Abstract

The hallmark of an infection with human immunodeficiency virus (HIV) is a selective depletion of CD4+ lymphocytes and an associated progressive decline of immunological function to the point the host becomes overwhelmed by opportunistic infections or malignancies (McChesney and Oldstone, 1989; Schupbach, 1989). Since CD4+ cells are essential components of effective host defense against most of the systemic mycotic agents, patients with acquired immunodeficiency syndrome (AIDS) frequently suffer from fulminating fungal infections (Armstrong, 1988; Spencer and Jackson, 1989). The two dimorphic fungi which are most commonly isolated from individuals infected with HIV are Histoplasma capsulatum and Coccidioides immitis, (Armstrong, 1988; Spencer and Jackson, 1989; Cairns, 1988) but less frequently other dimorphic fungi such as Sporothrix schenckii, (Bibler et al., 1986; Kurosawa et al., 1988) and Paracoccidioides brasiliensis (Bakos et al., 1989) have been reported to be secondary invaders in AIDS patients. To understand the AIDS patients’ immunological responses to the opportunistic fungi, it is essential to first recognize the immunological status of the host at the onset of the fungal infection. So, before discussing the specific immune responses during systemic dimorphic fungal infections in AIDS patients, I want to define the state of immune function as an HIV infection progresses from the asymptomatic, seroconversion stage to AIDS and identify the stage(s) at which the host is most vulnerable to opportunistic infections. For this purpose, I will use the classification scheme proposed by the Walter Reed group which is based upon the classical immunological and clinical status of HIV infected persons.

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