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Herpes Simplex Inhibits the Capacity of Lymphoblastoid B Cell Lines to Stimulate CD4⁺ T Cells¹

Serge Barcy^2,* and Lawrence Corey^3,*,,

Departments of ^* Laboratory Medicine and Medicine, University of Washington, Seattle, WA 98195; and Program in Infectious Diseases, Fred Hutchinson Cancer Research Center, Seattle, WA 98109

HSV establish a lifelong persistent infection in their host even among immunocompetent persons. The viruses use a variety of immune evasion strategies, presumably to assist persistent replication in the human host. We have observed that infection of human B lymphoblastoid cells (B-LCL) by HSV resulted in a strong inhibition of their ability to induce CD4⁺ T cell clone proliferation and cytokine secretion. This inhibitory effect occurs in a variety of both HSV- and HIV-specific clones from three different patients. The inhibition is observed when the Ag is provided either as a soluble protein or as a synthetic peptide and is not associated with detectable down-modulation of the MHC class II molecules or costimulatory molecules. Expression of the HSV-1 unique sequence 1 gene (US1) is necessary and sufficient to induce this inhibition of APC function. US1 gene expression also made B-LCL less susceptible to CD4⁺ T cell-mediated lysis. These data indicate a novel immune evasion strategy by HSV-1 in which Ag-processing cells that become infected by HSV-1 are inhibited in their ability to induce subsequent CD4⁺ T cell activation.

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