National Institute for Medical Research (NIMR)-Mbeya Medical Research Centre, Mbeya, Tanzania.
National Institute for Medical Research (NIMR)-Mbeya Medical Research Centre, Mbeya, Tanzania; Division of Infectious Diseases and Tropical Medicine, Medical Center of the University of Munich (LMU), Munich, Germany.
PLoS Negl Trop Dis. 2014 Mar 27;8(3):e2755. doi: 10.1371/journal.pntd.0002755. eCollection 2014 Mar.
It has been hypothesized that helminth infections increase HIV susceptibility by enhancing systemic immune activation and hence contribute to elevated HIV-1 transmission in sub-Saharan Africa.
To study systemic immune activation and HIV-1 co-receptor expression in relation to different helminth infections and in response to helminth treatment.
HIV-negative adults with (n = 189) or without (n = 57) different helminth infections, as diagnosed by Kato-Katz, were enrolled in Mbeya, Tanzania. Blinded to helminth infection status, T cell differentiation (CD45RO, CD27), activation (HLA-DR, CD38) and CCR5 expression was determined at baseline and 3 months after Albendazole/Praziquantel treatment. Plasma cytokine levels were compared using a cytometric bead array.
Trichuris and Ascaris infections were linked to increased frequencies of "activated" CD4 and/or CD8 T cells (p<0.05), whereas Hookworm infection was associated with a trend towards decreased HLA-DR+ CD8 T cell frequencies (p = 0.222). In Trichuris infected subjects, there was a linear correlation between HLA-DR+ CD4 T cell frequencies and the cytokines IL-1β and IL-10 (p<0.05). Helminth treatment with Albendazole and Praziquantel significantly decreased eosinophilia for S. mansoni and Hookworm infections (p<0.005) but not for Trichuris infection and only moderately modulated T cell activation. CCR5 surface density on memory CD4 T cells was increased by 1.2-fold during Trichuris infection (p-value: 0.053) and reduced after treatment (p = 0.003).
Increased expression of T cell activation markers was associated with Trichuris and Ascaris infections with relatively little effect of helminth treatment.
有人假设，寄生虫感染通过增强全身免疫激活，从而增加艾滋病毒易感性，并导致撒哈拉以南非洲艾滋病毒-1 传播率升高。
研究全身免疫激活和 HIV-1 共受体表达与不同寄生虫感染的关系，并研究寄生虫感染治疗的反应。
坦桑尼亚姆贝亚招募了 HIV 阴性成人，他们（n = 189）或没有（n = 57）不同的寄生虫感染，通过加藤厚涂片法诊断。在不了解寄生虫感染状态的情况下，在基线和阿苯达唑/吡喹酮治疗 3 个月后，确定 T 细胞分化（CD45RO、CD27）、激活（HLA-DR、CD38）和 CCR5 的表达。使用流式细胞术微珠阵列比较血浆细胞因子水平。
鞭虫和蛔虫感染与“激活”的 CD4 和/或 CD8 T 细胞频率增加有关（p<0.05），而钩虫感染与 HLA-DR+CD8 T 细胞频率下降趋势有关（p = 0.222）。在感染鞭虫的患者中，HLA-DR+CD4 T 细胞频率与细胞因子 IL-1β 和 IL-10 呈线性相关（p<0.05）。用阿苯达唑和吡喹酮治疗寄生虫可显著降低曼氏血吸虫和钩虫感染的嗜酸性粒细胞（p<0.005），但对感染鞭虫没有影响，仅适度调节 T 细胞激活。在感染鞭虫期间，记忆 CD4 T 细胞上的 CCR5 表面密度增加了 1.2 倍（p 值：0.053），治疗后降低（p = 0.003）。
T 细胞激活标志物表达增加与鞭虫和蛔虫感染有关，寄生虫感染治疗的效果相对较小。
