The lifecycle of HIV

Infection by HIV is initiated when either cell-free or cell-associated virus binds to a receptor in the target cell by means of the virus envelope. The major receptor for HIV, CD4 (see below), is a membrane protein found on the surface of certain hematopoietic cells, such as T helper lymphocytes and monocytes.

After fusion of the virus envelope protein with the cell membrane, the virus core enters the cell and single-stranded RNA, still associated with capsid protein, is converted to double-stranded proviral DNA through the dual polymerase and ribonuclease activities of the viral reverse transcriptase.

In T cells, the newly made provirus then enters the nucleus, integrates with host DNA by the action of the viral integrase and establishes an infection which is lifelong. The proviral DNA acts as a template for the production of viral RNA. This, in turn, serves both as messenger for synthesis of new viral proteins and as genomic RNA which is subsequently packaged into viral particles. Virus assembly occurs at the surface of the membrane. First, the capsid protein condenses beneath the cell membrane to form the budding particle. The viral RNA attached to the capsid precursor is folded into the particle while the envelope protein aggregates on the outer surface. The virus particle is then released from the cell surface and the capsid protein is processed into mature proteins by the viral protease. This completes the life cycle.

Replication of HIV is determined at least in parr by the level of activation of the target cell. It is well established that HIV will not replicatc in resting T cells, one level of restriction is at the level of provirus synthesis. Apparently, only a partial provirus is formed in the resting cell and upon activation provirus goes on to completion. Another restriction is at the level of RNA transcription. The HIV LTR contains binding sites for at least two transcription factors which are activated in stimulated T cells. These arc Spl and NEkB. Interaction of one of these two factors with the LTR sequences is sufficient to confer the virus with responsiveness to mitogenic stimulation. A number of DNA viruses (CMV, HSV), as well as the human T cell leukemia virus (HTI.V- li, have been shown to activate the NFkB site. Many-other cellular factors bind to specific DNA sequences in the HIV LTR and conceivably regulate HIV expression. The abundance and variety of these factors will vary according to cell type and cell cycle.

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