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Human immunodeficiency virus type 1 enhances intracellular growth of Mycobacterium avium in human macrophages

G Källenius1, T Koivula, K J Rydgård

  • 1National Bacteriological Laboratory, Karolinska Institute, Stockholm, Sweden.

Insights

Human immunodeficiency virus (HIV) infection accelerates Mycobacterium avium growth in macrophages. This interaction may explain the poor control of mycobacterial infections in patients with acquired immunodeficiency syndrome (AIDS).

Area of Science:

  • Immunology
  • Virology
  • Microbiology

Background:

  • Disseminated Mycobacterium avium infections are prevalent in acquired immunodeficiency syndrome (AIDS) patients, reducing life expectancy.
  • Human monocytes/macrophages are key target cells for both human immunodeficiency virus (HIV) and Mycobacterium avium (M. avium).

Purpose of the Study:

  • To investigate the in vitro interaction between M. avium and human immunodeficiency virus type 1 (HIV-1) within human macrophages.
  • To elucidate the impact of HIV-1 pre-infection on M. avium intracellular growth and cytokine production in macrophages.

Main Methods:

  • Human monocytes from healthy donors were isolated and differentiated into macrophages.
  • Macrophages were infected with HIV-1, M. avium, or co-infected with both.
  • Intracellular M. avium growth and HIV-1 replication were monitored for up to 5 weeks.
  • Interleukin 1 alpha and beta production was measured in infected macrophages.

Main Results:

  • Intracellular growth of M. avium was observed in all infected macrophage cultures.
  • M. avium infection led to increased production of interleukin 1 alpha and beta.
  • Pre-infection with HIV-1 reduced interleukin 1 production and significantly accelerated intracellular M. avium growth.

Conclusions:

  • HIV-1 infection enhances the intracellular proliferation of M. avium in human macrophages.
  • The observed interaction, including reduced interleukin 1 production, may contribute to the impaired control of mycobacterial infections in AIDS patients.

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