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Institute of Human Anatomy, University of Ferrara, Via Fossato di Mortara 66, 44100 Ferrara [G. Z., D. M., M. M., P. B., S. C.], Italy, and Institute of Microbiology, University of Bologna, Via Massarenti 9, 40138 Bologna [D. G., M. L. P], Italy
2 To whom requests for reprints should be addressed, at Institute of Human Anatomy, University of Ferrara, Via Fossato di Mortara 66, 44100 Ferrara, Italy.
We report here that the tat gene product of human immunodeficiency virus type 1 was able to protect lymphoblastoid (Jurkat), epithelial (293) and neuronal (PC12) cell lines from apoptotic death induced by serum withdrawal. The rescue from apoptosis by Tat was reflected by an increased expression of Bcl-2 protein in tat-positive Jurkat cells with respect to mock-transfected Jurkat cells after 3-6 days of serum-free cultures. We propose that the ability of the regulatory human immunodeficiency virus type 1 Tat protein to suppress apoptosis might have important implications in understanding the pathogenesis of frequent neoplastic disorders observed in human immunodeficiency virus type 1-seropositive individuals.
1 This research was supported by the AIDS project of the Italian Ministry of Health; by CNR Grants ACRO and FATMA, and MURST 40 and 60%.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 7/22/93. Accepted 8/19/93.
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