Báo cáo khoa học: "The relationship of interacting immunological components in dengue pathogenesis"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: The relationship of interacting immunological components in dengue pathogenesis | Virology Journal BioMed Central Open Access Review The relationship of interacting immunological components in dengue pathogenesis David G Nielsen Address Department of Microbiology and Immunology Tulane University 1430 Tulane Avenue SL-38 New Orleans Louisiana 70112-2699 USA Email David G Nielsen - dnielsen@ Published 27 November 2009 Virology Journal 2009 6 211 doi l743-422X-6-2l I Received 27 October 2009 Accepted 27 November 2009 This article is available from http content 6 l 2ll 2009 Nielsen licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract__ The World Health Organization WHO estimates that there are over 50 million cases of dengue fever reported annually and approximately billion people are at risk. Mild dengue fever presents with headache fever rash myalgia osteogenic pain and lethargy. Severe disease can manifest as dengue shock syndrome DSS or dengue hemorrhagic fever DHF . Symptoms of DSS DHF are leukopenia low blood volume and pressure encephalitis cold and sweaty skin gastrointestinal bleeding and spontaneous bleeding from gums and nose. Currently there are no therapeutics available beyond supportive care and untreated complicated dengue fever can have a 50 mortality rate. According to WHO DSS DHF is the leading cause of childhood mortality in some Asian countries. Dendritic cells are professional antigen presenting cells that are primary targets in a dengue infection. Dengue binds to Dendritic Cell-Specific Intercellular adhesion molecule-3-Grabbing Non-integrin DC-SIGN . DC-SIGN has a high affinity for ICAM3 which is expressed in activating T-cells. Previous studies have demonstrated

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