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Entry Inhibitors: A New Class of HIV Medications

October 2003

This material was developed independently through an unrestricted educational grant from Trimeris.

How Does HIV Enter Our Cells?
To damage the immune system, HIV must first get inside your CD4 cells, which are responsible for fighting off diseases inside your body. After HIV enters your CD4 cells, it uses several enzymes to turn the cells into factories that produce more HIV. Two of the key enzymes that HIV uses once it gets inside a CD4 cell are the reverse transcriptase and protease enzymes, which have been the focus of the first three available classes of HIV medications.

Researchers have figured out several of the critical steps that HIV follows to get inside CD4 cells. This has been broken down into a few stages. Here's a play-by-play look at what happens:

  • First, HIV attaches to a CD4 receptor.
  • Then HIV attaches to a "co-receptor."
  • After this dual attachment (to CD4 and then to a co-receptor), HIV inserts a harpoon-like anchor called a glycoprotein into the CD4 cell wall.
  • Then HIV "zips" together the two ends of this glycoprotein (one end is in the CD4 cell; the other end is still attached to the virus). This action allows HIV to literally pull itself close enough to the CD4 cell wall so it can actually fuse with the CD4 cell.
  • To complete this step of connection (or fusion), an opening is created in the CD4 cell, and -- through a process scientists still do not completely understand -- HIV inserts its viral RNA into the CD4 cell. This allows HIV to begin the process of completely taking over the CD4 cell.

The goal of Fuzeon, the first entry inhibitor to be approved in the U.S., is to prevent HIV from entering CD4 cells by stopping it from "zipping" together the two ends of the glycoprotein.

Now HIV can be targeted both inside and outside the CD4 Cell

Previous | Next: How Does Fuzeon Work?




  
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