Human immunodeficiency virus type 1 attachment, coreceptor, and fusion inhibitors are active against both direct and trans infection of primary cells.

Abstract

Inhibitors of human immunodeficiency virus type 1 attachment (CD4-immunoglobulin G subclass 2), CCR5 usage (PRO 140), and fusion (T-20) were tested on diverse primary cell types that represent the major targets both for infection in vivo and for the inhibition of trans infection of target cells by virus bound to dendritic cells. Although minor cell-type-dependent differences in potency were observed, each inhibitor was active on each cell type and trans infection was similarly vulnerable to inhibition at each stage of the fusion cascade.

• Authors: Thomas J Ketas, Ines Frank, Per Johan Klasse, Brian M Sullivan, Jason P Gardner, Catherine Spenlehauer, Mirjana Nesin, William C Olson, John P Moore, Melissa Pope
• Journal: Journal of virology (J Virol) Vol. 77 Issue 4 Pg. 2762-7 (Feb 2003) ISSN: 0022-538X [Print] United States
• PMID: 12552019 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Anti-HIV Agents
• CD4 Immunoadhesins
• CD4-IgG(2)
• Chemokine CCL5
• HIV Envelope Protein gp41
• Peptide Fragments
• Receptors, HIV
• Enfuvirtide

Topics

• Anti-HIV Agents (pharmacology)
• CD4 Immunoadhesins (pharmacology)
• Chemokine CCL5 (pharmacology)
• Dendritic Cells (virology)
• Enfuvirtide
• Fetal Blood (virology)
• HIV Envelope Protein gp41 (pharmacology)
• HIV-1 (drug effects, metabolism, pathogenicity, physiology)
• Humans
• Leukocytes, Mononuclear (virology)
• Macrophages (virology)
• Membrane Fusion (drug effects)
• Peptide Fragments (pharmacology)
• Receptors, HIV (drug effects)