• CXCR4-Tropic, But Not CCR5-Tropic, Human Immunodeficiency Virus Infection Is Inhibited by the Lipid Raft-Associated Factors, Acyclic Retinoid Analogs, and Cholera Toxin B Subunit

Kamiyama, Haruka

Kakoki, Katsura

Shigematsu, Sayuri

Izumida, Mai

Yashima, Yuka

Tanaka, Yuetsu

Hayashi, Hideki

Matsuyama, Toshifumi

Sato, Hironori

Yamamoto, Naoki

Sano, Tetsuro

Shidoji, Yoshihiro

Kubo, Yoshinao

    • This is a copy of an article published in the AIDS Research and Human Retroviruses © 2013 Mary Ann Liebert, Inc.; AIDS Research and Human Retroviruses is available online at:
  • Other chemokine receptor CCR5
  • Other chemokine receptor CXCR4
  • Other cholera toxin B subunit
  • Other geranylgeranoic acid
  • Other peretinoin
  • Other retinoid derivative
  • Other transactivator protein
  • Other unclassified drug
  • Other virus envelope protein
  • Other virus vector
  • Other antiviral therapy
  • Other article
  • Other cell viability
  • Other controlled study
  • Other human
  • Other human cell
  • Other Human immunodeficiency virus 1 infection
  • Other lipid raft
  • Other membrane fusion
  • Other nonhuman
  • Other priority journal
  • Other protein depletion
  • Other protein expression
  • Other target cell
  • Other viral tropism
  • Other virus particle
  • Other virus strain
  • Development of an effective low-cost anti-acquired immunodeficiency syndrome (AIDS) drugs is needed for treatment of AIDS patients in developing countries. Host cell lipid raft microdomains, which are enriched with cholesterol, glycolipids, ceramide, and gangliosides, are important for human immunodeficiency virus type 1 (HIV-1) entry. Retinoid analogs have been shown to modulate ceramide levels in the cell membrane, while cholera toxin B subunit (CT-B) specifically binds to the ganglioside GM1. In this study, we found that the acyclic retinoid analogs geranylgeranoic acid (GGA) and NIK-333 as well as CT-B efficiently attenuate CXCR4-tropic, but not CCR5-tropic, HIV-1 vector infection. We also found that GGA and NIK-333 suppress CXCR4-tropic HIV-1 infection by attenuating CXCR4 expression. CT-B also attenuated CXCR4-tropic HIV-1 infection, but did not suppress CXCR4 expression. These results suggest a distinct role for lipid raft microdomains in CXCR4- and CCR5-tropic HIV-1 infections and illuminate novel agents for the development of AIDS therapy.
  • identifier:AIDS Research and Human Retroviruses, 29(2), pp.279-288; 2013
  • identifier:19318405
PublisherMary Ann Liebert Inc.
Date Issued 2013-01-21
NIItypejournal article
Identifier URI
  • isIdenticalTo DOI
    • ISSN 0889-2229
    • AIDS Research and Human Retroviruses
    29(2), 279-288