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|108||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 RB; Gomo E; van Dam GJ; Deelder AM; Butterworth AE; Pedersen BK; Ostrowski SR; Gerstoft J; Ullum H
Am J Trop Med Hyg 2008; 79(3): 331-7
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.
PubMed ID: 18784223 Reprint: Download PDF (225 kB)