Schistosomiasis and infection with human immunodeficiency virus 1 in rural Zimbabwe: systemic inflammation during co-infection and after treatment for schistosomiasis

C. Erikstrup; P. Kallestrup; R.B. Zinyama-Gutsire; E. Gomo; G.J. van Dam; A.M. Deelder; A.E. Butterworth; Bente Klarlund Pedersen; S.R. Ostrowski; J. Gerstoft; H. Ullum

Schistosomiasis and infection with human immunodeficiency virus 1 in rural Zimbabwe: systemic inflammation during co-infection and after treatment for schistosomiasis

C. Erikstrup, P. Kallestrup, R.B. Zinyama-Gutsire, E. Gomo, G.J. van Dam, A.M. Deelder, A.E. Butterworth, Bente Klarlund Pedersen, S.R. Ostrowski, J. Gerstoft, H. Ullum

Department of Clinical Medicine

19 Citations (Scopus)

Abstract

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
Udgivelsesdato: 2008/9

Original language	English
Journal	American Journal of Tropical Medicine and Hygiene
Volume	79
Issue number	3
Pages (from-to)	331-337
Number of pages	6
ISSN	0002-9637
Publication status	Published - 2008

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Cite this

Erikstrup, C., Kallestrup, P., Zinyama-Gutsire, R. B., Gomo, E., Dam, G. J. V., Deelder, A. M., Butterworth, A. E., Pedersen, B. K., Ostrowski, S. R., Gerstoft, J., & Ullum, H. (2008). Schistosomiasis and infection with human immunodeficiency virus 1 in rural Zimbabwe: systemic inflammation during co-infection and after treatment for schistosomiasis. American Journal of Tropical Medicine and Hygiene, 79(3), 331-337.

Schistosomiasis and infection with human immunodeficiency virus 1 in rural Zimbabwe: systemic inflammation during co-infection and after treatment for schistosomiasis. / Erikstrup, C.; Kallestrup, P.; Zinyama-Gutsire, R.B. et al.

In: American Journal of Tropical Medicine and Hygiene, Vol. 79, No. 3, 2008, p. 331-337.

Research output: Contribution to journal › Journal article › Research › peer-review

Erikstrup, C, Kallestrup, P, Zinyama-Gutsire, RB, Gomo, E, Dam, GJV, Deelder, AM, Butterworth, AE, Pedersen, BK, Ostrowski, SR, Gerstoft, J & Ullum, H 2008, 'Schistosomiasis and infection with human immunodeficiency virus 1 in rural Zimbabwe: systemic inflammation during co-infection and after treatment for schistosomiasis', American Journal of Tropical Medicine and Hygiene, vol. 79, no. 3, pp. 331-337.

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abstract = "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 Udgivelsesdato: 2008/9",

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AB - 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 Udgivelsesdato: 2008/9

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