Biological effects of HIV‐1 glycoprotein gp120's interaction with CD4+ T cells

Abstract

HIV (human immunodeficiency virus) access to CD4+ T cells depends on the interaction of gp120 (viral envelope glycoprotein) with CD4+ receptor molecules on the targeted cells. Gp120 projects from the surface of HIV like small spikes and is the only extracellular protein on the virus envelope. The contact made between CD4+ T cells and gp120 is essential for virus interaction, but it also can mediate other effects, such as apoptosis or activation of T cells. In our study, we evaluated whether HIV‐1 glycoprotein interaction with CD4+T cells leads to apoptosis or activation of T cells. To do this, we allowed CD4+ T cells to interact with gp120/ICAM‐1 on filter of transwells and analyzed the cells migrating through the wells after interaction with gp120 + ICAM‐1 or ICAM‐1 alone. The data shows: gp120 temporarily stops the CD4+ T cells from migrating, and then resumes migration after one hour, the cells interaction with gp120 + ICAM‐1 did not display any change in expression of apoptosis markers and with stimulation of gp120, CD4+ T cells could still proliferate in response to IL‐2 and allogenic stimulation. These data indicate that the CD4‐‐gp120 interaction, on its own, is not likely to make CD4+ T cells more susceptible to apoptosis. Rather, this interaction may activate the cells to support HIV‐1 infection more efficiently.