Influence of membrane fluidity on human immunodeficiency virus type 1 entry.
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.
Harada
Shinji
S
Department of Medical Virology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556, Japan. biodef@gpo.kumamoto-u.ac.jp
Yusa
Keisuke
K
Monde
Kazuaki
K
Akaike
Takaaki
T
Maeda
Yosuke
Y
D002213:Capsid / Q000378:metabolism*; D015497:HIV-1 / Q000472:pathogenicity / Q000502:physiology*; D006801:Humans; D007938:Leukemia / Q000821:virology*; D008560:Membrane Fluidity / Q000502:physiology*; D008561:Membrane Fusion / Q000502:physiology*; D019718:Receptors, CXCR4 / Q000378:metabolism*; D013696:Temperature; D014407:Tumor Cells, Cultured
D019718:Receptors, CXCR4