Objective: To evaluate serum chemokines, macrophage inflammatory prote
in (MIP)-1 alpha, MIP-1 beta and RANTES, concentrations in non-progres
sing HIV-infected patients and AIDS patients. Setting: University Hosp
ital-based AIDS Clinical Trials Unit. Design/Methods: Serum MIP-1 alph
a, MIP-1 beta and RANTES levels were determined by enzyme-linked immun
osorbent assay using archived serum specimens obtained on two occasion
s at least 1.8 years apart. Patient selection: Long-term non-progressi
ng HIV-infected adult patients were identified from clinic records. Fo
r each non-progressing patient, two adult AIDS patients with initial d
ocumentation of seropositivity the same year and the same length of fo
llow-up were selected. Results: Four long-term non-progressing patient
s and eight AIDS patients were studied. Neither the duration of known
HIV positivity at the time of specimen collection nor the length of ti
me between specimen collections differed significantly between non-pro
gressing patients and AIDS patients. Serum levels of MIP-1 alpha, MIP-
1 beta and RANTES in specimens obtained either early or later in the c
ourse of HIV infection did not differ significantly between non-progre
ssing patients and AIDS patients. In the two patient subsets, signific
ant differences in serum chemokine levels over time were not observed.
The rate of change of serum chemokine concentration over time also di
d not differ between non-progressing patients and AIDS patients. Serum
MIP-1 alpha and MIP-1 beta levels did not reach levels reported to su
ppress HIV proliferation in vitro. When expressed as a quantity per pe
ripheral blood CD8+ lymphocyte, AIDS patients exhibited significantly
greater levels of MIP-1 alpha, MIP-1 beta and RANTES than non-progress
ing HIV patients (P < 0.05). These values did not exhibit a significan
t variation over time. Conclusions: Serum MIP-1 alpha, MIP-1 beta and
RANTES levels do not distinguish patients with AIDS from patients with
non-progressing HIV infection. Variations in levels of these chemokin
es do not explain individual variation in the natural history of HIV i
nfection.