Author:
ProCite
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Reference Manager
BibTeX
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-
1
UNAIDS. UNAIDS: 2007 Epidemic Update. 2007; Available at: http://www.unaids.org/en/KnowledgeCentre/HIVData/EpiUpdate/EpiUpdArchive/2007/. Accessed July 16, 2008.
-
2
Chitsulo L, Loverde P, Engels D, 2004. Schistosomiasis. Nat Rev Microbiol 2 :12–13.
-
3
Kallestrup P, Zinyama R, Gomo E, Butterworth AE, van Dam GJ, Erikstrup C, Ullum H, 2005. Schistosomiasis and HIV-1 infection in rural Zimbabwe: implications of coinfection for excretion of eggs. J Infect Dis 191 :1311–1320.
-
4
Brown M, Kizza M, Watera C, Quigley MA, Rowland S, Hughes P, Whitworth JAG, Elliott AM, 2004. Helminth infection is not associated with faster progression of HIV disease in coinfected adults in Uganda. J Infect Dis 190 :1869–1879.
-
5
Brown M, Mawa PA, Joseph S, Bukusuba J, Watera C, Whitworth JA, Dunne DW, Elliott AM, 2005. Treatment of Schistosoma mansoni infection increases helminth-specific type 2 cytokine responses and HIV-1 loads in coinfected Ugandan adults. J Infect Dis 191 :1648–1657.
-
6
Lawn SD, Karanja DM, Mwinzia P, Andove J, Colley DG, Folks TM, Secor WE, 2000. The effect of treatment of schistosomiasis on blood plasma HIV-1 RNA concentration in coinfected individuals. AIDS 14 :2437–2443.
-
7
Kallestrup P, Zinyama R, Gomo E, Butterworth AE, Mudenge B, van Dam GJ, Gerstoft J, Erikstrup C, Ullum H, 2005. Schistosomiasis and HIV-1 infection in rural Zimbabwe: effect of treatment of schistosomiasis on CD4 cell count and plasma HIV-1 RNA load. J Infect Dis 192 :1956–1961.
-
8
Lähdevirta J, Maury CP, Teppo AM, Repo H, 1988. Elevated levels of circulating cachectin/tumor necrosis factor in patients with acquired immunodeficiency syndrome. Am J Med 85 :289–291.
-
9
Breen EC, Rezai AR, Nakajima K, Beall GN, Mitsuyasu RT, Hirano T, Kishimoto T, Martinez-Maza O, 1990. Infection with HIV is associated with elevated IL-6 levels and production. J Immunol 144 :480–484.
-
10
Stylianou E, Aukrust P, Kvale D, Müller F, Frøland SS, 1999. IL-10 in HIV infection: increasing serum IL-10 levels with disease progression–down-regulatory effect of potent anti-retroviral therapy. Clin Exp Immunol 116 :115–120.
-
11
Kalinkovich A, Weisman Z, Leng Q, Borkow G, Stein M, Greenberg Z, Zlotnikov S, Eitan S, Bentwich Z, 1999. Increased CCR5 expression with decreased beta chemokine secretion in Ethiopians: relevance to AIDS in Africa. J Hum Virol 2 :283–289.
-
12
Kalinkovich A, Borkow G, Weisman Z, Tsimanis A, Stein M, Bentwich Z, 2001. Increased CCR5 and CXCR4 expression in Ethiopians living in Israel: environmental and constitutive factors. Clin Immunol 100 :107–117.
-
13
Griffin GE, Leung K, Folks TM, Kunkel S, Nabel GJ, 1991. Induction of NF-kappa B during monocyte differentiation is associated with activation of HIV-gene expression. Res Virol 142 :233–238.
-
14
Herbein G, Gordon S, 1997. 55- and 75-kilodalton tumor necrosis factor receptors mediate distinct actions in regard to human immunodeficiency virus type 1 replication in primary human macrophages. J Virol 71 :4150–4156.
-
15
Lane BR, Lore K, Bock PJ, Andersson J, Coffey MJ, Strieter RM, Markovitz DM, 2001. Interleukin-8 stimulates human immunodeficiency virus type 1 replication and is a potential new target for antiretroviral therapy. J Virol 75 :8195–8202.
-
16
Poli G, Kinter A, Justement JS, Kehrl JH, Bressler P, Stanley S, Fauci AS, 1990. Tumor necrosis factor alpha functions in an autocrine manner in the induction of human immunodeficiency virus expression. Proc Natl Acad Sci USA 87 :782–785.
-
17
Weissman D, Poli G, Fauci AS, 1994. Interleukin 10 blocks HIV replication in macrophages by inhibiting the autocrine loop of tumor necrosis factor alpha and interleukin 6 induction of virus. AIDS Res Hum Retroviruses 10 :1199–1206.
-
18
Tesselaar K, Arens R, van Schijndel GM, Baars PA, van der Valk MA, Borst J, van Oers MH, van Lier RA, 2003. Lethal T cell immunodeficiency induced by chronic costimulation via CD27-CD70 interactions. Nat Immunol 4 :49–54.
-
19
Bentwich Z, Weisman Z, Moroz C, Bar-Yehuda S, Kalinkovich A, 1996. Immune dysregulation in Ethiopian immigrants in Israel: relevance to helminth infections? Clin Exp Immunol 103 :239–243.
-
20
Kalinkovich A, Weisman Z, Greenberg Z, Nahmias J, Eitan S, Stein M, Bentwich Z, 1998. Decreased CD4 and increased CD8 counts with T cell activation is associated with chronic helminth infection. Clin Exp Immunol 114 :414–421.
-
21
Montenegro SM, Miranda P, Mahanty S, Abath FG, Teixeira KM, Coutinho EM, Brinkman J, Gonçalves I, Domingues LA, Domingues AL, Sher A, Wynn TA, 1999. Cytokine production in acute versus chronic human Schistosomiasis mansoni: the cross-regulatory role of interferon-gamma and interleukin-10 in the responses of peripheral blood mononuclear cells and splenocytes to parasite antigens. J Infect Dis 179 :1502–1514.
-
22
Hoffmann KF, Wynn TA, Dunne DW, 2002. Cytokine-mediated host responses during schistosome infections; walking the fine line between immunological control and immunopathology. Adv Parasitol 52 :265–307.
-
23
Maizels RM, Yazdanbakhsh M, 2003. Immune regulation by helminth parasites: cellular and molecular mechanisms. Nat Rev Immunol 3 :733–744.
-
24
Pearce EJ, MacDonald AS, 2002. The immunobiology of schistosomiasis. Nat Rev Immunol 2 :499–511.
-
25
McElroy MD, Elrefaei M, Jones N, Ssali F, Mugyenyi P, Barugahare B, Cao H, 2005. Coinfection with Schistosoma mansoni is associated with decreased HIV-specific cytolysis and increased IL-10 production. J Immunol 174 :5119–5123.
-
26
Mwinzi PN, Karanja DM, Colley DG, Orago AS, Secor WE, 2001. Cellular immune responses of schistosomiasis patients are altered by human immunodeficiency virus type 1 coinfection. J Infect Dis 184 :488–496.
-
27
Aderka D, 1996. The potential biological and clinical significance of the soluble tumor necrosis factor receptors. Cytokine Growth Factor Rev 7 :231–240.
-
28
van Deuren M, 1994. Kinetics of tumour necrosis factor-alpha, soluble tumour necrosis factor receptors, interleukin 1-beta and its receptor antagonist during serious infections. Eur J Clin Microbiol Infect Dis 13 (Suppl 1):S12–S16.
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29
Mott KE, Baltes R, Bambagha J, Baldassini B, 1982. Field studies of a reusable polyamide filter for detection of Schistosoma haematobium eggs by urine filtration. Tropenmed Parasitol 33 :227–228.
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Kallestrup P, Zinyama R, Gomo E, Butterworth AE, van Dam GJ, Gerstoft J, Erikstrup C, Ullum H, 2006. Schistosomiasis and HIV in rural Zimbabwe: efficacy of treatment of schistosomiasis in individuals with HIV coinfection. Clin Infect Dis 42 :1781–1789.
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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
Christian Erikstrup
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
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Per Kallestrup
Per Kallestrup
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
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Rutendo B. L. Zinyama-Gutsire
Rutendo B. L. Zinyama-Gutsire
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
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Exnevia Gomo
Exnevia Gomo
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
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Govert J. van Dam
Govert J. van Dam
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
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André M. Deelder
André M. Deelder
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
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Anthony E. Butterworth
Anthony E. Butterworth
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
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Bente Klarlund Pedersen
Bente Klarlund Pedersen
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
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Sisse R. Ostrowski
Sisse R. Ostrowski
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
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Jan Gerstoft
Jan Gerstoft
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
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Henrik Ullum
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
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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-α 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.
Author Notes
ProCite
RefWorks
Reference Manager
BibTeX
Zotero
EndNote
-
1
UNAIDS. UNAIDS: 2007 Epidemic Update. 2007; Available at: http://www.unaids.org/en/KnowledgeCentre/HIVData/EpiUpdate/EpiUpdArchive/2007/. Accessed July 16, 2008.
-
2
Chitsulo L, Loverde P, Engels D, 2004. Schistosomiasis. Nat Rev Microbiol 2 :12–13.
-
3
Kallestrup P, Zinyama R, Gomo E, Butterworth AE, van Dam GJ, Erikstrup C, Ullum H, 2005. Schistosomiasis and HIV-1 infection in rural Zimbabwe: implications of coinfection for excretion of eggs. J Infect Dis 191 :1311–1320.
-
4
Brown M, Kizza M, Watera C, Quigley MA, Rowland S, Hughes P, Whitworth JAG, Elliott AM, 2004. Helminth infection is not associated with faster progression of HIV disease in coinfected adults in Uganda. J Infect Dis 190 :1869–1879.
-
5
Brown M, Mawa PA, Joseph S, Bukusuba J, Watera C, Whitworth JA, Dunne DW, Elliott AM, 2005. Treatment of Schistosoma mansoni infection increases helminth-specific type 2 cytokine responses and HIV-1 loads in coinfected Ugandan adults. J Infect Dis 191 :1648–1657.
-
6
Lawn SD, Karanja DM, Mwinzia P, Andove J, Colley DG, Folks TM, Secor WE, 2000. The effect of treatment of schistosomiasis on blood plasma HIV-1 RNA concentration in coinfected individuals. AIDS 14 :2437–2443.
-
7
Kallestrup P, Zinyama R, Gomo E, Butterworth AE, Mudenge B, van Dam GJ, Gerstoft J, Erikstrup C, Ullum H, 2005. Schistosomiasis and HIV-1 infection in rural Zimbabwe: effect of treatment of schistosomiasis on CD4 cell count and plasma HIV-1 RNA load. J Infect Dis 192 :1956–1961.
-
8
Lähdevirta J, Maury CP, Teppo AM, Repo H, 1988. Elevated levels of circulating cachectin/tumor necrosis factor in patients with acquired immunodeficiency syndrome. Am J Med 85 :289–291.
-
9
Breen EC, Rezai AR, Nakajima K, Beall GN, Mitsuyasu RT, Hirano T, Kishimoto T, Martinez-Maza O, 1990. Infection with HIV is associated with elevated IL-6 levels and production. J Immunol 144 :480–484.
-
10
Stylianou E, Aukrust P, Kvale D, Müller F, Frøland SS, 1999. IL-10 in HIV infection: increasing serum IL-10 levels with disease progression–down-regulatory effect of potent anti-retroviral therapy. Clin Exp Immunol 116 :115–120.
-
11
Kalinkovich A, Weisman Z, Leng Q, Borkow G, Stein M, Greenberg Z, Zlotnikov S, Eitan S, Bentwich Z, 1999. Increased CCR5 expression with decreased beta chemokine secretion in Ethiopians: relevance to AIDS in Africa. J Hum Virol 2 :283–289.
-
12
Kalinkovich A, Borkow G, Weisman Z, Tsimanis A, Stein M, Bentwich Z, 2001. Increased CCR5 and CXCR4 expression in Ethiopians living in Israel: environmental and constitutive factors. Clin Immunol 100 :107–117.
-
13
Griffin GE, Leung K, Folks TM, Kunkel S, Nabel GJ, 1991. Induction of NF-kappa B during monocyte differentiation is associated with activation of HIV-gene expression. Res Virol 142 :233–238.
-
14
Herbein G, Gordon S, 1997. 55- and 75-kilodalton tumor necrosis factor receptors mediate distinct actions in regard to human immunodeficiency virus type 1 replication in primary human macrophages. J Virol 71 :4150–4156.
-
15
Lane BR, Lore K, Bock PJ, Andersson J, Coffey MJ, Strieter RM, Markovitz DM, 2001. Interleukin-8 stimulates human immunodeficiency virus type 1 replication and is a potential new target for antiretroviral therapy. J Virol 75 :8195–8202.
-
16
Poli G, Kinter A, Justement JS, Kehrl JH, Bressler P, Stanley S, Fauci AS, 1990. Tumor necrosis factor alpha functions in an autocrine manner in the induction of human immunodeficiency virus expression. Proc Natl Acad Sci USA 87 :782–785.
-
17
Weissman D, Poli G, Fauci AS, 1994. Interleukin 10 blocks HIV replication in macrophages by inhibiting the autocrine loop of tumor necrosis factor alpha and interleukin 6 induction of virus. AIDS Res Hum Retroviruses 10 :1199–1206.
-
18
Tesselaar K, Arens R, van Schijndel GM, Baars PA, van der Valk MA, Borst J, van Oers MH, van Lier RA, 2003. Lethal T cell immunodeficiency induced by chronic costimulation via CD27-CD70 interactions. Nat Immunol 4 :49–54.
-
19
Bentwich Z, Weisman Z, Moroz C, Bar-Yehuda S, Kalinkovich A, 1996. Immune dysregulation in Ethiopian immigrants in Israel: relevance to helminth infections? Clin Exp Immunol 103 :239–243.
-
20
Kalinkovich A, Weisman Z, Greenberg Z, Nahmias J, Eitan S, Stein M, Bentwich Z, 1998. Decreased CD4 and increased CD8 counts with T cell activation is associated with chronic helminth infection. Clin Exp Immunol 114 :414–421.
-
21
Montenegro SM, Miranda P, Mahanty S, Abath FG, Teixeira KM, Coutinho EM, Brinkman J, Gonçalves I, Domingues LA, Domingues AL, Sher A, Wynn TA, 1999. Cytokine production in acute versus chronic human Schistosomiasis mansoni: the cross-regulatory role of interferon-gamma and interleukin-10 in the responses of peripheral blood mononuclear cells and splenocytes to parasite antigens. J Infect Dis 179 :1502–1514.
-
22
Hoffmann KF, Wynn TA, Dunne DW, 2002. Cytokine-mediated host responses during schistosome infections; walking the fine line between immunological control and immunopathology. Adv Parasitol 52 :265–307.
-
23
Maizels RM, Yazdanbakhsh M, 2003. Immune regulation by helminth parasites: cellular and molecular mechanisms. Nat Rev Immunol 3 :733–744.
-
24
Pearce EJ, MacDonald AS, 2002. The immunobiology of schistosomiasis. Nat Rev Immunol 2 :499–511.
-
25
McElroy MD, Elrefaei M, Jones N, Ssali F, Mugyenyi P, Barugahare B, Cao H, 2005. Coinfection with Schistosoma mansoni is associated with decreased HIV-specific cytolysis and increased IL-10 production. J Immunol 174 :5119–5123.
-
26
Mwinzi PN, Karanja DM, Colley DG, Orago AS, Secor WE, 2001. Cellular immune responses of schistosomiasis patients are altered by human immunodeficiency virus type 1 coinfection. J Infect Dis 184 :488–496.
-
27
Aderka D, 1996. The potential biological and clinical significance of the soluble tumor necrosis factor receptors. Cytokine Growth Factor Rev 7 :231–240.
-
28
van Deuren M, 1994. Kinetics of tumour necrosis factor-alpha, soluble tumour necrosis factor receptors, interleukin 1-beta and its receptor antagonist during serious infections. Eur J Clin Microbiol Infect Dis 13 (Suppl 1):S12–S16.
-
29
Mott KE, Baltes R, Bambagha J, Baldassini B, 1982. Field studies of a reusable polyamide filter for detection of Schistosoma haematobium eggs by urine filtration. Tropenmed Parasitol 33 :227–228.
-
30
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