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Journal of Virology, February 2004, p. 1464-1472, Vol. 78, No. 3
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.3.1464-1472.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Dysregulation of the Polo-Like Kinase Pathway in CD4+ T Cells Is Characteristic of Pathogenic Simian Immunodeficiency Virus Infection

Pavel Bostik,* Geraldine L. Dodd, Francois Villinger, Ann E. Mayne, and Aftab A. Ansari

Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, Georgia 30322

Received 13 February 2003/ Accepted 21 October 2003

CD4+ T-cell dysfunction highlighted by defects within the intracellular signaling cascade and cell cycle has long been characterized as a direct and/or indirect consequence of human immunodeficiency virus (HIV) infection in humans and simian immunodeficiency virus (SIV) infection in rhesus macaques (RM). Dysregulation of the M phase of the cell cycle is a well-documented effect of HIV or SIV infection both in vivo and in vitro. In this study the effect of SIV infection on the modulation of two important regulators of the M phase—polo-like kinases Plk3 and Plk1—was investigated. We have previously shown that Plk3 is markedly downregulated in CD4+ T cells from SIV-infected disease-susceptible RM but not SIV-infected disease-resistant sooty mangabeys (SM), denoting an association of downregulation with disease progression. Here we show that, in addition to the downregulation, Plk3 exhibits aberrant activation patterns in the CD4+ T cells from SIV-infected RM following T-cell receptor stimulation. Interestingly, in vitro SIV infection of CD4+ T cells leads to the upregulation, rather than downregulation, of Plk3, suggesting that different mechanisms operate in vitro and in vivo. In addition, CD4+ T cells from RM with high viral loads exhibited consistent and significant upregulation of Plk1, concurrent with an aberrant activation-induced Plk1 response, suggesting complex mechanisms of SIV-induced M-phase abnormalities in vivo. Altogether this study presents a novel mechanism underlying M-phase defects observed in CD4+ T cells from HIV or SIV-infected disease-susceptible humans and RM which may contribute to aberrant T-cell responses and disease pathogenesis.

* Corresponding author. Mailing address: Department of Pathology and Laboratory Medicine, Emory University, WMB Room 2337A, 1639 Pierce Dr., Atlanta, GA 30322. Phone: (404) 712-2835. Fax: (404) 712-1771. E-mail: pbostik{at}emory.edu.

Journal of Virology, February 2004, p. 1464-1472, Vol. 78, No. 3
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.3.1464-1472.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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