2. Academic Validation
  3. Inhibition of HIV-1 entry by the tricyclic coumarin GUT-70 through the modification of membrane fluidity

Inhibition of HIV-1 entry by the tricyclic coumarin GUT-70 through the modification of membrane fluidity

  • Biochem Biophys Res Commun. 2015 Feb 13;457(3):288-94. doi: 10.1016/j.bbrc.2014.12.102.
Kouki Matsuda 1,  Shinichiro Hattori 1,  Ryusho Kariya 1,  Yuji Komizu 2,  Eriko Kudo 1,  Hiroki Goto 1,  Manabu Taura 1,  Ryuichi Ueoka 2,  Shinya Kimura 3,  Seiji Okada 4
Affiliations

Affiliations

  • 1 Division of Hematopoiesis, Center for AIDS Research, Kumamoto University, 2-2-1 Honjo, Chuo-ku, Kumamoto 860-0811, Japan.
  • 2 Division of Applied Life Science, Graduate School of Engineering, Sojo University, 4-22-1 Ikeda, Nishi-ku, Kumamoto 860-0082, Japan.
  • 3 Division of Hematology, Respiratory Medicine and Oncology, Department of Internal Medicine, Faculty of Medicine, Saga University, 5-1-1 Nabeshima, Saga 849-8501, Japan.
  • 4 Division of Hematopoiesis, Center for AIDS Research, Kumamoto University, 2-2-1 Honjo, Chuo-ku, Kumamoto 860-0811, Japan. Electronic address: okadas@kumamoto-u.ac.jp.
PMID: 25576356 DOI: 10.1016/j.bbrc.2014.12.102
Abstract

Membrane fusion between host cells and HIV-1 is the initial step in HIV-1 Infection, and plasma membrane fluidity strongly influences infectivity. In the present study, we demonstrated that GUT-70, a natural product derived from Calophyllum brasiliense, stabilized plasma membrane fluidity, inhibited HIV-1 entry, and down-regulated the expression of CD4, CCR5, and CXCR4. Since GUT-70 also had an inhibitory effect on viral replication through the inhibition of NF-κB, it is expected to be used as a dual functional and viral mutation resistant reagent. Thus, these unique properties of GUT-70 enable the development of novel therapeutic agents against HIV-1 Infection.

Keywords

Cell fusion; GUT-70; HIV-1 infection; Membrane fluidity; Viral entry.

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