As a result of this experiment, conclusions have been made about viral binding.  The viral membrane and the target cell membrane fuse together due to the recognition by the surface proteins of HIV.  GP120 functions in the positioning and timing of this fusion.  If this fusion can be interrupted at the level of gp120, then perhaps infection can be stopped or inhibited.

    The virus enters the cell by first binding to the cellular receptor CD4.  This binding is initiated by D1D2-a portion of CD4 in the ternary complex.  Once CD4 and gp120 are bound, gp120 undergoes conformational changes.  The gp120 surface is oriented by the movement of sequenced structures which expose the binding site itself.  The next step of entry involves the gp120-CD4 complex with the chemokine receptor.  With this binding, the gp120 moves close to the chemokine receptor in the host membrane.  CD4 is very flexible to promote HIV entry.  This receptor induces changes that cause exposure of the gp41 ectodomain.  Thus, the HIV virus invades a human cell and causes infection.

Implications of this experiment

     Although the isolation and crystallization of the gp120-CD4 complex is a milestone for HIV research, there is still much work to be done.  With further research of this nature, we can learn even more about the initial interactions between HIV and the human lymphocyte cells.  The more we learn about these interactions, the closer researchers will come to developing some type drug to prevent infection.  In this case the ultimate goal is to discover some type of chemical that will bind to gp120 and keep it from binding to CD4.  However, as there is currently no cure for AIDS, and the drugs to ease the disease's symptoms tend to be quite expensive, it is crucial that each and every person be properly educated about AIDS prevention.

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 Group 2
The Biology Project
University of Arizona
Tucson, AZ. 85719