The clinical consequences of human immunodeficiency virus (HIV) infection are due to the ability of this retrovirus to disarm the host immune system, a process that occurs by virtue of the fact that the primary target for the virus is the helper-inducer subset of lymphocytes. This lymphocyte subset, defined by its surface expression of the CD4 molecule, acts as the pivotal orchestrator of a myriad of immune functions. HIV-1 infection can therefore be considered a disease of the immune system, characterized by the progressive loss of CD4-positive (CD4+) lymphocytes, with ultimately fatal consequences for the infected host.
Despite this immunosuppression induced by HIV, a number of specific immunologic defenses against the virus are generated in infected individuals and may contribute to the long, asymptomatic phase that follows infection by keeping the virus at least partially contained.
TABLE: POTENTIAL CAUSES OF CD4+ CELL DEPLETION
1. Direct toxic consequences of infection
2. Syncytia formation
3. Innocent bystander destruction of cells with adsorbed gp120
4. Impaired regeneration of the peripheral T cell compartment
5. Autoimmune destruction
The potential significance of such responses is also underscored by the recent demonstration in animal AIDS models that a state of vaccine-induced protective immunity can be achieved against retroviruses related to HIV, and by the identification of infected persons who maintain control of HIV-1 viremia without drug therapy. An understanding of the immunology related to HIV provides insight not only into the clinical sequelae of infection, but also into the prospects for development of an effective vaccine against HIV.
Revision date: June 14, 2011
Last revised: by Andrew G. Epstein, M.D.