Disruption of the Actin Cytoskeleton Can Complement the Ability of Nef To Enhance Human Immunodeficiency Virus Type 1 Infectivity

• Edward M. Campbell

  Department of Microbiology and Immunology

• Rafael Nunez

  Department of Medicine, University of Illinois at Chicago, Chicago, Illinois 60612

• Thomas J. Hope

  Department of Microbiology and Immunology

抄録

The human immunodeficiency virus (HIV) protein Nef has been shown to increase the infectivity of HIV at an early point during infection. Since Nef is known to interact with proteins involved in actin cytoskeleton rearrangements, we tested the possibility that Nef may enhance HIV infectivity via a mechanism that involves the actin cytoskeleton. We find that disruption of the actin cytoskeleton complements the Nef infectivity defect. The ability of disruption of the actin cytoskeleton to complement the Nef defect was specific to envelopes that fuse at the cell surface, including a variety of HIV envelopes and the murine leukemia virus amphotropic envelope. In contrast, the infectivity of HIV virions pseudotyped to enter cells via endocytosis, which is known to complement the HIV Nef infectivity defect and can naturally penetrate the cortical actin barrier, was not altered by actin cytoskeleton disruption. The results presented here suggest that Nef functions to allow the HIV genome to penetrate the cortical actin network, a known barrier for intracellular parasitic organisms.

収録刊行物

• Journal of Virology

  Journal of Virology 78 (11), 5745-5755, 2004-06

  American Society for Microbiology

キーワード

• Virology
• Insect Science
• Immunology
• Microbiology

詳細情報

• CRID: 1361137044117763200
• NII論文ID: 30020800009
• DOI: 10.1128/jvi.78.11.5745-5755.2004
• ISSN: 10985514
• ISSN: 0022538X
• Web Site: https://journals.asm.org/doi/pdf/10.1128/JVI.78.11.5745-5755.2004
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