HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Zou, J. X. Articles by Luciw, P. A. Search for Related Content PubMed PubMed Citation Articles by Zou, J. X. Articles by Luciw, P. A. Agricola Articles by Zou, J. X. Articles by Luciw, P. A.

The requirement for Vif of SIVmac is cell-type dependent

Department of Medical Pathology, University of California, Davis, CA 95616, USA

The vif gene (viral infectivity factor) of the human and simian immunodeficiency viruses (HIV and SIV) is present in almost all members of the lentivirus group of retroviruses. This gene is highly conserved among different HIV and SIV isolates and is therefore presumed to play an important role in pathogenesis. To analyse the role of Vif in SIV, three SIVmac mutants have been constructed by introducing site-specific mutations or deletions into vif of the pathogenic molecular clone SIVmac239. The effect of Vif on viral replication in T cells was examined by transfecting equal amounts of either vif-positive or vif-negative viral DNA into SupT1, CEM-SS and H9 cells. Reverse transcriptase assay of supernatants from transfected cultures revealed that both SupT1 and CEM-SS cell lines supported replication of all three vif mutants to a level comparable to the parental vif-positive virus, whereas vif mutants did not replicate in H9 cells. Our results demonstrate that the requirement for Vif in SIVmac replication is cell-type dependent and that sequences near both the N and C termini are required for its function. Vif-defective SIVmac239, produced in transfected SupT1 and CEM-SS cells, failed to infect primary T lymphocytes, whereas both vif-positive and vif-defective viruses established productive infection in CEMx174 cells. These findings in primary cells suggest that Vif plays an important role in viral replication in vivo.

^* Author for correspondence. Fax +1 916 752 4548.

Received 27 July 1995; accepted 14 November 1995.

This article has been cited by other articles:

				Y. Guan, J. B. Whitney, M. Detorio, and M. A. Wainberg Construction and In Vitro Properties of a Series of Attenuated Simian Immunodeficiency Viruses with All Accessory Genes Deleted J. Virol., May 1, 2001; 75(9): 4056 - 4067. [Abstract] [Full Text]

				S. M. White, M. Renda, N.-Y. Nam, E. Klimatcheva, Y. Zhu, J. Fisk, M. Halterman, B. J. Rimel, H. Federoff, S. Pandya, et al. Lentivirus Vectors Using Human and Simian Immunodeficiency Virus Elements J. Virol., April 1, 1999; 73(4): 2832 - 2840. [Abstract] [Full Text]