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The Lack of the Association of the CCR5 Genotype with the Clinical Presentation and Frequency of Tick-Borne Encephalitis in the Polish Population
Background: The host factors influencing the susceptibility to and the severity of tick-borne encephalitis (TBE) are poorly defined. The loss-of-function Δ32 mutation in the chemokine receptor gene CCR5 was identified as a risk factor for West Nile encephalitis and possibly for TBE, suggesting a pro...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8955457/ https://www.ncbi.nlm.nih.gov/pubmed/35335642 http://dx.doi.org/10.3390/pathogens11030318 |
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author | Grygorczuk, Sambor Dunaj-Małyszko, Justyna Sulik, Artur Toczyłowski, Kacper Czupryna, Piotr Żebrowska, Agnieszka Parczewski, Miłosz |
author_facet | Grygorczuk, Sambor Dunaj-Małyszko, Justyna Sulik, Artur Toczyłowski, Kacper Czupryna, Piotr Żebrowska, Agnieszka Parczewski, Miłosz |
author_sort | Grygorczuk, Sambor |
collection | PubMed |
description | Background: The host factors influencing the susceptibility to and the severity of tick-borne encephalitis (TBE) are poorly defined. The loss-of-function Δ32 mutation in the chemokine receptor gene CCR5 was identified as a risk factor for West Nile encephalitis and possibly for TBE, suggesting a protective role of CCR5 in Flavivirus encephalitis. Methods: We studied the CCR5 genotype in 205 TBE patients stratified by a clinical presentation and 257 controls from the same endemic area (Podlasie, Poland). The genotype distribution between the groups and differences between TBE patients with different genotypes were analyzed. Results: There were 36 (17.6%) CCR5Δ32 heterozygotes and 3 (1.5%) homozygotes in the TBE group, with no statistically significant difference in comparison with the controls. The CCR5Δ32 allele did not associate with the clinical presentation or the severity of TBE. The cerebrospinal fluid (CSF) inflammatory parameters did not differ between the wild-type (wt/wt) and wt/Δ32 genotype patients. The TBE clinical presentation and CSF parameters in three Δ32/Δ32 homozygotes were unremarkable. Conclusions: The lack of association of CCR5Δ32 with the risk and clinical presentation of TBE challenges the suspected CCR5 protective role. CCR5 is not indispensable for the effective immune response against the TBE virus. |
format | Online Article Text |
id | pubmed-8955457 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-89554572022-03-26 The Lack of the Association of the CCR5 Genotype with the Clinical Presentation and Frequency of Tick-Borne Encephalitis in the Polish Population Grygorczuk, Sambor Dunaj-Małyszko, Justyna Sulik, Artur Toczyłowski, Kacper Czupryna, Piotr Żebrowska, Agnieszka Parczewski, Miłosz Pathogens Article Background: The host factors influencing the susceptibility to and the severity of tick-borne encephalitis (TBE) are poorly defined. The loss-of-function Δ32 mutation in the chemokine receptor gene CCR5 was identified as a risk factor for West Nile encephalitis and possibly for TBE, suggesting a protective role of CCR5 in Flavivirus encephalitis. Methods: We studied the CCR5 genotype in 205 TBE patients stratified by a clinical presentation and 257 controls from the same endemic area (Podlasie, Poland). The genotype distribution between the groups and differences between TBE patients with different genotypes were analyzed. Results: There were 36 (17.6%) CCR5Δ32 heterozygotes and 3 (1.5%) homozygotes in the TBE group, with no statistically significant difference in comparison with the controls. The CCR5Δ32 allele did not associate with the clinical presentation or the severity of TBE. The cerebrospinal fluid (CSF) inflammatory parameters did not differ between the wild-type (wt/wt) and wt/Δ32 genotype patients. The TBE clinical presentation and CSF parameters in three Δ32/Δ32 homozygotes were unremarkable. Conclusions: The lack of association of CCR5Δ32 with the risk and clinical presentation of TBE challenges the suspected CCR5 protective role. CCR5 is not indispensable for the effective immune response against the TBE virus. MDPI 2022-03-04 /pmc/articles/PMC8955457/ /pubmed/35335642 http://dx.doi.org/10.3390/pathogens11030318 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Grygorczuk, Sambor Dunaj-Małyszko, Justyna Sulik, Artur Toczyłowski, Kacper Czupryna, Piotr Żebrowska, Agnieszka Parczewski, Miłosz The Lack of the Association of the CCR5 Genotype with the Clinical Presentation and Frequency of Tick-Borne Encephalitis in the Polish Population |
title | The Lack of the Association of the CCR5 Genotype with the Clinical Presentation and Frequency of Tick-Borne Encephalitis in the Polish Population |
title_full | The Lack of the Association of the CCR5 Genotype with the Clinical Presentation and Frequency of Tick-Borne Encephalitis in the Polish Population |
title_fullStr | The Lack of the Association of the CCR5 Genotype with the Clinical Presentation and Frequency of Tick-Borne Encephalitis in the Polish Population |
title_full_unstemmed | The Lack of the Association of the CCR5 Genotype with the Clinical Presentation and Frequency of Tick-Borne Encephalitis in the Polish Population |
title_short | The Lack of the Association of the CCR5 Genotype with the Clinical Presentation and Frequency of Tick-Borne Encephalitis in the Polish Population |
title_sort | lack of the association of the ccr5 genotype with the clinical presentation and frequency of tick-borne encephalitis in the polish population |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8955457/ https://www.ncbi.nlm.nih.gov/pubmed/35335642 http://dx.doi.org/10.3390/pathogens11030318 |
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