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149 Impact of Acute Vivax Malaria on the Immune System of HIV-Positive Subjects
X.-P. Chen*, B.-Q. Xiao, W.-J. Shi, H.-F. Xu, K. Gao, J.-L. Rao, and Z.-B. Zhang
Municipal Hlth. and Anti-Epidemic Station of Guangzhou, Guangzhou, China
Background: A beneficial interaction of malaria and HIV coinfection has been reported in a hospital-based study and in a well-controlled cohort study in Africa. In our previous studies there was an increase in total trend of CD4 cell counts in HIV-positive subjects during 2 years of follow-up to malariotherapy (therapeutic vivax malaria).
Methods: A total of 12 HIV-1-positive patients were grouped by CD4 cell count baselines: total group (TG) for all represented CD4 range from 1217 to 15/muL, subgroup 1 (SG1) for 5 patients with CD4 counts ( 500/muL, subgroup 2 (SG2) for 5 patients with CD4 counts from 499 to 200/muL. Two patients with CD4 counts < 200/muL were not included as a subgroup for statistic analysis. Plasmodium vivax was intravenously injected into the HIV patients to induce therapeutic malaria and the malaria was terminated with chloroquine after 10 fever episodes. ELISA was used to measure the plasma levels of cytokines and soluble activation markers including TNF-a, INF-r, sTNF-RII, NPT, sIL-2R, and b2M. Flow cytometry was used to measure the levels of CD4+, CD8+, CD25+, CD4+CD25+, HLA-DR+, and CD8+HLA-DR+ lymphocytes and the percentage of apoptotic CD4 cells. Samples were taken and tested at the first pre-malaria (pre1), second pre-malaria (pre2), first malarial fever episode (f1), fifth episode (f5), tenth episode (f10), day 10 after termination of malaria (pd10), and 1 month (m1) and 3 months (m3) of follow-up.
Results: Levels of plasma TNF-a, sTNF-RII, NPT, and sIL-2R significantly elevated during malaria and sharply reduced to baselines post malaria in all groups, but much stronger responses of these factors were seen in SG2 than in SG1 (p = 0.081, 0.001, 0.013, and 0.020) during malaria. In TG, CD4 number, CD25+, and CD4+CD25+ percentages decreased (not significantly for CD4, significantly for other 2) during malaria then rebounded to over baseline levels post malaria. CD4 percentage and CD4/CD8 ratio increased either during or post malaria (p = 0.048 for %CD4 at m3). In SG1, CD4 and CD8 numbers significantly decreased during malaria then rebounded to baseline levels post malaria. In SG2, CD4 number and percentage, CD4/CD8 ratio, and CD25+ and CD4+CD25+ percentages increased either during or post malaria (p < 0.001 for %CD4 at m3). Changes of HLA-DR+ and CD8+HLA-DR+ percentages were somewhat different among different groups. Percentage of apoptotic CD4 cells rose during malaria (p = 0.015) and then sharply reduced to lower than the baseline in all groups (p = 0.148 for TG).
Conclusions: Relatively stronger responses of CD4 cell (especially its percentage) and CD4/CD8 ratio elevation and much stronger responses of plasma cytokines and immune activation markers to therapeutic acute vivax malaria were seen in HIV-positive subjects with CD4 baseline level from 499 to 200/muL. The effects on CD4 cells and other phenotypic changes might follow from the cytokine responses.
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