title: Gene expression profile of HIV-1 Tat expressing cells: a close interplay between proliferative and differentiation signals.
abstract: BACKGROUND
  Expression profiling holds great promise for rapid host genome functional analysis. It is plausible that host expression profiling in an infection could serve as a universal phenotype in virally infected cells. Here, we describe the effect of one of the most critical viral activators, Tat, in HIV-1 infected and Tat expressing cells. We utilized microarray analysis from uninfected, latently HIV-1 infected cells, as well as cells that express Tat, to decipher some of the cellular changes associated with this viral activator.
  
  
  RESULTS
  Utilizing uninfected, HIV-1 latently infected cells, and Tat expressing cells, we observed that most of the cellular host genes in Tat expressing cells were down-regulated. The down-regulation in Tat expressing cells is most apparent on cellular receptors that have intrinsic receptor tyrosine kinase (RTK) activity and signal transduction members that mediate RTK function, including Ras-Raf-MEK pathway. Co-activators of transcription, such as p300/CBP and SRC-1, which mediate gene expression related to hormone receptor genes, were also found to be down-regulated. Down-regulation of receptors may allow latent HIV-1 infected cells to either hide from the immune system or avoid extracellular differentiation signals. Some of the genes that were up-regulated included co-receptors for HIV-1 entry, translation machinery, and cell cycle regulatory proteins.
  
  
  CONCLUSIONS
  We have demonstrated, through a microarray approach, that HIV-1 Tat is able to regulate many cellular genes that are involved in cell signaling, translation and ultimately control the host proliferative and differentiation signals.
authors.affiliation: Department of Biochemistry and Molecular Biology George Washington University School of Medicine Washington DC 20037, USA. bcmfxk@gwumc.edu
authors.forename: Cynthia
authors.initials: C
authors.lastname: de la Fuente
authors.forename: Francisco
authors.initials: F
authors.lastname: Santiago
authors.forename: Longwen
authors.initials: L
authors.lastname: Deng
authors.forename: Carolyne
authors.initials: C
authors.lastname: Eadie
authors.forename: Irene
authors.initials: I
authors.lastname: Zilberman
authors.forename: Kylene
authors.initials: K
authors.lastname: Kehn
authors.forename: Anil
authors.initials: A
authors.lastname: Maddukuri
authors.forename: Shanese
authors.initials: S
authors.lastname: Baylor
authors.forename: Kaili
authors.initials: K
authors.lastname: Wu
authors.forename: Chee Gun
authors.initials: CG
authors.lastname: Lee
authors.forename: Anne
authors.initials: A
authors.lastname: Pumfery
authors.forename: Fatah
authors.initials: F
authors.lastname: Kashanchi
mesh_terms: D002453:Cell Cycle / Q000235:genetics; D002454:Cell Differentiation / Q000235:genetics; D002455:Cell Division / Q000235:genetics; D002843:Chromatin / Q000235:genetics; D020869:Gene Expression Profiling / Q000379:methods*; D005786:Gene Expression Regulation / Q000235:genetics; D015696:Gene Products, tat / Q000235:genetics*; D015497:HIV-1 / Q000235:genetics*; D006367:HeLa Cells / Q000166:cytology / Q000378:metabolism / Q000821:virology; D006801:Humans; D014176:Protein Biosynthesis / Q000235:genetics; D015398:Signal Transduction / Q000235:genetics*; D013947:Thymosin / Q000235:genetics; D014157:Transcription Factors / Q000235:genetics; D014158:Transcription, Genetic / Q000235:genetics; D014407:Tumor Cells, Cultured; D054322:tat Gene Products, Human Immunodeficiency Virus
chemical_list: D002843:Chromatin; D015696:Gene Products, tat; D014157:Transcription Factors; D054322:tat Gene Products, Human Immunodeficiency Virus; D013947:Thymosin