Short report
Cofilin activation in peripheral CD4 T cells of HIV-1 infected patients: a pilot study
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* Corresponding author: Yuntao Wu ywu8@gmu.edu
1 Department of Molecular and Microbiology, George Mason University, Manassas, VA, 20110, USA
2 Clinical Alliance For Research & Education – Infectious Diseases, LLC, Annandale, VA, 22003, USA
3 Department of Genetics and Genomics, Boston University School of Medicine, Boston, MA, 02118, USA
Retrovirology 2008, 5:95 doi:10.1186/1742-4690-5-95
Published: 17 October 2008Abstract
Cofilin is an actin-depolymerizing factor that regulates actin dynamics critical for T cell migration and T cell activation. In unstimulated resting CD4 T cells, cofilin exists largely as a phosphorylated inactive form. Previously, we demonstrated that during HIV-1 infection of resting CD4 T cells, the viral envelope-CXCR4 signaling activates cofilin to overcome the static cortical actin restriction. In this pilot study, we have extended this in vitro observation and examined cofilin phosphorylation in resting CD4 T cells purified from the peripheral blood of HIV-1-infected patients. Here, we report that the resting T cells from infected patients carry significantly higher levels of active cofilin, suggesting that these resting cells have been primed in vivo in cofilin activity to facilitate HIV-1 infection. HIV-1-mediated aberrant activation of cofilin may also lead to abnormalities in T cell migration and activation that could contribute to viral pathogenesis.