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Summary
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During the M-tropic phase of HIV infection, the virus
favors macrophages, which it invades by binding (through its gp120
protein) to the molecules CD4 and CCR5 on the macrophage surface.
Eventually, however, HIV-1 can become dual-tropic. Such strains
produce gp120 molecules capable of recognizing the CXCR4 protein on
CD4-bearing T-cells. During this phase HIV-1 may infect both macrophages
and T-cells. Still later, the bulk of the viral population may switch it's
preference to the CXCR4 receptor and become T-tropic. T-tropic
viruses readily destroy infected T-cells, contributing to the collapse of
the immune system and the onset of AIDS. Alternatively, some
viruses, such as certain strains of HIV-2 could attach to CXCR4 quickly
leading to AIDS.
Interactions
Between HIV-1 and the Cell Surface
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| HIV-1 interacts with
a cell-surface receptor, primarily CD4, and through conformational
changes becomes more closely associated with the cell through
interactions with other cell-surface molecules, such as the
chemokine receptors CXCR4 and CCR5. The likely steps in HIV
infection are as follows: |
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The CD4-binding site
on HIV-1 gp120 interacts with the CD4 molecule on the cell surface. |
| Conformational
changes in both the viral envelope and the CD4 receptor permit the
binding of gp120 to another cell-surface receptor, such as CCR5. |
 |
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This second
attachment brings the viral envelope closer to the cell surface,
allowing interaction between gp41 on the viral envelope and a fusion
domain on the cell surface. HIV then fuses with the cell. |
| Subsequently, the
viral nucleoid enters into the cell, most likely by means of other
cellular events. Once this stage is achieved, the cycle of
viral replication begins. |
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Illustrations
and content based on "Infection by Human Immunodeficiency Virus - CD4 Is
Not Enough" by Levy, J.A. - The New England Journal of
Medicine, Vol 335, no 20, pages 1525-1527, Nov., 1996. Illustrations
(c) Massachusetts Medical Society.
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