Serum levels of MIP-1beta and RANTES in HIV-1 subtype CRF01_AE infected patients with different rates of disease progression.

ABSTRACT

The beta-chemokines have been shown to inhibit HIV replication in vitro. To evaluate the role of serum beta-chemokines in disease progression and their anti-viral role in vivo, we determined serum levels of macrophage inflammatory protein-1beta (MIP-1beta) and regulated upon activation normal T-cell expressed and secreted (RANTES) of twenty HIV-1 subtype CRF01_AE infected patients nine progressors (PRs, follow-up CD4+ cell count < 200/mm3 and progression to AIDS or death) and eleven slower progressors (SPs, asymptomatic and/or follow-up CD4+ cell counts > 350/mm3 at the end of follow-up) and determined their plasma viral loads. The subjects were followed for at least 36 months. All had initial CD4 values > 350 cells/mm3. In this longitudinal study, serum levels of MIP-1beta and RANTES in specimens obtained either early or later in the course of HIV infection did not differ significantly between progressors and slower progressors (p > 0.05). There were no significant changes in serum MIP-1beta and RANTES levels over time in either patient group (p > 0.05). No significant associations were observed between plasma viral loads and the measured beta-chemokines (r = -0.205, p = 0.21 for MIP-1beta and r = -0.12, p = 0.492 for RANTES). The results suggest these chemokines do not play a major systemic role in control of viremia or protection against the progression of HIV disease.