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Journal of Virology, November 2004, p. 12041-12046, Vol. 78, No. 21
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.21.12041-12046.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Further Investigation of Simian Immunodeficiency Virus Vif Function in Human Cells

Nathan C. Gaddis,1 Ann M. Sheehy,1,2 K. Muneer Ahmad,2 Chad M. Swanson,1,2 Kate N. Bishop,2 Brigitte E. Beer,3 Preston A. Marx,4 Feng Gao,5 Frederic Bibollet-Ruche,6 Beatrice H. Hahn,6 and Michael H. Malim1,2*

Department of Microbiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania,1 Department of Infectious Diseases, Guy's, King's and St. Thomas' School of Medicine, King's College London, London, United Kingdom,2 Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland,3 National Primate Research Center, Tulane University Health Sciences Center, Covington, Louisiana,4 Department of Medicine, Duke University, Durham, North Carolina,5 Departments of Medicine and Microbiology, University of Alabama at Birmingham, Birmingham, Alabama6

Received 7 August 2003/ Accepted 27 July 2004

Primate lentivirus Vif proteins function by suppressing the antiviral activity of the cell-encoded apolipoprotein B mRNA-editing enzyme-catalytic polypeptide-like (APOBEC) proteins APOBEC3G and APOBEC3F. It has been hypothesized that species-specific susceptibilities of APOBEC proteins to Vif proteins may help govern the transmission of primate lentiviruses to new host species. Consistent with this view and with previous results, we report that the Vif proteins of several diverse simian immunodeficiency viruses (SIVs) that are not known to infect humans are not effective inhibitors of human APOBEC3G or APOBEC3F when assessed in transient-transfection experiments. Unexpectedly, this lack of SIV Vif function did not prevent the replication of two vif-deficient SIVs (SIVtan and SIVmnd1; isolated from tantalus monkeys and mandrills, respectively) in a human T-cell line, HUT78, that expresses both APOBEC 3G and APOBEC3F, a finding which demonstrates that some SIVs are partially resistant to the antiretroviral effects of these enzymes irrespective of Vif function. Additional virus replication studies also revealed that the Vif protein of SIVtan is, in fact, active in human T cells, as it substantially enhanced the replication of its cognate virus and human immunodeficiency virus type 1. In sum, we now consider it improbable that species-specific restrictions to SIV Vif function can explain the lack of human infection with certain SIVs. Instead, our data reveal that the species-specific modulation of Vif function is more complex than previously envisioned and that additional (as-yet-unidentified) viral or host factors may be involved in regulating this dynamic interaction between host and pathogen.

* Corresponding author. Mailing address: Department of Infectious Diseases, Guy's, King's and St. Thomas' School of Medicine, King's College London, 2nd Floor, New Guy's House, GKT Guy's Hospital, London SE1 9RT, United Kingdom. Phone: (44) 20 718 80149. Fax: (44) 20 718 80147. E-mail: michael.malim{at}kcl.ac.uk.

Journal of Virology, November 2004, p. 12041-12046, Vol. 78, No. 21
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.21.12041-12046.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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