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Aggravation of both Trypanosoma cruzi and murine leukemia virus by concomitant infections

J S Silva1, M Barral-Netto, S G Reed

  • 1School of Medicine of Ribeirao Preto, University of Sao Paulo, Brazil.

The American Journal of Tropical Medicine and Hygiene
|November 1, 1993
PubMed

Insights

Murine leukemia virus (MuLV) infection reactivated Trypanosoma cruzi (T. cruzi) infections and worsened MuLV-induced disease. This highlights risks of co-infection with retroviruses and protozoan parasites in humans.

Area of Science:

  • Immunology
  • Infectious Diseases
  • Parasitology

Background:

  • Acquired immunodeficiency syndrome (AIDS) is spreading in Latin America, a region endemic for Chagas' disease.
  • This creates a significant risk for co-infections with human immunodeficiency virus (HIV) and Trypanosoma cruzi.
  • Murine acquired immunodeficiency syndrome (MAIDS) models HIV-like immunologic alterations.

Purpose of the Study:

  • To investigate the effects of co-infection with a retrovirus and Trypanosoma cruzi using a MAIDS model.
  • To understand how murine leukemia virus (MuLV) impacts T. cruzi infection and vice versa.

Main Methods:

  • Utilized a murine acquired immunodeficiency syndrome (MAIDS) model induced by murine leukemia virus (MuLV).
  • Studied C57Bl/10 mice infected with MuLV and T. cruzi, assessing parasitemia, cardiac inflammation, T cell responses, and antibody levels.
  • Investigated MAIDS-resistant B6D2 mice infected sequentially with MuLV and T. cruzi.

Main Results:

  • MuLV infection reactivated T. cruzi in mice, evidenced by increased parasitemia and myocardial inflammation.
  • Dual infection led to suppressed T cell responses to T. cruzi antigens and elevated IL-10 levels.
  • T. cruzi-specific antibodies were reduced in dually infected animals.
  • In MAIDS-resistant mice, dual infection resulted in higher parasitemia and the development of MAIDS.

Conclusions:

  • Murine leukemia virus (MuLV) can activate latent Trypanosoma cruzi infections.
  • Trypanosoma cruzi infection can aggravate MuLV-induced disease, potentially leading to MAIDS development.
  • These findings have implications for understanding and managing retroviral and protozoan co-infections in humans.

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