ABSTRACT
Acquired immunodeficiency syndrome (AIDS) is characterized by infection with human immunodeficiency virus (HIV) and progressive depletion of CD4+(helper) T cells, leading to opportunistic infections and malignancies (1). In addition to CD4+ cell loss, HIV-infected patients manifest impairment of immune response, affecting both CD4+ and CD8+ T-cell subsets, that resembles an anergic state of immune dysfunction (2). These defective immunological responses include decreased interleukin-2 (IL-2) secretion and unresponsiveness to recall antigens or stimulation through the CD3/TCR complex (3).
