Endogenous levels of C-C chemokines MIP-1 alpha, MIP-1 beta, and RANTES donot reflect the disease course in HIV-seropositive individuals

Citation
Ka. Kreuzer et al., Endogenous levels of C-C chemokines MIP-1 alpha, MIP-1 beta, and RANTES donot reflect the disease course in HIV-seropositive individuals, INT J CL L, 30(4), 2000, pp. 163-168
Citations number
18
Categorie Soggetti
Medical Research Diagnosis & Treatment
Journal title
INTERNATIONAL JOURNAL OF CLINICAL & LABORATORY RESEARCH
ISSN journal
09405437 → ACNP
Volume
30
Issue
4
Year of publication
2000
Pages
163 - 168
Database
ISI
SICI code
0940-5437(200012)30:4<163:ELOCCM>2.0.ZU;2-#
Abstract
It has been shown that the beta (C-C) chemokines macrophage inflammatory pr otein-1 alpha/beta (MIP-1 alpha/beta) and RANTES, which are released by CD8 (+) T cells, are potent inhibitors of HIV viral replication in vitro. To in vestigate whether serum concentrations of these chemokines reflect such a p rotective effect in vivo, we measured these in peripheral blood of 60 HIV s eropositive patients, 10 healthy subjects, and 10 disease controls. Values were compared with the CDC disease stages and immunological surrogate marke rs of disease progression, such as CD4(+) count, beta (2)-microglobulin and 5'-neopterin serum levels. In addition, HIV RNA was measured in sera. All three chemokines were not significantly different between HIV patients and healthy individuals, nor were differences of chemokine levels between the C DC stages significant. Instead, disease controls exhibited significantly mo re MIP-1 alpha and MIP-1 beta than normals or HIV patients. Furthermore, wi thin the HIV-seropositive subjects we did not observe any relationship with the surrogate markers of HIV disease, CD4(+) count, CD4(+)/CD8(+) ratio, b eta (2)-microglobulin, and 5'-neopterin (all correlations NS). HIV viral lo ad did not correlate with the measured chemokine concentrations (r < 0.1, N S). In conclusion, endogenous levels of MIP-la, MIP-IP, and RANTES do not r eflect the hypothesized protective effect on disease progression in HIV inf ection. Thus, despite potential beneficial effects of the investigated chem okines, other factors may equally contribute to HPV replication control in vivo.