Propranolol Decreases Proliferation of Endothelial Cells Transformed by Kaposi's Sarcoma-Associated Herpesvirus and Induces Lytic Viral Gene Expression
Author(s) -
Shane C. McAllister,
Ryan S. Hanson,
Rory D. Manion
Publication year - 2015
Publication title -
journal of virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.617
H-Index - 292
eISSN - 1070-6321
pISSN - 0022-538X
DOI - 10.1128/jvi.01569-15
Subject(s) - biology , downregulation and upregulation , propranolol , cyclin dependent kinase 6 , cancer research , lytic cycle , kaposi's sarcoma associated herpesvirus , virology , sarcoma , cyclin dependent kinase , immunology , cell cycle , virus , gene , herpesviridae , endocrinology , viral disease , medicine , genetics , pathology
Kaposi's sarcoma (KS) is common in Africa, but economic constraints hinder successful treatment in most patients. Propranolol, a generic β-adrenergic antagonist, decreased proliferation of KS-associated herpesvirus (KSHV)-infected cells. Downregulation of cyclin A2 and cyclin-dependent kinase 1 (CDK1) recapitulated this phenotype. Additionally, propranolol induced lytic gene expression in association with downregulation of CDK6. Thus, propranolol has diverse effects on KSHV-infected cells, and this generic drug has potential as a therapeutic agent for KS.
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