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Human acid-labile interferon alpha.

¹Laboratory of Virology, Polish Academy of Sciences, Wrocław, Poland.

Archivum Immunologiae Et Therapiae Experimentalis

|April 15, 1999

Summary

High levels of acid-labile interferon-alpha (al-IFN-alpha) are found in AIDS and autoimmune diseases. This study investigates the nature of al-IFN-alpha, suggesting a plasma factor interaction rather than synergistic interferon effects.

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Area of Science:

Immunology
Virology
Molecular Biology

Background:

Elevated plasma interferon (IFN) levels, specifically acid-labile IFN-alpha (al-IFN-alpha), are observed in acquired immune deficiency syndrome (AIDS) and autoimmune diseases like systemic lupus erythematosus (SLE).
The precise nature of al-IFN-alpha remains unknown, with several hypotheses proposed, including distinct gene products, post-transcriptional modification, synergistic interferon interactions, or interaction with plasma factors.

Purpose of the Study:

To experimentally investigate the hypothesis that al-IFN-alpha results from synergistic interactions between acid-stable IFN-alpha and acid-labile IFN-gamma.
To elucidate the underlying mechanisms contributing to the presence of al-IFN-alpha in certain disease states.

Main Methods:

Creation of artificial mixtures of normal human IFN-alpha (nHuIFN-alpha) and recombinant human IFN-gamma (rHuIFN-gamma).
Treatment of these mixtures with acid (pH 2) and anti-IFN-gamma antibodies to assess synergistic effects.
Analysis of acid lability and antibody neutralization of IFN in AIDS patient serum (al-IFN-gamma).

Main Results:

Synergistic effects in artificial mixtures were abolished by acid or anti-IFN-gamma treatment, with residual activity matching acid-stable IFN-alpha.
AIDS-derived al-IFN-gamma showed high sensitivity to acid treatment, with minimal neutralization by anti-IFN-gamma serum.
These findings indicate that synergistic interferon interactions play a minor role in the acid lability of IFN-alpha.

Conclusions:

The phenomenon of acid-labile IFN-alpha in AIDS and autoimmune diseases is unlikely to be solely due to synergistic interactions between IFN-alpha and IFN-gamma.
The hypothesis involving interaction of IFN-alpha with unknown plasma factor(s) warrants further investigation to explain the occurrence of al-IFN-alpha.

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