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The lectins griffithsin, cyanovirin-N and scytovirin inhibit HIV-1 binding to the DC-SIGN receptor and transfer to CD4(+) cells

  1. Author:
    Alexandre, K. B.
    Gray, E. S.
    Mufhandu, H.
    McMahon, J. B.
    Chakauya, E.
    O'Keefe, B. R.
    Chikwamba, R.
    Morris, L.

  2. Author Address

    [Alexandre, Kabamba B.; Gray, Elin S.; Morris, Lynn] Natl Inst Communicable Dis, ZA-2131 Johannesburg, South Africa. [Mufhandu, Hazel; Chakauya, Ereck; Chikwamba, Rachel] CSIR, Pretoria, South Africa. [McMahon, James B.; O'Keefe, Barry R.] NCI Frederick, Mol Targets Lab, Ctr Canc Res, Frederick, MD USA.;Morris, L (reprint author), Natl Inst Communicable Dis, Private Bag X4, ZA-2131 Johannesburg, South Africa;lynnm@nicd.ac.za
    1. Year: 2012
    2. Date: Feb
  2. Journal: Virology
    1. 423
    2. 2
    3. Pages: 175-186
  4. Type of Article: Article
  5. ISSN: 0042-6822
  1. Abstract:

    It is generally believed that during the sexual transmission of HIV-1, the glycan-specific DC-SIGN receptor binds the virus and mediates its transfer to CD4(+) cells. The lectins griffithsin (GRFT), cyanovirin-N (CV-N) and scytovirin (SVN) inhibit HIV-1 infection by binding to mannose-rich glycans on gp120. We measured the ability of these lectins to inhibit both the HIV-1 binding to DC-SIGN and the DC-SIGN-mediated HIV-1 infection of CD4(+) cells. While GRFT, CV-N and SVN were moderately inhibitory to DC-SIGN binding, they potently inhibited DC-SIGN-transfer of HIV-1. The introduction of the 234 glycosylation site abolished HIV-1 sensitivity to lectin inhibition of binding to DC-SIGN and virus transfer to susceptible cells. However, the addition of the 295 glycosylation site increased the inhibition of transfer. Our data suggest that GRFT. CV-N and SVN can block two important stages of the sexual transmission of HIV-1, DC-SIGN binding and transfer, supporting their further development as microbicides. (C) 2011 Elsevier Inc. All rights reserved.

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External Sources

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  2. DOI: 10.1016/j.virol.2011.12.001
  3. View record in Web of Science®
  4. WOS: 000299803300008

Library Notes

  1. Fiscal Year: FY2011-2012
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