of helper T-cell killing. Many scientists believe that the host cell is worn down from reproducing so many virus particles and releasing them to the environment. Eventually the host cell simply dies. Added to this very direct interaction is a wealth of indirect interactions between pathogen and host.
One theory that has received much attention concerns the role of the lollipop-shaped glycoproteins. Gp120, the candy part of the lollipop-shaped gp160 complex, sticks out of the surface of the virus and facilitates viral binding to the CD4 receptor on host T-helper cells and macrophages. Fragments of these and other viral proteins are displayed by the host cell on its surface. The foreign peptide sticking out of the infected host cell serves as a red flag to the immune system, alerting the immune cells that a host cell has been invaded by a foreign pathogen. The infected cell is now targeted for destruction by the killer T-cells.
But the killing might not stop there. Research has shown that infected cells shed gp120 molecules. These free-floating molecules can be captured by uninfected helper T-cells. In some cases the healthy helper T-cell may display the shed gp120 molecules on its surface, so now it looks to the immune system just like an infected cell. Even though the healthy cell has no virus inside it, it becomes a target for immune destruction and is eliminated by killer T-cells as though it were infected. Such a mechanism would raise the number of helper cells killed without necessarily increasing the number of cells infected.
Shedding of molecules is not the only indirect effect of HIV infection. The gp120 molecules sticking out of an infected cell may also have direct contact with other uninfected cells. Since gp120 can bind to CD4 molecules, it is possible that infected cells actually bind to and fuse with uninfected cells via the gp120-CD4 interaction. The result of this fusion is the formation of giant masses of infected and uninfected cells in what is technically called a syncytium. Syncytia have been observed in the test tube when infected and uninfected cells are mixed together. Some scientists believe that syncytia may form in people with AIDS as well, but no such syncytium has ever been isolated from an AIDS patient. Other scientists interpret this discrepancy to mean that syncytia are only a test tube phenomenon but that it might hint at some other harmful interaction between infected and uninfected cells in the HIV seropositive individual.
Gp120 is not the only molecule that can pass from infected to uninfected cells. The Tat protein also may diffuse from cell to cell. If that is the case, scientists have identified several potential consequences. For one thing Tat is a potent activator of viral gene expression, so it is