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The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
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Updated: Apr 17, 2026

An In Vitro Model for Measuring Immune Responses to Malaria in the Context of HIV Co-infection
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HIV Coinfection Enhances Complement Activation During Sepsis.

Michaëla A M Huson1, Diana Wouters2, Gerard van Mierlo2

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The Journal of Infectious Diseases
|February 7, 2015
PubMed
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Human immunodeficiency virus (HIV) activates the complement system, particularly the classical pathway, leading to increased C4 activation. This immune response may contribute to tissue injury in chronic HIV infection and sepsis.

Keywords:
HIVcomplement system proteinsmalariamannose-binding lectinsepsis

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Area of Science:

  • Immunology
  • Infectious Diseases
  • Complement System Biology

Background:

  • Human immunodeficiency virus (HIV) infection is linked to chronic immune activation.
  • HIV may influence the complement system during acute illnesses like sepsis and malaria.

Purpose of the Study:

  • To determine the impact of HIV infection on the complement system.
  • To investigate complement activation in asymptomatic HIV, sepsis, and malaria patients.

Main Methods:

  • Prospective observational study of 268 subjects with or without HIV.
  • Measured complement activation products (C3bc, C4bc) and native proteins (C3, C4).
  • Assessed mannose-binding lectin and C1q-C4 for lectin and classical pathway activation.

Main Results:

  • Asymptomatic HIV infection showed increased C4 activation and elevated C1q-C4 levels, especially with high viral loads.
  • Sepsis and malaria also increased C4 activation and C1q-C4 concentrations.
  • HIV coinfection amplified C4 activation in sepsis but not malaria; mannose-binding lectin deficiency had no effect.

Conclusions:

  • HIV predominantly activates the complement system via the classical pathway.
  • Increased C4 activation and consumption occur during sepsis in HIV-infected individuals.
  • HIV-induced complement activation may contribute to tissue injury in chronic and acute infections.