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Journal of Virology, March 2000, p. 2594-2602, Vol. 74, No. 6
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Partial Rescue of the Vif-Negative Phenotype of Mutant Human Immunodeficiency Virus Type 1 Strains from Nonpermissive Cells by Intravirion Reverse Transcription

Geethanjali Dornadula, Shicheng Yang, Roger J. Pomerantz, and Hui Zhang*

The Dorrance H. Hamilton Laboratories, Center for Human Virology, Division of Infectious Diseases, Department of Medicine, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania 19107

Received 10 September 1999/Accepted 8 December 1999

Virion infectivity factor (Vif) is a protein encoded by human immunodeficiency virus type I (HIV-1) and is essential for viral replication. It appears that Vif functions in the virus-producing cells and affects viral assembly. Viruses with defects in the vif gene (vif-) generated from the "nonpermissive cells" are not able to complete reverse transcription. In previous studies, it was demonstrated that defects in the vif gene also affect endogenous reverse transcription (ERT) when mild detergents were utilized to permeabilize the viral envelope. In this report, we demonstrate that defects in the vif gene have much less of an effect on ERT if detergent is not used. When ERT was driven by addition of deoxyribonucleoside triphosphates (dNTPs) at high concentrations, certain levels of plus-strand viral DNA could also be achieved. Interestingly, if vif- viruses, generated from nonpermissive cells and harboring large quantities of viral DNA generated by ERT, were allowed to infect permissive cells, they could partially bypass the block at intracellular reverse transcription, through which vif- viruses without dNTP treatment could not pass. Consequently, viral infectivity can be partially rescued from the vif- phenotype. Based on our observations, we suggest that vif defects may cause the reverse transcription complex (RT complex) to become sensitive to mild detergent treatments within HIV-1 virions and become unstable in the target cells, such that the process of reverse transcription cannot be efficiently supported. Further dissection of RT complexes of vif- viruses may be key to uncovering the molecular mechanism(s) of Vif in HIV-1 pathogenesis.

* Corresponding author. Mailing address: The Dorrance H. Hamilton Laboratories, Center for Human Virology, Division of Infectious Diseases, Department of Medicine, Jefferson Medical College, Thomas Jefferson University, 1020 Locust St., Suite 329, Philadelphia, PA 19107. Phone: (215) 503-0163. Fax: (215) 923-1956. E-mail: hui.zhang{at}mail.tju.edu.

Journal of Virology, March 2000, p. 2594-2602, Vol. 74, No. 6
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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