siglecs facilitate hiv-1 infection of macrophages through adhesion with viral sialic acidssiglecs促进hiv - 1感染的巨噬细胞粘附与病毒唾液酸.pdfVIP
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siglecs facilitate hiv-1 infection of macrophages through adhesion with viral sialic acidssiglecs促进hiv - 1感染的巨噬细胞粘附与病毒唾液酸
Siglecs Facilitate HIV-1 Infection of Macrophages
through Adhesion with Viral Sialic Acids
1. 1. 2 1 1
Zhongcheng Zou , Ashley Chastain , Susan Moir , Jennifer Ford , Kathryn Trandem , Elena
2 2 3 2 1
Martinelli , Claudia Cicala , Paul Crocker , James Arthos , Peter D. Sun *
1 Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, United States of America,
2 Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America, 3 Cell
Biology and Immunology, College of Life Sciences, University of Dundee, Dundee, United Kingdom
Abstract
Background: Human immunodeficiency virus type 1 (HIV-1) infects macrophages effectively, despite relatively low levels of
cell surface-expressed CD4. Although HIV-1 infections are defined by viral tropisms according to chemokine receptor usage
(R5 and X4), variations in infection are common within both R5- and X4-tropic viruses, indicating additional factors may
contribute to viral tropism.
Methodology and Principal Findings: Using both solution and cell surface binding experiments, we showed that R5- and
X4-tropic HIV-1 gp120 proteins recognized a family of I-type lectin receptors, the Sialic acid-binding immunoglobulin-like
lectins (Siglec). The recognition was through envelope-associated sialic acids that promoted viral adhesion to macrophages.
The sialic acid-mediated viral-host interaction facilitated both R5-tropic pseudovirus and HIV-1BaL infection of macrophages.
The high affinity Siglec-1 contribute
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