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CCR5 mediates Fas- and caspase-8 dependent apoptosis of both uninfected and HIV infected primary human CD4 T cells
TLDR
CCR5 is ascribed to CCR5 a novel role in activating the Fas pathway and caspase-8 as well as triggering FasL production when activated by R5 Env, ultimately causing CD4 T cell death.
G Protein-Coupled Chemokine Receptors Induce Both Survival and Apoptotic Signaling Pathways1
TLDR
Giα protein-coupled chemokine receptors can function as death prone receptors and the balance between the above signaling pathways will ultimately mandate the fate of the activated cell.
Chemokine-receptor activation by env determines the mechanism of death in HIV-infected and uninfected T lymphocytes.
TLDR
It is suggested that activation of the chemokine receptor by HIVenv determines the mechanism of death for both infected and uninfected T lymphocytes.
Human immunodeficiency virus-induced apoptosis of human hepatocytes via CXCR4.
TLDR
HIV can directly cause hepatocyte death in humans by signaling through CXCR4, without infecting the cell.
Comparison of the metabolic effects of ritonavir-boosted darunavir or atazanavir versus raltegravir, and the impact of ritonavir plasma exposure: ACTG 5257.
TLDR
Ritonavir C24 was not different in the PI arms and had no relationship with the modest but comparable increases in lipids observed with either atazanavir or darunavir, and raltegravir produced the most favorable lipid profile.
Effectiveness of highly active antiretroviral therapy (HAART) among HIV-infected patients in Mexico.
TLDR
Implementation of NGP for HAART access in a specialized care setting in Mexico resulted in an excellent virologic response, and younger age was a significant risk factor for VF.
Prospective, Randomized, Open Label Trial of Efavirenz vs Lopinavir/Ritonavir in HIV+ Treatment-Naive Subjects With CD4+<200 cell/mm3 in Mexico
TLDR
In these very advanced HIV-infected ARV-naive subjects, EFV-based highly active antiretroviral therapy had superior virologic efficacy than LPV/r-basedhighly active antifungal therapy, with a more favorable lipid profile.
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