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Decay-accelerating factor (CD55) protects human immunodeficiency virus type 1 from inactivation by human complement

P Marschang1, J Sodroski, R Würzner

  • 1Institut für Hygiene, Leopold-Franzens-Universität, Innsbruck, Austria.

European Journal of Immunology
|January 1, 1995
PubMed
Summary

Human cells protect HIV-1 from complement lysis by acquiring decay-accelerating factor (DAF). This host factor shields the virus from immune attack, explaining species-specific protection against human complement.

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Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • Human Immunodeficiency Virus type 1 (HIV-1) evades human complement lysis, unlike animal retroviruses.
  • Animal sera readily inactivate HIV-1, suggesting a species-specific immune evasion mechanism.

Purpose of the Study:

  • To investigate the species-specific protection mechanism of HIV-1 against human complement.
  • To identify host-derived factors on HIV-1 virions that confer resistance to complement-mediated lysis.

Main Methods:

  • Recombinant HIV-1 was produced in human (HEp-2), monkey (COS-1), and mink cells.
  • Infectivity of HIV-1 was assessed in CD4-positive target cells after incubation with human serum.
  • Virus capture assays and antibody blocking experiments were used to detect and analyze viral surface proteins.

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Main Results:

  • HIV-1 produced in non-human cells was significantly inactivated (5-10 fold reduction in infectivity) by human serum, while HIV-1 from human cells was resistant.
  • Human serum efficiently lysed HIV-1 from non-human cells but not from human cells.
  • Decay-accelerating factor (DAF) and CD59 were detected on HIV-1 virions; antibodies against DAF blocked complement resistance in HIV-1 from human cells.

Conclusions:

  • HIV-1 acquires host-derived decay-accelerating factor (DAF) during budding from human cells.
  • DAF on the viral surface confers species-specific resistance to human complement-mediated lysis.
  • This mechanism highlights viral adaptation for immune evasion within the host species.