Kubar J, Marty P, Lelièvre A, Quaranta J F, Staccini P, Caroli-Bosc C, Le Fichoux Y
Groupe de Recherche en Immunopathologie de la Leishmaniose, Laboratoire de Parasitologie, Faculté de Médecine de Nice, France.
AIDS. 1998 Nov 12;12(16):2147-53. doi: 10.1097/00002030-199816000-00009.
To discriminate cases of visceral leishmaniosis (VL) following a primary infection from cases originating in a reactivation of a latent Leishmania infection and to assess the impact of CD4+ T-cell counts on the occurrence of VL in patients with HIV disease.
We searched by Western blotting for the presence of Leishmania infantum-specific antibodies in the sera of 236 HIV-positive patients. We performed a follow-up of antileishmanial serology and analysed the evolution of the CD4+ T-cell counts for 14 HIV-positive VL patients and for 18 HIV-positive Leishmania-seropositive patients without VL.
This study (1) showed that the VL disease/Leishmania infection ratio in HIV-positive individuals is high (1 : 10); (2) discriminated between a primary Leishmania infection (five patients who converted from Leishmania-seronegative to Leishmania-seropositive) and a reactivation of a latent infection (seven patients); (3) showed that HIV-positive individuals with dramatically low CD4+ T-cell counts maintained or generated a specific antileishmanial antibody production; (4) demonstrated that the primary-VL appeared at significantly higher (P = 0.028) CD4+ T-cell levels than the reactivation-VL; (5) documented the existence of HIV-positive Leishmania-seropositive individuals who despite a severe and prolonged immunosuppression did not develop VL (eight of 18).
Our data stress the utility of the follow-up by Western blotting for an early diagnosis of VL, and therefore an early treatment, for HIV-positive patients living in endemic areas. They suggest that in a latent Leishmania infection supplementary control mechanism(s) might operate in addition to the T-cell-mediated response, and provide a further example of non-appearance of an opportunistic infection despite a severe reduction in CD4+ T cells.
区分原发性感染后发生的内脏利什曼病(VL)病例与潜伏性利什曼原虫感染激活引发的病例,并评估CD4+ T细胞计数对HIV疾病患者发生VL的影响。
我们通过蛋白质印迹法检测了236例HIV阳性患者血清中婴儿利什曼原虫特异性抗体的存在情况。我们对14例HIV阳性VL患者和18例HIV阳性利什曼原虫血清阳性但无VL的患者进行了抗利什曼原虫血清学随访,并分析了CD4+ T细胞计数的变化情况。
本研究(1)表明HIV阳性个体中VL疾病/利什曼原虫感染率很高(1:10);(2)区分了原发性利什曼原虫感染(5例从利什曼原虫血清阴性转为血清阳性的患者)和潜伏感染激活(7例患者);(3)表明CD4+ T细胞计数极低的HIV阳性个体维持或产生了特异性抗利什曼原虫抗体;(4)证明原发性VL出现时的CD4+ T细胞水平显著高于激活型VL(P = 0.028);(5)记录了尽管存在严重且长期的免疫抑制但仍未发生VL的HIV阳性利什曼原虫血清阳性个体(18例中有8例)。
我们的数据强调了通过蛋白质印迹法进行随访对生活在流行地区的HIV阳性患者早期诊断VL从而早期治疗的实用性。这些数据表明,在潜伏性利什曼原虫感染中,除了T细胞介导的反应外,可能还存在其他补充控制机制,并提供了尽管CD4+ T细胞严重减少但机会性感染未出现的又一实例。