AJTMH ASTMH MEMBERSHIP INFORMATION: astmh@astmh.org
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am. J. Trop. Med. Hyg., 49(5), 1993, pp. 589-597
Copyright © 1993 by The American Society of Tropical Medicine and Hygiene

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Silva, J. S.
Right arrow Articles by Reed, S. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Silva, J. S.
Right arrow Articles by Reed, S. G.

Aggravation of Both Trypanosoma Cruzi and Murine Leukemia Virus by Concomitant Infections

Joao S. Silva, Manoel Barral-Netto AND Steven G. Reed
School of Medicine of Ribeirao Preto, University of Sao Paulo, Ribeirao Preto, Brazil; Federal University of Bahia School of Medicine, Salvador, Bahia, Brazil; Seattle Biomedical Research Institute, Seattle, Washington; Department of Medicine, Division of International Medicine, Cornell University Medical College, New York, New York

Given the dissemination of acquired immunodeficiency syndrome (AIDS) in Latin America, where Chagas' disease is endemic, there is a present and increasing risk of concurrent infections with human immunodeficiency virus (HIV) and Trypanosoma cruzi. We used the model of murine acquired immunodeficiency syndrome (MAIDS) caused by a murine leukemia virus (MuLV) that induces immunologic alterations with similarities to those accompanying human HIV infection to study aspects of concomitant infections. The MuLV infection was found to reactivate T. cruzi infection in C57BI/10 mice, as indicated by elevated parasitemia and lymphocytic infiltration in the myocardium. The T cells from these animals did not respond to T. cruzi antigens (lymphocyte proliferation, interferon-gamma, or interleukin-2 [IL-2] production) but had increased levels of IL-10. Trypanosoma cruzi-specific antibody was decreased but not absent in dually infected animals. In a second set of experiments, we infected MAIDS-resistant B6D2 mice with MuLV, followed by infection with T. cruzi. These animals had higher parasitemia than those infected with T. cruzi alone. More interestingly, only dually infected animals developed MAIDS. The present report describes the activation of T. cruzi infection by MuLV as well as the aggravation of MuLV infection by T. cruzi. These results may be relevant to coinfections with retrovirus and protozoan parasites in humans.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1993 by the American Society of Tropical Medicine and Hygiene.