Changing Virus‐Host Interactions in the Course of HIV‐1 Infection

Acquired immunodeficiency syndrome (AIDS) patients may present with various clinical symptoms related to severe immunodeficiency resulting from persistent infection with the human immunodeficiency virus-l (HIV-1). CD4+ T-helper (Th) cells are an important target for HIV (Klatzmann et al. 1984, Dalgleish et al. 1984, McDougal et al. 1985), and loss of these eells in relatively late stages of HIV infection is well documented and known to be predictive for progression (Meibye et al. 1986, Fahey et al. 1984). In addition to depletion of Th eells, leukocytes from AIDS patients display a variety of functional defects finally resulting in a general disturbance of immune reactivity that includes almost all leukocyte functions. At that stage, the patient is extremely susceptible to diseases related to a variety of intracellular pathogens but also has a moderately increased risk for pyogenic infections particularly with encapsulated bacteria. Moreover, in addition to Kaposi's sarcomas, opportunistic neoplasia frequently develop (Fauci 1988). One feature of HIV-1 is its great variability with respect to biological properties such as syncytium inducing (SI) capacity, replication rate and cytotropism (ChengMayer et al. 1988, Asjo et al. 1986, Von Briesen et al. 1987, Evans et al. 1987, Tersmette et al. 1988). HIV-1 isolates recovered from peripheral blood mononuclear cells of asymptomatic subjects are able to grow in phytohemagglutinin (PHA)-stimulated primary blood lymphocytes (PBL) but, in contrast to isolates