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The bis-azo compound FP-21399 inhibits HIV-1 replication by preventing viral entry

Academic Article
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Overview

authors

  • Zhang, J. L.
  • Choe, Hyeryun
  • Dezube, B. J.
  • Farzan, Michael
  • Sharma, P. L.
  • Zhou, X. C.
  • Chen, L. B.
  • Ono, M.
  • Gillies, S.
  • Wu, Y. M.
  • Sodroski, J. G.
  • Crumpacker, C. S.

publication date

  • 1998

journal

  • Virology  Journal

abstract

  • The bis-azo compound FP-21399 inhibits HIV-1 infection. We now show that FP-21399 acts on the HIV-1 envelope glycoprotein to prevent viral replication. This compound targets the entry step of the HIV-1 replication cycle as demonstrated by time-of-addition and single cycle viral entry assays. The entry of SIVmac239, which uses the same coreceptors (CD4/CCR5) as HIV-1, was not inhibited by FP-21399, indicating that the antiviral effect of FP-21399 is specific for the HIV-1 envelope glycoprotein and is not dependent upon the cellular receptors CD4 and CCR5. FP-21399 inhibits neither the activity of HIV-1 reverse transcriptase nor the expression of HIV-1 early mRNA. Finally, this compound inhibits gp120 shedding of the T-tropic virus. Our results suggest that the anti-HIV activity of FP-21399 is due to its interaction with HIV-1 gp120/41 complex during viral entry.

subject areas

  • Animals
  • Anti-HIV Agents
  • Base Sequence
  • Chlorobenzenes
  • DNA Primers
  • Gene Expression
  • HIV Envelope Protein gp120
  • HIV Envelope Protein gp41
  • HIV Infections
  • HIV-1
  • Humans
  • In Vitro Techniques
  • Leukocytes, Mononuclear
  • Membrane Fusion
  • Naphthalenes
  • RNA, Messenger
  • RNA, Viral
  • Receptors, CCR5
  • Receptors, CXCR4
  • Simian Acquired Immunodeficiency Syndrome
  • Simian Immunodeficiency Virus
  • Virus Replication
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Identity

International Standard Serial Number (ISSN)

  • 0042-6822

Digital Object Identifier (DOI)

  • 10.1006/viro.1998.9115

PubMed ID

  • 9601521
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Additional Document Info

start page

  • 530

end page

  • 541

volume

  • 244

issue

  • 2

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