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Influence of membrane fluidity on human immunodeficiency virus type 1 entry.

Harada S, Yusa K, Monde K, Akaike T, Maeda Y

Department of Medical Virology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556, Japan. biodef@gpo.kumamoto-u.ac.jp

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 degrees 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 degrees 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.

Published 1 March 2005 in Biochem Biophys Res Commun, 329(2): 480-6.
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