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Preparation of Quality Inositol Pyrophosphates
10:34

Preparation of Quality Inositol Pyrophosphates

Published on: September 3, 2011

HIV infection of H9 lymphoblastoid cells chronically activates the inositol polyphosphate pathway

K E Nye1, A J Pinching

  • 1Department of Immunology, St Mary's Hospital Medical School, London, UK.

AIDS (London, England)
|January 1, 1990
PubMed

Insights

HIV infection disrupts cellular signaling in CD4+ lymphocytes, causing chronic activation and impaired calcium responses. This study reveals how these signal transduction defects contribute to immune dysfunction in HIV.

Area of Science:

  • Immunology
  • Cell Biology
  • Virology

Background:

  • Human Immunodeficiency Virus (HIV) infection impairs CD4+ lymphocyte function.
  • HIV leads to reduced CD4+ cell numbers and functional abnormalities in various cell types.

Purpose of the Study:

  • To investigate the impact of HIV infection on signal transduction pathways in the H9 CD4+ lymphoblastoid cell line.
  • To elucidate the mechanisms underlying CD4+ lymphocyte dysfunction in HIV.

Main Methods:

  • Studied signal transduction in HIV-infected H9 cells.
  • Measured inositol polyphosphate metabolites (InsP3, InsP4) and intracellular free calcium concentrations.
  • Stimulated cells with phytohemagglutinin (PHA) and anti-CD3 antibody.

Main Results:

  • Resting HIV-infected H9 cells exhibit chronic activation with elevated InsP3 and InsP4 levels, and increased intracellular calcium.
  • PHA stimulation caused a decrease in InsP3 but an increase in InsP4.
  • Both PHA and anti-CD3 antibody elicited an attenuated intracellular calcium rise in HIV-infected cells.

Conclusions:

  • HIV infection alters inositol polyphosphate metabolism and calcium signaling in CD4+ cells.
  • These signal transduction abnormalities provide a potential mechanism for CD4+ lymphocyte functional defects in HIV.
  • The findings may also explain functional issues in other cell types affected by HIV.

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