HIV-1 infection causes a down-regulation of genes involved in ribosome biogenesis

PLoS One. 2014 Dec 2;9(12):e113908. doi: 10.1371/journal.pone.0113908. eCollection 2014.

Abstract

HIV-1 preferentially infects CD4+ T cells, causing fundamental changes that eventually lead to the release of new viral particles and cell death. To investigate in detail alterations in the transcriptome of the CD4+ T cells upon viral infection, we sequenced polyadenylated RNA isolated from Jurkat cells infected or not with HIV-1. We found a marked global alteration of gene expression following infection, with an overall trend toward induction of genes, indicating widespread modification of the host biology. Annotation and pathway analysis of the most deregulated genes showed that viral infection produces a down-regulation of genes associated with the nucleolus, in particular those implicated in regulating the different steps of ribosome biogenesis, such as ribosomal RNA (rRNA) transcription, pre-rRNA processing, and ribosome maturation. The impact of HIV-1 infection on genes involved in ribosome biogenesis was further validated in primary CD4+ T cells. Moreover, we provided evidence by Northern Blot experiments, that host pre-rRNA processing in Jurkat cells might be perturbed during HIV-1 infection, thus strengthening the hypothesis of a crosstalk between nucleolar functions and viral pathogenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • CD4-Positive T-Lymphocytes / immunology
  • Down-Regulation / genetics*
  • Gene Expression Profiling
  • HIV Infections / genetics*
  • HIV Infections / immunology*
  • HIV-1 / physiology*
  • Humans
  • Jurkat Cells
  • RNA Precursors / genetics
  • RNA Processing, Post-Transcriptional / genetics
  • Real-Time Polymerase Chain Reaction
  • Reproducibility of Results
  • Ribosomes / metabolism*
  • Sequence Analysis, RNA

Substances

  • RNA Precursors

Grants and funding

This study was supported in part by the Ministry of Health, ‘Programma Nazionale di ricerca sull’AIDS' in collaboration with ISS to A. M. and by grants of the Ministry of Health, Ricerca Finalizzata, and Ricerca Corrente co-funded by the Italian 5×1000 contribution to M.D. C.L.K. was the recipient of a fellowship award from the Fonds de Recherche du Québec-Santé. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.