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The acquired immune deficiency syndrome (AIDS) is caused by human immunodeficiency virus type 1 or 2 (HIV-l or HIV-2). The disease is characterized by a high susceptibility to opportunistic infections or to malignant diseases, such as Kaposi’s sarcoma. The major immunologic abnormality is the selective depletion of CD4
+
T-cells together with decreased capacity to secrete or respond to lymphokines, such as interleukin 2. During infection, HIV induces both a humor-al and cell-mediated immune response to its viral components. However, the response cannot cope with progressive infection. An antibody response to the virion surface proteins,
env
(gp120, gp41), and the core protein,
gag
(p24, p17), is observed in most instances 4–8 wk after infection with the virus. The antibody response clears the virus from the circulation, but does not eliminate cells that become latently infected. As infected individuals progress from the asymptomatic state to produce AIDS-related complex (ARC) and subsequently to full-blown AIDS, anti-p24 titers are reduced and the viral antigen appears in the circulation of patients. The significance of this reduction in p24 antibody for disease progression is presently not known. High levels of antibodies to
env
gene products are also found in HIV-l positive patients, but no real relationship has been noted between their titers or their neutralizing capacities and progression to AIDS (
1
,
2
).
