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Journal of Virology, March 2000, p. 2594-2602, Vol. 74, No. 6
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
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
) 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.
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