Characterization of the human chemerin receptor - ChemR23/CMKLR1 - as co-receptor for human and simian immunodeficiency virus infection, and identification of virus-binding receptor domains.
(2006) In Virology 355(Aug 9). p.6-17- Abstract
- Studies were conducted to elucidate co-receptor spectrum and function of the inflammatory receptor, CMKLR1/ChemR23, which was recently identified as the receptor for the cystatin-like chemoattractant, TIG2, also named chemerin. An infection model was applied based on stably transfiected NP-2.CD4 host cells expressing various co-receptor constructs and exposed to panels of HIV-1, HIV-2 and SIV primary isolates. In a panel of 27 HIV-1 isolates tested, 12 isolates could use CMKLR1/ChemR23. As expected from a relatively high sequence homology with the extracellular domains of CCR3, HIV-1 isolates showing R3 tropism were particularly efficient in using CMKLR1/ChemR23. In addition, 5 out of 7 HIV-2 isolates and 13 out of 15 SIV (SMM-3 origin)... (More)
- Studies were conducted to elucidate co-receptor spectrum and function of the inflammatory receptor, CMKLR1/ChemR23, which was recently identified as the receptor for the cystatin-like chemoattractant, TIG2, also named chemerin. An infection model was applied based on stably transfiected NP-2.CD4 host cells expressing various co-receptor constructs and exposed to panels of HIV-1, HIV-2 and SIV primary isolates. In a panel of 27 HIV-1 isolates tested, 12 isolates could use CMKLR1/ChemR23. As expected from a relatively high sequence homology with the extracellular domains of CCR3, HIV-1 isolates showing R3 tropism were particularly efficient in using CMKLR1/ChemR23. In addition, 5 out of 7 HIV-2 isolates and 13 out of 15 SIV (SMM-3 origin) used CMKLR1/ChemR23, in accordance with the previously documented ability of these isolates to use several co-receptors. In order to define important extracellular epitopes for the viral interaction, a hybrid receptor model was applied. This was based on the fact that the rat receptor, although structurally very similar to the human orthologue, was inefficient as viral co-receptor. When the rat receptor was "humanized" to include regions unique to the human receptor (N-terminus or second extracellular loop), exposure to HIV-1, HIV-2 and SIV isolates resulted in infection. The relative importance of the two critical receptor regions differed between HIV-1/HIV-2 on the one hand and SIV on the other. The results strongly support that the chemerin receptor, in the presence of CD4, functions as a "minor co-receptor" promoting infection by these classes of viruses. (c) 2006 Elsevier Inc. All rights reserved. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/160127
- author
- Mårtensson, Ulrika LU ; Fenyö, Eva Maria LU ; Olde, Björn LU and Owman, Christer LU
- organization
- publishing date
- 2006
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- hybrid receptor model, SIV, chemerin receptor, G-protein coupled receptor, HIV-2, HIV-1
- in
- Virology
- volume
- 355
- issue
- Aug 9
- pages
- 6 - 17
- publisher
- Elsevier
- external identifiers
-
- wos:000241740100002
- scopus:33750076356
- ISSN
- 1096-0341
- DOI
- 10.1016/j.virol.2006.07.010
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Division of Medical Microbiology (013250400), Molecular Neurobiology (0131000140), Drug Target Discovery (013212045)
- id
- 8e7d4f39-840e-4c66-81d6-f35b9326ec9c (old id 160127)
- alternative location
- http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16904155&dopt=Abstract
- date added to LUP
- 2016-04-01 16:10:17
- date last changed
- 2022-04-22 20:04:08
@article{8e7d4f39-840e-4c66-81d6-f35b9326ec9c,
abstract = {{Studies were conducted to elucidate co-receptor spectrum and function of the inflammatory receptor, CMKLR1/ChemR23, which was recently identified as the receptor for the cystatin-like chemoattractant, TIG2, also named chemerin. An infection model was applied based on stably transfiected NP-2.CD4 host cells expressing various co-receptor constructs and exposed to panels of HIV-1, HIV-2 and SIV primary isolates. In a panel of 27 HIV-1 isolates tested, 12 isolates could use CMKLR1/ChemR23. As expected from a relatively high sequence homology with the extracellular domains of CCR3, HIV-1 isolates showing R3 tropism were particularly efficient in using CMKLR1/ChemR23. In addition, 5 out of 7 HIV-2 isolates and 13 out of 15 SIV (SMM-3 origin) used CMKLR1/ChemR23, in accordance with the previously documented ability of these isolates to use several co-receptors. In order to define important extracellular epitopes for the viral interaction, a hybrid receptor model was applied. This was based on the fact that the rat receptor, although structurally very similar to the human orthologue, was inefficient as viral co-receptor. When the rat receptor was "humanized" to include regions unique to the human receptor (N-terminus or second extracellular loop), exposure to HIV-1, HIV-2 and SIV isolates resulted in infection. The relative importance of the two critical receptor regions differed between HIV-1/HIV-2 on the one hand and SIV on the other. The results strongly support that the chemerin receptor, in the presence of CD4, functions as a "minor co-receptor" promoting infection by these classes of viruses. (c) 2006 Elsevier Inc. All rights reserved.}},
author = {{Mårtensson, Ulrika and Fenyö, Eva Maria and Olde, Björn and Owman, Christer}},
issn = {{1096-0341}},
keywords = {{hybrid receptor model; SIV; chemerin receptor; G-protein coupled receptor; HIV-2; HIV-1}},
language = {{eng}},
number = {{Aug 9}},
pages = {{6--17}},
publisher = {{Elsevier}},
series = {{Virology}},
title = {{Characterization of the human chemerin receptor - ChemR23/CMKLR1 - as co-receptor for human and simian immunodeficiency virus infection, and identification of virus-binding receptor domains.}},
url = {{http://dx.doi.org/10.1016/j.virol.2006.07.010}},
doi = {{10.1016/j.virol.2006.07.010}},
volume = {{355}},
year = {{2006}},
}