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Modulation of HIV-1 Replication by a Novel RhoA Effector Activity¹

Liping Wang^*,, Hangchun Zhang^,§, Patricia A. Solski^,, Matthew J. Hart^¶, Channing J. Der^, and Lishan Su^2,*,

Departments of ^* Microbiology and Immunology and Pharmacology, Lineberger Comprehensive Cancer Center, School of Medicine, and ^§ Department of Epidemiology, School of Public Health, University of North Carolina, Chapel Hill, NC 27599; and ^¶ Onyx Pharmaceuticals, Richmond, CA 94806

The RhoA GTPase is involved in regulating actin cytoskeletal organization, gene expression, cell proliferation, and survival. We report here that p115-RhoGEF, a specific guanine nucleotide exchange factor (GEF) and activator of RhoA, modulates HIV-1 replication. Ectopic expression of p115-RhoGEF or G13, which activates p115-RhoGEF activity, leads to inhibition of HIV-1 replication. RhoA activation is required and the inhibition affects HIV-1 gene expression. The RhoA effector activity in inhibiting HIV-1 replication is genetically separable from its activities in transformation of NIH3T3 cells, activation of serum response factor, and actin stress fiber formation. These findings reveal that the RhoA signal transduction pathway regulates HIV-1 replication and suggest that RhoA inhibits HIV-1 replication via a novel effector activity.

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