Alpha interferon and HIV infection cause activation of human T cells in NSG-BLT mice

J Virol. 2012 Mar;86(6):3327-36. doi: 10.1128/JVI.06676-11. Epub 2012 Jan 11.

Abstract

The development of small animal models for the study of HIV transmission is important for evaluation of HIV prophylaxis and disease pathogenesis. In humanized bone marrow-liver-thymus (BLT) mice, hematopoiesis is reconstituted by implantation of human fetal liver and thymus tissue (Thy/Liv) plus intravenous injection of autologous liver-derived hematopoietic stem progenitor cells (HSPC). This results in reconstitution of human leukocytes in the mouse peripheral blood, lymphoid organs, and mucosal sites. NOD-scid interleukin-2 receptor-negative (IL-2Rγ(-/-)) (NSG)-BLT mice were inoculated intravaginally with HIV and were monitored for plasma viremia by a branched DNA assay 4 weeks later. T-cell activation was determined by expression of CD38 and HLA-DR on human CD4(+) and CD8(+) T cells in mouse peripheral blood at the time of inoculation and 4 weeks later. Additional BLT mice were treated with human alpha interferon 2b (IFN-α2b) (intron A) and assessed for T-cell activation. Productive HIV infection in BLT mice was associated with T-cell activation (increases in CD38 mean fluorescence intensity and both the frequency and absolute number of CD38(+) HLA-DR(+) T cells) that correlated strongly with plasma viral load and was most pronounced in the CD8(+) T-cell compartment. This T-cell activation phenotype was recapitulated in NSG-BLT mice treated with intron A. HIV susceptibility correlated with the number of HSPC injected, yet a number of mice receiving the Thy/Liv implant alone, with no HSPC injection, were also susceptible to intravaginal HIV. These results are consistent with studies linking T-cell activation to progressive disease in humans and lend support for the use of NSG-BLT mice in studies of HIV pathogenesis.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Disease Models, Animal
  • Female
  • HIV Infections / immunology*
  • HIV Infections / virology
  • HIV-1 / immunology
  • HIV-1 / physiology*
  • Humans
  • Interferon alpha-2
  • Interferon-alpha / immunology*
  • Lymphocyte Activation*
  • Mice
  • Mice, Inbred NOD
  • Mice, Knockout
  • Mice, SCID
  • Receptors, Interleukin-2 / genetics
  • Receptors, Interleukin-2 / immunology
  • Recombinant Proteins / immunology
  • T-Lymphocytes / immunology*
  • T-Lymphocytes / physiology

Substances

  • Interferon alpha-2
  • Interferon-alpha
  • Receptors, Interleukin-2
  • Recombinant Proteins