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The formation of a complex between CXCR4, CD4 and X4 HIV-1 envelope glycoprotein is inhibited in resistant to infection and fusion promonocytic U937 cells

  1. Author:
    Xiao, X.
    Norwood, D.
    Feng, Y.
    Moriuchi, H.
    Moriuchi, M.
    Earl, P.
    Broder, C. C.
    Fauci, A. S.
    Dimitrov, D. S.
    1. Year of Conference: 1999
  2. Conference Name: Conference on Retroviruses and Opportunistic Infections
    1. Pages: 166 (abstract no. 522)
  4. Type of Work: Meeting Abstract
  1. Abstract:

    We have previously reported that certain subclones of U937 cells (minus clones) do not support infection and fusion mediated by X4 HIV-1 strains (J. Virol., 71:9664). Based on our previous observation that gp120 from X4 HIV-1 strains forms a complex with CD4 and CXCR4 (Science, 274:602) we hypothesized that the mechanism of resistance to HIV-1 entry in these cells is caused by inhibition of the gp120-CD4-CXCR4 complex formation. Following incubation with oligomeric HIV-1 IIIB gp120 (gp140), CD4 was efficiently coimmunoprecipitated by anti-CXCR4 monoclonal antibodies (mAbs) from U937 cells which support HIV-1 entry and fusion (plus clones) but not from the minus cells. Similar concentrations of CXCR4 and CD4 at the surface of the minus and plus cells were detected by flow cytometry with the same anti-CXCR4 mAbs used in the coimmunoprecipitation and with anti-CD4 mAbs, respectively. However, the amount of immunoprecipitated 40-46 kDa CXCR4 in the minus cells was much smaller or undetectable compared to that in the plus cells and another higher molecular weight band was found in the minus but not in the plus cells. We propose that the resistance to HIV-1 entry in the U937 minus cells is due to the inability of CXCR4 expressed in these cells to form a complex with the HIV-1 envelope glycoprotein and CD4, and that a similar mechanism determines the resistance to X4 HIV-1 entry in macrophages.

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