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Brief Report: CD14brightCD16- monocytes and sCD14 level negatively associate with CD4-memory T-cell frequency and
Chelsey J Judge1, Johan K Sandberg, Nicholas T Funderburg
1*Department of Pathology, The Cleveland VA Medical Center, Case Western Reserve University, Cleveland, OH; †Center for Infection Medicine, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden; ‡School of Health and Rehabilitation Sciences, Division of Medical Laboratory Science, The Ohio State University, Columbus, OH; §University of Cincinnati Medical Center, Cincinnati, OH; ‖Weill Cornell Medical College, New York, NY; ¶Hamd Healthcare Quality Institute and Hamad Medical Corporation, Doha, Qatar; #Harvard T.H. Chan School of Public Health, Boston, MA, USA **Rush University Medical Center, Chicago, IL; and ††Department of Medicine, University Hospitals Case Medical Center, and the Center for AIDS Research, Cleveland, OH.
Abstract:
During HIV+ hepatitis C virus (HCV)+ coinfection CD14CD16 monocytes produce soluble immune-activation markers that predict disease progression and poor response to interferon (IFN)-α treatment. We evaluated relationships among immune activation, monocyte phenotype, CD4-memory T cells, and HCV-, cytomegalovirus-, and cytomegalovirus/Epstein-Barr virus/influenza-specific IFN-γ-response before and during IFN-α treatment. Effector-memory and central-memory CD4 T-cell frequencies were lower in HCV+ HIV+ donors than in uninfected donors and correlated negatively with HCV level, CD14CD16 monocytes, and plasma sCD14. sCD14 and CD14CD16 monocytes negatively correlated with IFN-α-dependent HCV decline. CD4 effector-memory T cells positively associated with cytomegalovirus/Epstein-Barr virus/influenza(CEF)-specific IFN-γ response, while sCD14 negatively associated with both CD4 effector-memory T cells and CEF-specific IFN-γ response. These data support a role for memory-CD4 T cells in HCV containment and link immune activation and CD14CD16-monocyte frequency to the failure of IFN-dependent HCV clearance.
