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Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: "Blockade of chemokine-induced signalling inhibits CCR5-dependent HIV infection in vitro without blocking gp120/CCR5 interaction. | Retrovirology BioMed Central Research Open Access Blockade of chemokine-induced signalling inhibits CCR5-dependent HIV infection in vitro without blocking gp120 CCR5 interaction David J Grainger and Andrew ML Lever Address Department of Medicine University of Cambridge Box 157 Addenbrooke s Hospital Hills Road Cambridge CB2 2QQ UK Email David J Grainger - djg15@cam.ac.uk Andrew ML Lever - amll1@mole.bio.cam.ac.uk Corresponding author Published 04 April 2005 Received 02 March 2005 Retrovirology 2005 2 23 doi l0.ll86 l742-4690-2-23 Accepted 04 April 2005 This article is available from http www.retrovirology.cOm content 2 1 23 2005 Grainger and Lever licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http creativecommons.org licenses by 2.0 which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Cellular infection with human immunodeficiency virus HIV both in vitro and in vivo requires a member of the chemokine receptor family to act as a co-receptor for viral entry. However it is presently unclear to what extent the interaction of HIV proteins with chemokine receptors generates intracellular signals that are important for productive infection. Results In this study we have used a recently described family of chemokine inhibitors termed BSCIs which specifically block chemokine-induced chemotaxis without affecting chemokine ligands binding to their receptors. The BSCI termed Peptide 3 strongly inhibited CCR5 mediated HIV infection of THP-l cells 83 7 inhibition assayed by immunofluoresence staining but had no effect on gpl20 binding to CCR5. Peptide 3 did not affect CXCR4-dependent infection of Jurkat T cells. Conclusion These observations suggest that in some cases intracellular signals generated by the chemokine coreceptor may be required for a productive HIV infection. Background Human immunodeficiency
