HIV entry into host cells is a complex process initiated by the interaction of the viral envelope glycoprotein gp120 with specific receptors on the surface of the target cell. This interaction primarily involves the CD4 receptor, a protein found on immune cells like T helper cells. Following CD4 binding, gp120 undergoes conformational changes that allow it to interact with a co-receptor, typically CCR5 or CXCR4. This crucial co-receptor binding event triggers further changes in the viral envelope, ultimately facilitating fusion between the viral and cellular membranes. The virus then releases its genetic material into the host cell.
Understanding the precise molecular mechanisms governing this viral entry process is paramount for developing effective antiviral therapies. By targeting the specific interactions between viral and cellular proteins, researchers can design drugs that block HIV entry and prevent infection. The discovery of co-receptors and their role in HIV entry was a major breakthrough in HIV research, opening new avenues for drug development. Current antiretroviral therapies include entry inhibitors that specifically target these interactions, significantly improving the prognosis for individuals living with HIV.
