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Journal of Virology, February 2007, p. 1534-1536, Vol. 81, No. 3
0022-538X/07/$08.00+0     doi:10.1128/JVI.02099-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Selective Restriction of Nef-Defective Human Immunodeficiency Virus Type 1 by a Proteasome-Dependent Mechanism{triangledown}

Mingli Qi and Christopher Aiken*

Department of Microbiology and Immunology, Vanderbilt University School of Medicine, A-5301 Medical Center North, Nashville, Tennessee 37232-2363

Received 25 September 2006/ Accepted 5 November 2006

The Nef protein enhances human immunodeficiency virus type 1 (HIV-1) infectivity by facilitating an early postentry step in the virus life cycle. We report here that the addition of MG132 or lactacystin, each a specific inhibitor of cellular proteasome activity, preferentially enhances cellular permissiveness to infection by Nef-defective versus wild-type HIV-1. Pseudotyping by the glycoprotein of vesicular stomatitis virus rendered Nef-defective HIV-1 particles minimally responsive to the enhancing effects of proteasome inhibitors. These results suggest that Nef enhances the infectivity of HIV-1 particles by reducing their susceptibility to proteasomal degradation in target cells.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232-2363. Phone: (615) 343-7037. Fax: (615) 343-7392. E-mail: chris.aiken{at}vanderbilt.edu.

{triangledown} Published ahead of print on 15 November 2006.

Journal of Virology, February 2007, p. 1534-1536, Vol. 81, No. 3
0022-538X/07/$08.00+0     doi:10.1128/JVI.02099-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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