Interaction between the viral envelope proteins (gp120) and receptors on the cell membrane is critical for the HIV to enter and infect the host cell. High concentrations of the CD4 molecule and co-receptors have been detected on the surface of T-lymphocytes and macrophages. Other cells that have been found to have CD4 molecules on their surface include the Langerhans cells (found in the skin) and the microglial cells of the brain.
Following entry of the HIV into a susceptible host cell, using the enzyme reverse transcriptase, the viral genome copies itself from RNA to DNA genetic material. The viral DNA copy enters the nucleus of the host cell and becomes intimately incorporated into the host cell’s own DNA using the enzyme integrase. The virus thus becomes a permanent part of an infected person’s nuclear proteins. There follows a latent period during which the provirus in the infected host cell nucleus is waiting for an external stimulus to start reproducing.
CD4+ T lymphocytes when stimulated by new HIV, other infections and infestations which would normally result in the CD4+ T lymphocyte reproducing itself, now respond to these stimuli by manufacturing HIV. As more and more viruses are produced and leave the host cell, the cell membrane weakens leading eventually to the death of the infected CD4+ T lymphocytes. Other factors, most of which are still unknown, lead to the rapid depletion of the CD4+ T lymphocytes. The decline in the CD4+ T lymphocytes count is a reflection of the declining cellular immunity, which eventually manifests itself by the appearance of opportunistic infections.