Plasmodium vivax infections seldom kill directly but do cause indirect mortality by reducing birth weight and causing abortion. Cytoadherence and séquestration in the microvasculature are central to the pathogenesis of severe Plasmodium falciparum malaria, but the contribution of cytoadherence to pathology in other human malarias is less clear.The adhérence properties of P. vivax infected red blood cells (PvIRBC) were evaluated under static and flow conditions.P. vivax isolates from 33 patients were studied. None adhered to immobilized CD36, ICAM-1, or thrombospondin, putative ligands for P. falciparum vascular cytoadherence, or umbilical vein endothelial cells, but all adhered to immobilized chondroitin sulphate A (CSA) and hyaluronic acid (HA), the receptors for adhesion of P. falciparum in the placenta. PvIRBC also adhered to fresh placental cells (N = 5). Pre-incubation with chondroitinase prevented PvIRBC adherence to CSA, and reduced binding to HA, whereas preincubation with hyaluronidase prevented adhérence to HA, but did not reduce binding to CSA significantly. Pre-incubation of PvIRBC with soluble CSA and HA reduced binding to the immobilized receptors and prevented placental binding. PvIRBC adhesion was prevented by pre-incubation with trypsin, inhibited by heparin, and reduced by EGTA. Under laminar flow conditions the mean (SD) shear stress reducing maximum attachment by 50% was 0.06 (0.02) Pa but, having adhered, the PvIRBC could then resist detachment by stresses up to 5 Pa. At 37 °C adherence began approximately 16 hours after red cell invasion with maximal adherence at 30 hours. At 39 °C adherence began earlier and peaked at 24 hours.Adherence of P. vivax-infected erythrocytes to glycosaminoglycans may contribute to the pathogenesis of vivax malaria and lead to intra-utérine growth retardation.

Plasmodium vivax infections seldom kill directly but do cause indirect mortality by reducing birth weight and causing abortion. Cytoadherence and sequestration in the microvasculature are central to the pathogenesis of severe Plasmodium falciparum malaria, but the contribution of cytoadherence to pathology in other human malarias is less clear.The adherence properties of P. vivax infected red blood cells (PvIRBC) were evaluated under static and flow conditions.P. vivax isolates from 33 patients were studied. None adhered to immobilized CD36, ICAM-1, or thrombospondin, putative ligands for P. falciparum vascular cytoadherence, or umbilical vein endothelial cells, but all adhered to immobilized chondroitin sulphate A (CSA) and hyaluronic acid (HA), the receptors for adhesion of P. falciparum in the placenta. PvIRBC also adhered to fresh placental cells (N = 5). Pre-incubation with chondroitinase prevented PvIRBC adherence to CSA, and reduced binding to HA, whereas preincubation with hyaluronidase prevented adherence to HA, but did not reduce binding to CSA significantly. Pre-incubation of PvIRBC with soluble CSA and HA reduced binding to the immobilized receptors and prevented placental binding. PvIRBC adhesion was prevented by pre-incubation with trypsin, inhibited by heparin, and reduced by EGTA. Under laminar flow conditions the mean (SD) shear stress reducing maximum attachment by 50% was 0.06 (0.02) Pa but, having adhered, the PvIRBC could then resist detachment by stresses up to 5 Pa. At 37 °C adherence began approximately 16 hours after red cell invasion with maximal adherence at 30 hours. At 39 °C adherence began earlier and peaked at 24 hours.Adherence of P. vivax-infected erythrocytes to glycosaminoglycans may contribute to the pathogenesis of vivax malaria and lead to intrauterine growth retardation.

Plasmodium vivax infections seldom kill directly but do cause indirect mortality by reducing birth weight and causing abortion. Cytoadherence and sequestration in the microvasculature are central to the pathogenesis of severe Plasmodium falciparum malaria, but the contribution of cytoadherence to pathology in other human malaria is less clear. The adherence properties of P. vivax infected red blood cells (PvIRBC) were evaluated under static and flow conditions. P. vivax isolates from 33 patients were studied. None adhered to immobilized CD36, ICAM-1, or thrombospondin, putative ligands for P. falciparum vascular cytoadherence, or umbilical vein endothelial cells, but all adhered to immobilized chondroitin sulphate A (CSA) and hyaluronic acid (HA), the receptors for adhesion of P. falciparum in the placenta. PvIRBC also adhered to fresh placental cells (N = 5). Pre-incubation with chondroitinase prevented PvIRBC adherence to CSA, and reduced binding to HA, whereas preincubation with hyaluronidase prevented adherence to HA, but did not reduce binding to CSA significantly. Pre-incubation of PvIRBC with soluble CSA and HA reduced binding to the immobilized receptors and prevented placental binding. PvIRBC adhesion was prevented by pre-incubation with trypsin, inhibited by heparin, and reduced by EGTA. Under laminar flow conditions the mean (SD) shear stress reducing maximum attachment by 50% was 0.06 (0.02) Pa but, having adhered, the PvIRBC could then resist detachment by stresses up to 5 Pa. At 37°C adherence began approximately 16 hours after red cell invasion with maximal adherence at 30 hours. At 39°C adherence began earlier and peaked at 24 hours. Adherence of P. vivax-infected erythrocytes to glycosaminoglycans may contribute to the pathogenesis of vivax malaria and lead to intrauterine growth retardation.

نادراً ما تقتل عدوى المتصورة النشيطة بشكل مباشر ولكنها تسبب وفيات غير مباشرة عن طريق تقليل الوزن عند الولادة والتسبب في الإجهاض. يعد الارتباط الخلوي والعزل في الأوعية الدموية الدقيقة أمرًا أساسيًا في التسبب في ملاريا المتصورة المنجلية الحادة، لكن مساهمة الالتزام الخلوي في علم الأمراض في الملاريا البشرية الأخرى أقل وضوحًا. تم تقييم خصائص الالتزام لخلايا الدم الحمراء المصابة بـ P. vivax (PvIRBC) في ظل ظروف ثابتة وتدفق. تمت دراسة عزلات P. vivax من 33 مريضًا. لم يلتصق أي منها بـ CD36 أو ICAM -1 أو thrombospondin المثبت، أو الأربطة المفترضة للالتصاق الخلوي الوعائي لـ P. falciparum، أو الخلايا البطانية للوريد السري، ولكن جميعها التزمت بكبريتات شوندروتن A المثبتة (CSA) وحمض الهيالورونيك (HA)، مستقبلات التصاق P. falciparum في المشيمة. التزم PvIRBC أيضًا بالخلايا المشيمية الطازجة (N = 5). منع الحضانة المسبقة مع شوندروتيناز التزام PvIRBC بـ CSA، وخفض الارتباط بـ HA، في حين منع الحضانة المسبقة مع الهيالورونيداز الالتزام بـ HA، لكنه لم يقلل من الارتباط بـ CSA بشكل كبير. قلل الحضانة المسبقة لـ PvIRBC مع CSA و HA القابلين للذوبان من الارتباط بالمستقبلات المثبتة ومنع ربط المشيمة. تم منع التصاق PvIRBC عن طريق الحضانة المسبقة مع التربسين، وتم تثبيطه بواسطة الهيبارين، وتم تقليله بواسطة EGTA. في ظل ظروف التدفق الصفحي، كان متوسط إجهاد القص (SD) الذي يقلل من أقصى ارتباط بنسبة 50 ٪ هو 0.06 (0.02) باسكال، ولكن بعد الالتزام، يمكن لـ PvIRBC بعد ذلك مقاومة الانفصال من خلال ضغوط تصل إلى 5 باسكال. عند 37 درجة مئوية، بدأ الالتزام بعد حوالي 16 ساعة من غزو الخلايا الحمراء مع الالتزام الأقصى عند 30 ساعة. عند 39 درجة مئوية، بدأ الالتزام في وقت مبكر وبلغ ذروته في 24 ساعة. قد يساهم التزام كريات الدم الحمراء المصابة بـ P. vivax إلى glycosaminoglycans في التسبب في ملاريا vivax ويؤدي إلى تأخر النمو داخل الرحم.