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Journal of Virology, December 1999, p. 10020-10028, Vol. 73, No. 12
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Species-Specific, Postentry Barriers to Primate Immunodeficiency Virus Infection

Wolfgang Hofmann,1 David Schubert,1 Jason LaBonte,1 Linda Munson,2 Susan Gibson,3 Jonathan Scammell,4 Paul Ferrigno,5 and Joseph Sodroski1,6,7,*

Department of Cancer Immunology and AIDS1 and Department of Cancer Biology,5 Dana-Farber Cancer Institute, Department of Pathology, Harvard Medical School,6 and Department of Immunology and Infectious Diseases, Harvard School of Public Health,7 Boston, Massachusetts 02115; Department of Veterinary Medicine-PMI, University of California, Davis, California 956162; and College of Medicine3 and Department of Pharmacology,4 University of South Alabama, Mobile, Alabama 36688

Received 6 July 1999/Accepted 26 August 1999

By using replication-defective vectors derived from human immunodeficiency virus type 1 (HIV-1), simian immunodeficiency virus (SIVmac), and murine leukemia virus (MuLV), all of which were pseudotyped with the vesicular stomatitis virus (VSV) G glycoprotein, the efficiency of postentry, early infection events was examined in target cells of several mammalian species. Titers of HIV-1 vectors were significantly lower than those of SIVmac and MuLV vectors in most cell lines and primary cells from Old World monkeys. By contrast, most New World monkey cells exhibited much lower titers for the SIVmac vector compared with those of the HIV-1 vector. Prosimian cells were resistant to both HIV-1 and SIVmac vectors, although the MuLV vector was able to infect these cells. Cells from other mammalian species were roughly equivalent in susceptibility to the three vectors, with the exception of rabbit cells, which were specifically resistant to the HIV-1 vector. The level of HIV-1 vector expression was very low in transduced cells of rodent, rabbit, cow, and pig origin. Early postentry restriction of primate immunodeficiency virus infection exhibits patterns largely coincident with species borders and applies to diverse cell types within an individual host, suggesting the involvement of species-specific, widely expressed cellular factors.

* Corresponding author. Mailing address: Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, 44 Binney St., JFB 824, Boston, MA 02115. Phone: (617) 632-3371. Fax: (617) 632-4338. E-mail: joseph_sodroski{at}dfci.harvard.edu.

Journal of Virology, December 1999, p. 10020-10028, Vol. 73, No. 12
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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