Imbalance in cytokine production by whole blood related to presence of cytopathogenic HIV-1 strains in HIV-1-infected patients

Infection. 1998 Mar-Apr;26(2):109-12. doi: 10.1007/BF02767770.

Abstract

The possible association between the emergence of cytopathogenic HIV-1 variants and disturbance of the cytokine production in the course of HIV-1 infection was studied in 18 infected patients. The cytopathogenicity of the isolates was studied in a microassay based on the use of HIV-1-infectible Hela-CD4 cells carrying the bacterial LacZ gene under the control of the HIV-LTR (P4 cells). In addition, the production of cytokines by heparinized whole blood (HWB) obtained the same day from HIV-1(+) patients was measured. TNF-alpha was determined in a one-step procedure combining HWB culture in the presence of LPS+PHA for 24 h and detection of cytokines in the same wells. In separate experiments HWB was cultured in the presence of LPS+PHA for 48 h, then the supernatants were collected and stored until assayed by ELISa for IFN-gamma and IL-4. Higher TNF-alpha levels were found in activated HWB of patients with cytopathic strains (n = 9) than in patients with non-cytopathic strains (n = 9, p = 0.02) assessed with P4 cells. A defective production of type 1 cytokine (IFN-gamma) and no increased secretion of type 2 cytokines (IL-4) was observed in patients with cytopathic strains. IFN-gamma/IL-4 ratios were significantly lower in patients with cytopathic strains (n = 9) than in other patients (n = 9, p = 0.009). The results show that the disarray of cytokine production, as assessed with whole blood culture, is associated with the cytopathogenicity of HIV-1 isolates in HIV-1-infected individuals.

MeSH terms

  • Acquired Immunodeficiency Syndrome / blood
  • Acquired Immunodeficiency Syndrome / immunology*
  • Acquired Immunodeficiency Syndrome / virology*
  • Antibodies, Viral / blood
  • Blotting, Western
  • Cells, Cultured
  • Cytopathogenic Effect, Viral
  • Enzyme-Linked Immunosorbent Assay
  • HIV-1 / metabolism
  • HIV-1 / pathogenicity*
  • Humans
  • Interferon-gamma / blood*
  • Interleukin-4 / blood*
  • Phenotype
  • Tumor Necrosis Factor-alpha / metabolism*

Substances

  • Antibodies, Viral
  • Tumor Necrosis Factor-alpha
  • Interleukin-4
  • Interferon-gamma