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AIDS as immune system activation: a model for pathogenesis.

M S Ascher1, H W Sheppard

  • 1Viral and Rickettsial Disease Laboratory, California Department of Health Services, Berkeley 94704.

Clinical and Experimental Immunology
|August 1, 1988
PubMed
Summary
This summary is machine-generated.

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The current model of human immunodeficiency virus (HIV) causing acquired immunodeficiency syndrome (AIDS) is challenged. A new hypothesis suggests indirect mechanisms, involving HIV-infected macrophages, cause immune deficiency, not direct T4 cell killing.

Area of Science:

  • Immunology
  • Virology
  • Pathogenesis

Background:

  • Epidemiological data strongly link human immunodeficiency virus (HIV) to acquired immunodeficiency syndrome (AIDS).
  • HIV infection progresses from acute illness to asymptomatic stages, then immune decline, characterized by T4 cell depletion and opportunistic infections.
  • The prevailing model attributes T4 cell loss to direct viral cytopathic effects or autoimmunity.

Purpose of the Study:

  • To critically evaluate the current model of HIV-induced immunodeficiency.
  • To propose an alternative hypothesis for AIDS pathogenesis.
  • To explain the latency period and progressive immune decline without direct widespread T cell infection.

Main Methods:

  • Review and critique of existing epidemiological and experimental evidence regarding HIV and AIDS.

Related Experiment Videos

  • Development of a novel hypothesis based on indirect pathogenic mechanisms.
  • Analysis of viral load and T cell infection data.

    • Main Results:

    • Evidence suggests limited and constant viraemia and T cell infection throughout disease progression, challenging direct cytopathic models.
    • The current model of HIV-induced pathology is deemed unsatisfactory.
    • An alternative hypothesis is advanced.

    Conclusions:

    • Progressive immunodeficiency in AIDS may result from indirect mechanisms rather than direct widespread T cell infection or autoimmunity.
    • HIV infection of macrophages could induce abnormal immune regulatory mechanisms.
    • The latency of AIDS may be due to the accumulation of immune insults, not delayed viral replication.