Human immunodeficiency virus type 1 chronic infection is associated with different gene expression in MT-4, H9 and U937 cell lines

Virus Res. 2009 Jan;139(1):22-31. doi: 10.1016/j.virusres.2008.09.010. Epub 2008 Nov 25.

Abstract

To investigate cellular factors involved in HIV-1 chronic infection, three cell lines chronically infected with the same HIV-1 viral isolate (s61) were studied by cDNA microarray analysis. Two T cell lines, H61 and M61, showed the characteristics of a persistent infection whereas U61 cell line displayed a latent infection pattern. Analysis of genes with altered expression in the three cell lines revealed evidence of apoptosis control by up-regulation of anti-apoptotic genes and down-regulation of pro-apoptotic genes. In addition, cell cycle control was affected in the two persistent T cell lines particularly through the down-regulation of cyclin-dependent kinase inhibitor 1A (CDKN1A/p21). Moreover, each cell line showed specific characteristics, like in M61 cells, genes related with cellular activation and with cell migration and motility. In U61 cells, genes associated with immune response were activated. Genes with altered expression in our experiments, and not previously related with HIV such as ANXA 1 or CFLAR were detected and validated. This work revealed that different cell mechanism such as control of apoptosis and cell cycle are important for "in vitro" HIV-1 chronic infections, and discovered new genes previously not related with HIV-1 replication.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line, Tumor
  • Chronic Disease
  • Gene Expression Profiling
  • Gene Expression Regulation, Viral*
  • Genes, Viral*
  • HIV Infections / genetics
  • HIV Infections / physiopathology*
  • HIV-1 / genetics
  • HIV-1 / pathogenicity
  • HIV-1 / physiology*
  • Humans
  • RNA, Viral / genetics
  • RNA, Viral / metabolism
  • U937 Cells
  • Virus Activation / genetics
  • Virus Activation / physiology*
  • Virus Latency / genetics
  • Virus Latency / physiology*
  • Virus Replication

Substances

  • RNA, Viral