منابع مشابه
HIV-1 Induced Bystander Apoptosis
Apoptosis of uninfected bystander cells is a key element of HIV pathogenesis and believed to be the driving force behind the selective depletion of CD4+ T cells leading to immunodeficiency. While several viral proteins have been implicated in this process the complex interaction between Env glycoprotein expressed on the surface of infected cells and the receptor and co-receptor expressing bysta...
متن کاملHIV-1 protease inhibitors.
Treatment of human immunodeficiency virus type 1 (HIV-1) infection with regimens that include protease inhibitors (PIs) has contributed to marked improvements in HIV-related disease progression and mortality. Five PIs are approved by the US Food and Drug Administration and have potent activity in vitro. PIs with 2 nucleoside analogue reverse transcriptase inhibitors have demonstrated prolonged ...
متن کاملDrug-Induced Reactivation of Apoptosis Abrogates HIV-1 Infection
HIV-1 blocks apoptosis, programmed cell death, an innate defense of cells against viral invasion. However, apoptosis can be selectively reactivated in HIV-infected cells by chemical agents that interfere with HIV-1 gene expression. We studied two globally used medicines, the topical antifungal ciclopirox and the iron chelator deferiprone, for their effect on apoptosis in HIV-infected H9 cells a...
متن کاملThe effect of an HIV-1 viral protease inhibitor on staurosporine-induced apoptosis in immortalized mesangial cells.
CONTEXT Progressive glomerular sclerosis is a condition characterized by the accumulation of glomerular extracellular matrix and a decrease in the number of glomerular cells. The mechanisms involved in the progressive loss of glomerular cells are not well understood but may involve the process of apoptosis. The principal mediators for the apoptotic pathway are a class of protease enzymes called...
متن کاملHIV Protease Inhibitor-induced Lipodystrophy Syndrome
s of the 37th ICAAC, San Diego, September, 1998 (ab-
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ژورنال
عنوان ژورنال: Retrovirology
سال: 2014
ISSN: 1742-4690
DOI: 10.1186/1742-4690-11-37