40) DNAJB1, whereas the IFN inducible gene STAT1, the MAPK1/ERK2 kinase regulator ST5, and the chemokine CXCL3 and SHC1 genes were induced by subtypes C and A/E. These analyses distinguish a temporally regulated host response to de novo HIV-1 infection in primary dendritic cells.

OSTI ID:
20850545
Journal Information:
Virology, Vol. 352, Issue 1; Other Information: DOI: 10.1016/j.virol.2006.04.010; PII: S0042-6822(06)00231-5; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0042-6822
Country of Publication:
United States
Language:
English