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Cell-Free Human Immunodeficiency Virus Type 1 Transcytosis through Primary Genital Epithelial Cells
TLDR
The transcellular migration of HIV-1 as a cell-free virus through primary genital epithelial cells (PGECs) is investigated and it is found that syndecans are abundantly expressed on PGECs and promote the initial attachment and subsequent entry of HIV, which demonstrates that the genital epithelium serves as a major barrier against HIV- 1.
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Syndecans Serve as Attachment Receptors for Human Immunodeficiency Virus Type 1 on Macrophages
TLDR
It is shown that CD4 alone is not sufficient to support the initial adsorption of HIV-1 to macrophages, and it is found that heparan sulfate proteoglycans (HSPGs) serve as the main class of attachment receptors for HIV- 1 on macrophage.
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Host cyclophilin A mediates HIV‐1 attachment to target cells via heparans
TLDR
HIV‐1 attachment to target cells is a multi‐step process that requires an initial CypA–heparan interaction followed by the gp120–CD4 interaction.
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DEB025 (Alisporivir) Inhibits Hepatitis C Virus Replication by Preventing a Cyclophilin A Induced Cis-Trans Isomerisation in Domain II of NS5A
TLDR
It was very difficult to select resistant replicons (genotype 1b) to DEB025, requiring an average of 20 weeks (four independent experiments), compared to the typically <2 weeks with protease or polymerase inhibitors, indicating a high genetic barrier to resistance forDEB025.
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Syndecan captures, protects, and transmits HIV to T lymphocytes.
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The cyclophilin inhibitor Debio‐025 shows potent anti–hepatitis C effect in patients coinfected with hepatitis C and human immunodeficiency virus
TLDR
These are the first preliminary human data supporting the hypothesis that CypB may play an important role in hepatitis C virus replication and that Cyp inhibition is a valid target for the development of anti–hepatitis C drugs.
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The Isomerase Active Site of Cyclophilin A Is Critical for Hepatitis C Virus Replication*
TLDR
The respective contribution of Cyp members to HCV replication is analyzed by specifically knocking down their expression by both transient and stable small RNA interference, suggesting for the first time that HCV exploits either the isomerase or the chaperone activity of CypA to replicate in hepatocytes and that CypA is the principal mediator of the Cyp inhibitor anti-HCV activity.
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Naturally Occurring Capsid Substitutions Render HIV-1 Cyclophilin A Independent in Human Cells and TRIM-cyclophilin-resistant in Owl Monkey Cells*
TLDR
This study demonstrates that specific capsid substitutions can release HIV-1 from both CypA dependence in human cells and TRIM-Cyp restriction in monkey cells.
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Syndecan-3 is a dendritic cell-specific attachment receptor for HIV-1
TLDR
Dendritic cells efficiently capture HIV-1 and mediate transmission to T cells, but the underlying molecular mechanism is still being debated, and an effective microbicide should target both syndecan-3 and DC-SIGN on DCs to prevent transmission.
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HCV resistance to cyclosporin A does not correlate with a resistance of the NS5A-cyclophilin A interaction to cyclophilin inhibitors.
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