Thippawan ChuenchitraChantapong WasiMark De SouzaSorachai NitayaphanSuda LouisirirotchanakulRuengpung SutthentArthur E. BrownDeborah L. BirxVictoria R. PolonisArmed Forces Research Institute of Medical Sciences, ThailandMahidol UniversityU.S. Military HIV Research ProgramUS Army Medical Materiel Development ActivityCenters for Disease Control and Prevention2018-07-122018-07-122008-09-01Southeast Asian Journal of Tropical Medicine and Public Health. Vol.39, No.5 (2008), 863-866012515622-s2.0-52649179841https://repository.li.mahidol.ac.th/handle/123456789/19567The β-chemokines have been shown to inhibit HIV replication in vitro. To evaluate the role of serum β-chemokines in disease progression and their anti-viral role in vivo, we determined serum levels of macrophage inflammatory protein-1β (MIP-1 β) 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/mm 3 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-1β 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-1β and RANTES levels over time in either patient group (p>0.05). No significant associations were observed between plasma viral loads and the measured β-chemokines (r = -0.205, p = 0.21 for MIP-1β 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.Mahidol UniversityMedicineArticleSCOPUS