Schistosomiasis and HIV-1 infection in rural Zimbabwe: Effect of treatment of schistosomiasis on CD4 cell count and plasma HIV-1 RNA load

被引:87
作者
Kallestrup, P
Zinyama, R
Gomo, E
Butterworth, AE
Mudenge, B
van Dam, GJ
Gerstoft, J
Erikstrup, C
Ullum, H
机构
[1] Rigshosp, Dept Infect Dis, Ctr Inflammat & Metab, DK-2100 Copenhagen, Denmark
[2] Rigshosp, Dept Clin Immunol, DK-2100 Copenhagen, Denmark
[3] Coll Hlth Sci, Natl Inst Hlth Res, Harare, Zimbabwe
[4] Coll Hlth Sci, Dept Immunol, Harare, Zimbabwe
[5] Univ Zimbabwe, Dept Med Microbiol, Harare, Zimbabwe
[6] Parirenyatwa Hosp, Biomed Res & Training Inst, Harare, Zimbabwe
[7] Parirenyatwa Hosp, Dept Hematol, Harare, Zimbabwe
[8] London Sch Hyg & Trop Med, London WC1, England
[9] Leiden Univ, Med Ctr, Dept Parasitol, Leiden, Netherlands
关键词
D O I
10.1086/497696
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
To determine whether treatment of schistosomiasis has an effect on the course of human immunodeficiency virus type 1 (HIV-1) infection, individuals with schistosomiasis and with or without HIV-1 infection were randomized to receive praziquantel treatment at inclusion or after a delay of 3 months; 287 participants were included in the study, and 227 (79%) were followed up. Among the 130 participants who were coinfected, those who received early treatment (n = 64) had a significantly lower increase in plasma HIV-1 RNA load than did those who received delayed treatment (n = 66) (P < .05); this difference was associated with no change in plasma HIV-1 RNA load in the early intervention group (P = .99) and an increase in plasma HIV-1 RNA load in the delayed intervention group (P < .01). Among the 227 participants who were followed up, those who received early treatment (n = 105) had an increase in CD4 cell count, whereas those who received delayed treatment (n = 122) did not (P < .05); this effect did not differ between participants when stratified by HIV-1 infection status (P = .17). The present study suggests that treatment of schistosomiasis can reduce the rate of viral replication and increase CD4 cell count in the coinfected host.
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页码:1956 / 1961
页数:6
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