Chemokine receptors are used by HIV-1 for entry into CD4+ T cells. The beta-chemokines are capable of inhibiting HIV replication. This study measured beta-chemokine macrophage inflammatory protein (MIP)-1alpha and MIP-1beta levels and determined the CCR5 and CXCR4 expression on T cells in HIV-1-infected patients treated with HAART. The time of known HIV infection and time of HAART use were similar between failure and successful groups. The CD4+ T cell nadir was 163 vs. 251 cells/mm3, p = 0.07, for failure and successful groups, respectively. The successfully treated group, when compared with the failure group, had a higher median CD4+ T cells count (667 vs. 257 cells/mm3; p = 0.003) as well as higher spontaneous MIP-1alpha (median of 4390 vs. 802 pg/ml, p = 0.03) and MIP-1beta (median of 2416 vs. 1117 pg/ml, p = 0.001) levels. The untreated patients had a higher number and intensity of CCR5- and CXCR4-expressing T cells. Higher levels of chemokines were not related to nadir CD4+ T and current CD8+ T cell counts. Successfully treated patients were able to produce higher amounts of beta-chemokines and normalize the coreceptor overexpression on T cells. These findings may have clinical implications, such as a new strategy of using chemokines as adjuvants in anti-HIV therapy.