Influence of membrane fluidity on human immunodeficiency virus type 1 entry

Journal Article · Fri Apr 08 04:00:00 EDT 2005 · Biochemical and Biophysical Research Communications

DOI:https://doi.org/10.1016/j.bbrc.2005.02.007· OSTI ID:20630918

Harada, Shinji ^[1]; Yusa, Keisuke ^[1]; Monde, Kazuaki ^[1]; Akaike, Takaaki ^[2]; Maeda, Yosuke ^[1]

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1. Department of Medical Virology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556 (Japan)
2. Department of Microbiology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556 (Japan)

For penetration of human immunodeficiency virus type 1 (HIV-1), formation of fusion-pores might be required for accumulating critical numbers of fusion-activated gp41, followed by multiple-site binding of gp120 with receptors, with the help of fluidization of the plasma membrane and viral envelope. Correlation between HIV-1 infectivity and fluidity was observed by treatment of fluidity-modulators, indicating that infectivity was dependent on fluidity. A 5% decrease in fluidity suppressed the HIV-1 infectivity by 56%. Contrarily, a 5% increase in fluidity augmented the infectivity by 2.4-fold. An increased temperature of 40 deg C or treatment of 0.2% xylocaine after viral adsorption at room temperature enhanced the infectivity by 2.6- and 1.5-fold, respectively. These were inhibited by anti-CXCR4 peptide, implying that multiple-site binding was accelerated at 40 deg C or by xylocaine. Thus, fluidity of both the plasma membrane and viral envelope was required to form the fusion-pore and to complete the entry of HIV-1.

• OSTI ID: 20630918
• Journal Information: Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 2 Vol. 329; ISSN BBRCA9; ISSN 0006-291X
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
AIDS VIRUS
FLUIDIZATION
INFECTIVITY
MEMBRANES
PEPTIDES
RECEPTORS