equipped to recognize that particular pathogen. The B-cells respond by secreting antibodies into the blood to help remove any circulating pathogen, and the killer cells destroy any host cells infected by the pathogen.

In an HIV infection, however, this scenario becomes a little more ambiguous. The cell-to-cell contact between macrophage and helper cell that serves as such an effective alert system against most pathogens activates the immune response against HIV. At the same time, it spreads the virus to more host cells. The presenting macrophage has CD4 molecules on its surface, so more than likely the presenting macrophage is actually infected with the virus. And, as fate would have it, the helper T-cell also has CD4 molecules on its surface and is a prime target for HIV infection. Many scientists now believe that the presentation process has been subverted by the virus to become a means of infecting the helper T-cells. In other words, the macrophages help spread the virus from the skin lining the body's orifices to the T-cells circulating in the blood as well as to those in the spleen, lymph nodes, and other tissues. Without a doubt, the infection of a cell as important to immune functions as the helper T-cell can deal a profound blow to the integrity of the immune system. For that reason, immunologists, virologists, and molecular biologists have all contributed their expertise in deciphering the events that follow the initial contact between the virus and the CD4 molecule.


We have already seen that a virus is one of the most minimalist forms of life, if it can be considered living at all. Basically, it is a protein-wrapped package of genes that has no other purpose than to create more packages like itself. The information for this replication is contained entirely within the viral genes, the protein coating being nothing more than protective packaging. As such, the mission of the virus infecting a cell is to inject its genes inside the cell. But the protein coat does not necessarily have to enter, and in the case of HIV some of that protein shell is left outside.

The specifics of this process, called uncoating, have not been worked out in their entirety for HIV. What is known, however, is that the glycoprotein gp120 on the surface of HIV contacts and binds to the CD4 receptor on the immune cell. Sometime afterwards the lipid membrane surrounding HIV fuses with the lipid membrane of the cell, an action that effectively opens the outer shell of the virus and juxtaposes the viral contents with the cell's interior. From that point it is an easy matter for

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