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Am. J. Trop. Med. Hyg., 79(3), 2008, pp. 331-337
Copyright © 2008 by The American Society of Tropical Medicine and Hygiene

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Schistosomiasis and Infection with Human Immunodeficiency Virus 1 in Rural Zimbabwe: Systemic Inflammation during Co-infection and after Treatment for Schistosomiasis

Christian Erikstrup*, Per Kallestrup, Rutendo B. L. Zinyama-Gutsire, Exnevia Gomo, Govert J. van Dam, André M. Deelder, Anthony E. Butterworth, Bente Klarlund Pedersen, Sisse R. Ostrowski, Jan Gerstoft, AND Henrik Ullum
Department of Clinical Immunology, Aarhus University Hospital, Skejby Sygehus, Aarhus, Denmark; Department of Clinical Immunology, Rigshospitalet, Copenhagen, Denmark; The Centre of Inflammation and Metabolism at the Department of Infectious Diseases, Rigshospitalet, Faculty of Health Sciences, and Cluster of International Health, University of Copenhagen, Denmark; National Institute of Health Research, Harare, Zimbabwe; Department of Immunology, College of Health Sciences, and Department of Medical Microbiology, University of Zimbabwe, Harare, Zimbabwe; Department of Parasitology, Leiden University Medical Center, Leiden, The Netherlands; Biomedical Research and Training Institute, Harare, Zimbabwe, London School of Hygiene and Tropical Medicine, London, United Kingdom

We previously reported that treatment for schistosomiasis in persons infected with human immunodeficiency virus 1 (HIV-1) attenuated HIV replication as measured by plasma HIV RNA. We investigated systemic inflammation as measured by plasma levels of soluble tumor necrosis factor-{alpha} receptor II (sTNF-rII), interleukin-8, (IL-8), and IL-10 during schistosomiasis and HIV co-infection and after schistosomiasis treatment. The cohort was composed of 378 persons who were or were not infected with HIV-1, Schistosoma haematobium, or S. mansoni. Schistosomiasis-infected persons were randomized to receive praziquantel (40 mg/kg) at baseline or at the three-month follow-up. sTNF-rII and IL-8 were positively associated with schistosomiasis intensity as measured by circulating anodic antigen (CAA), regardless of HIV status. Interleukin-10 was positively associated with CAA in HIV-negative participants. IL-8 levels were higher in S. mansoni-infected individuals. Treatment for schistosomiasis caused a decrease in levels of sTNF-rII (P < 0.05) and IL-10 (P < 0.001). Our results indicate that schistosomiasis treatment may attenuate HIV replication by decreasing systemic inflammation.


Received January 14, 2008. Accepted for publication June 5, 2008.

Acknowledgments: We thank the Mupfure Community; the Village Health Workers; the Environmental Health Technician; the technical team (E. N. Kurewa, N. Taremeredzwa, W. Mashange, C. Mukahiwa, S. Nyandoro, W. Soko, B. Mugwagwa, and E. Mashiri), the Department of Haematology at Parirenyatwa Hospital (R. Mafirakureba, D. Mawire, and B. Mudenge); and the Department of Virology at Rigshospitalet, Copenhagen (M. Luneborg-Nielsen) for their contributions to the study.

Financial support: This study was supported by grants from the Danish AIDS Foundation; Fonden Til Lægevidenskabens Fremme; The Essential National Health Research Fund of the Ministry of Health and Child Welfare of Zimbabwe (P355); The Danish Embassy in Zimbabwe (2001); The DANIDA Health Programme in Zimbabwe (2001); The U.S. Centers for Disease Control and Prevention Program in Zimbabwe; and the Centre of Inflammation and Metabolism (Danish National Research Foundation) (DG 02-512-555).

Disclosure: The authors have no commercial or other association that might pose a conflict of interest.

* Address correspondence to Christian Erikstrup, Department of Clinical Immunology, Aarhus University Hospital, Skejby Sygehus, Brendstrupgaardsvej 100, DK-8200 Aarhus N, Denmark. E-mail: christian{at}erikstrup.org

Authors’ addresses: Christian Erikstrup, Department of Clinical Immunology, Aarhus University Hospital, Skejby Sygehus, Brendstrup-gaardsvej 100, DK-8200 Aarhus N, Denmark, Tel: +45-40187491, Fax: +45-35457644, E-mail: Christian{at}erikstrup.org. Per Kallestrup, Bente Klarlund Pedersen, and Sisse R. Ostrowski, Centre of Inflammation and Metabolism, Department of Infectious Diseases 7641, Rigshospitalet, Blegdamsvej 9, 2100 Copenhagen, Denmark, E-mails: kallestrup{at}dadlnet.dk, bente.klarlund.pedersen{at}rh.regionh.dk, and sisse.ostrowski{at}gmail.com. Rutendo B. L. Zinyama-Gutsire, National Institute of Health Research, Corner Tongogara and Mazoe St, CY 573 Causeway, Harare, Zimbabwe, E-mail: gutsirerbl{at}yahoo.com. Exnevia Gomo, Research Support Centre, College of Medicine, University of Malawi, P.Bag 360, Chichiri, Blantyre 3, Malawi, E-mail: egomo{at}rsc.medcol.mw. Govert J. van Dam and André M. Deelder, Department of Parasitology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, The Netherlands, E-mails: G.J.van_Dam{at}lumc.nl and a.m.deelder{at}lumc.nl. Anthony E. Butterworth, Biomedical Research and Training Institute, PO Box CY 1753, Causeway, Harare, Zimbabwe, E-mail: aeb1{at}ecoweb.co.zw. Jan Gerstoft, Department of Infectious Diseases 5132, Rigshospitalet, Blegdamsvej 9, DK-2100 Copenhagen, Denmark, E-mail: jan.gerstoft{at}rh.regionh.dk. Henrik Ullum, Department of Clinical Immunology 2031, Rigshospitalet, Blegdamsvej 9, DK-2100, Copenhagen, Denmark, E-mail: henrik.ullum{at}rh.regionh.dk.

Reprint requests: Christian Erikstrup, Department of Clinical Immunology, Aarhus University Hospital, Skejby Sygehus, Brendstrup-gaardsvej 100, DK-8200 Aarhus N, Denmark.







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Copyright © 2008 by the American Society of Tropical Medicine and Hygiene.