Highly Active Antiretroviral Therapy Normalizes the Potential for MIP-1a Production in HIV Infection

The CC chemokines RANTES, MIP-1[alpha] and MIP-1[beta] are ligands for CCR5, which has been identified as the principal co-receptor for macrophage tropic strains of HIV-1. This study investigated whether the inducible levels of RANTES, MIP-1[alpha] and MIP-1[beta] produced by cultured whole blood sa...

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Bibliographic Details
Published in:The Journal of infection 2000-11, Vol.41 (3), p.252-255
Main Authors: Carter, L M, Peters, B S, Ellis, BA, Wolstencroft, R A
Format: Article
Language:English
Subjects:
CCR5 protein
Human immunodeficiency virus 1
MIP-1^a protein
MIP-1^b protein
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Summary:The CC chemokines RANTES, MIP-1[alpha] and MIP-1[beta] are ligands for CCR5, which has been identified as the principal co-receptor for macrophage tropic strains of HIV-1. This study investigated whether the inducible levels of RANTES, MIP-1[alpha] and MIP-1[beta] produced by cultured whole blood samples related to different rates of progression of HIV infection and to the introduction of Nelfinavir-based highly active anti-retroviral therapy (HAART). Study subjects were HIV-positive and categorized as "slow progressors" (n=8) or as "fast progressors" (n=7); the latter group were treated with HAART. MIP-1[alpha], MIP-1[beta] and RANTES production was determined using commercial ELISA kits. The inducible production of MIP-1[alpha] by whole blood cells in culture was significantly depressed in patients starting therapy compared with "slow progressors" and "normal donors". The levels of MIP-1[alpha] significantly increased with therapy at 12 weeks compared with pre-HAART levels (P=0.05) and became comparable to that of "normals" and "slow progressors". Differences in the inducible levels of MIP-1[beta] and RANTES for the separate subject groups were not significant. The increase in inducible MIP-1[alpha] production following HAART might suggest a role for the chemokines in HIV disease, either for monitoring the outcome of therapy of HIV disease, or as a direct therapeutic intervention.
ISSN:0163-4453