tailieunhanh - Báo cáo y học: " Role of the Fas/FasL Pathway in HIV or SIV Disease"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Retrovirology cung cấp cho các bạn kiến thức về ngành y đề tài: Role of the Fas/FasL Pathway in HIV or SIV Disease. | Retrovirology BioMed Central Review Role of the Fas FasL Pathway in HIV or SIV Disease Bhawna Poonia C David Pauza and Maria S Salvato Open Access Address Institute of Human Virology University of Maryland School of Medicine 725 W. Lombard Street Baltimore MD 21201 Email Bhawna Poonia - bpoonia@ C David Pauza - cdpauza@ Maria S Salvato - msalvato@ Corresponding author Published 15 October 2009 Received 21 July 2009 Retrovirology 2009 6 91 doi 1742-4690-6-91 Accepted 15 October 2009 This article is available from http content 6 1 91 2009 Poonia et al 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_ Human immunodeficiency virus disease involves progressive destruction of host immunity leading to opportunistic infections and increased rates for malignancies. Quantitative depletion of immune cell subsets and accruing defects in cell effector functions are together responsible for immunodeficiency The broad impact of HIV reflects a similarly broad spectrum of affected cells including subsets that do not express viral receptors or support viral replication. Indirect cell killing the destruction of uninfected cells is one important mechanism due partly to activation of the Fas FasL system for cell death. This death-signaling pathway is induced during HIV disease and contributes significantly to viral pathogenesis and disease. Background Changes in CD4 cell count and viral RNA burden are common markers for HIV disease progression. However evidence has existed for several years that many patients with HIV disease experience a broad loss of leukocyte subsets without an .

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