- Microbiology

After infection, HIV causes a reduction of the number of T-cells in the body, eventually resulting in an increased risk of disease. HIV enters the body -- through the usual means of unsafe sex, sharing contaminated needles, blood transfusions or from mother to child (vertical infection)and waits to bump into its host cell; the T-cell.

Once this happens, HIV will reprogram the host cell to make more copies of the virus, which infect more cells and on and on. For this to happen HIV has to complete its life cycle: The steps of the Viral life cycle all involve making more viruses.

Attachment and Fusion - Once HIV has come into contact with a T-cell, it must attach itself to the cell so that it can get its nucleic acid into the host. On the surface of your T-cells are receptors, Hiv binds to two in particular, CD4 and a chemokine receptor, are used by HIV to attach onto the cell in order to gain access. With these two receptors, HIV attaches to the cell and fuses with the cell's membrane, or outer surface.

Transcription - After HIV successfully attaches and fuses with the cell, it is ready to transfer its RNA, HIV needs to translate these RNA instructions into DNA first to create many, many more copies of the RNA. To do this, HIV uses an enzyme known as Reverse Transcriptase. This enzyme takes the single strand of viral RNA and transcribes it into a double strand of DNA. This enzyme is only found in Retroviruses (Viruses with RNA genomes). A class of drugs known as reverse transcriptase inhibitors inhibit this process. These inhibitors are currently part of our best treatment regime for AIDS.

Integration - After HIV has successfully translated its instructions from RNA to DNA, it is ready for the next step in its life cycle -- integration. Integration is the process by which HIV inserts its DNA into the cell's DNA. The new viral DNA will reprogram the cell to make HIV.

Packaging - Once the cell has the viral instructions in its nucleus and becomes activated, it is ready to make new HIV. The cell's nucleus commands the cell to reproduce HIV, and soon the building blocks for the new HIV viruses are produced in the cell, in the form of chains of coat proteins and RNA. HIV uses an enzyme called protease to cut the long chains of subunits so they can come together to form the new virus. The class of drugs called protease inhibitors are able to block the cutting action of the enzyme, thus preventing the reassembly of the new HIV. Once the subunits are cut by the protease enzyme they are ready to be put together to form the new viruses.

Budding - As the packaging step is completed, HIV moves to the outer part of the cell to escape. This process is known as budding . HIV actually uses part of the cell's outer coating, known as the cell membrane, to complete its final structure. Once this process is completed the new HIV particles leave the cell in search of new cells to infect and start the whole process over.

Resistance to infection with the HIV virus has been noted in a percentage of individuals who were at high risk of acquiring the disease. Resistance to HIV infection is a result of a defect in the gene for a chemokine receptor, CKR-5. In normal individuals, the product of this gene is deposited on the surface of the cell membrane and acts as a co-receptor with CD4 protein for binding the HIV virus and initiating the infection process. In resistant individuals, the gene for CKR-5 exhibits a 32 bp deletion which alters the protein product. The protein produced is not deposited on the surface membrane and as a result of this the HIV virus is unable to initiate successful binding and entry into the lymphocyte. (Lui, Rong et al . (1996). Homozygous Defect In HIV-1 Coreceptor Accounts For Resistance Of Some Multiply-Exposed Individuals To HIV-1 Infection. Cell, Vol. 86 (3))

Emerging Diseases