Do CCR5 (CCR5?32) and TLR3 (RS5743313) gene polymorphisms prevent chronic hepatitis B infection?

Basit Öğe Kaydı
dc.authoridAKSOY, Emel/0000-0001-9536-4322
dc.contributor.authorTuncel, Burcin
dc.contributor.authorKaygusuz, Sedat
dc.contributor.authorKocakap, Derya Beyza Sayin
dc.contributor.authorAksoy, Emel
dc.contributor.authorAzkur, Ahmet Kursat
dc.date.accessioned2025-01-21T16:37:46Z
dc.date.available2025-01-21T16:37:46Z
dc.date.issued2023
dc.departmentKırıkkale Üniversitesi
dc.description.abstractHepatitis B virus (HBV) is still a significant health problem in human. HBV severity or sensitivity of patients may be based on the individual genetic factors significantly. The aim of this study is to investigate the association of CCR5 (CCR5 Delta 32), TLR3 (rs5743313) functional gene polymorphisms, interferon-gamma (IFN-?) level in HBV infection, which are thought to play an important role in innate and acquired immunity in patients who have undergone HBV seroconversion and those who have chronic hepatitis B disease and receive treatment. One hundred patients who are became naturally immune against HBV infection (HBsAg negative, anti-HBc IgG, and anti-HBs IgG positive), and 100 patients with chronic hepatitis B infection (>6 months HBsAg positive) who are receiving oral antiviral therapy were compared for CCR5 Delta 32, TLR3 (rs5743313) genotypes and serum IFN-gamma level. It was found that CCR5 Delta 32 polymorphism (Wt/Delta 32 and Delta 32/Delta 32) was significantly higher in the chronic hepatitis B group (p=0.048) but not for TLR3 gene polymorphism. However, serum IFN-gamma level was significantly higher in the HBV seroconversion group (75 +/- 89ng/ml) than in the chronic hepatitis B group (4.35 +/- 17.27ng/ml) (p < 0.001). In conclusion, a higher CCR5 Delta 32 allele frequency in patients with chronic hepatitis B might be considered as a marker of progression to chronic hepatitis.
dc.description.sponsorshipKirikkale University Scientific Research Unit [2021/072]
dc.description.sponsorshipThe study was financially supported by Kirikkale University Scientific Research Unit with project number 2021/072.
dc.identifier.doi10.1002/jmv.28376
dc.identifier.issn0146-6615
dc.identifier.issn1096-9071
dc.identifier.issue1
dc.identifier.pmid36478230
dc.identifier.scopus2-s2.0-85145901207
dc.identifier.scopusqualityQ1
dc.identifier.urihttps://doi.org/10.1002/jmv.28376
dc.identifier.urihttps://hdl.handle.net/20.500.12587/24530
dc.identifier.volume95
dc.identifier.wosWOS:000911465200295
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherWiley
dc.relation.ispartofJournal of Medical Virology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_20241229
dc.subjectevolution; genetic variability; hepatitis B virus; immune system; pathogenesis; virus classification
dc.titleDo CCR5 (CCR5?32) and TLR3 (RS5743313) gene polymorphisms prevent chronic hepatitis B infection?
dc.typeArticle

Dosyalar

Koleksiyon

WOS İndeksli Yayınlar Koleksiyonu
PubMed İndeksli Yayınlar Koleksiyonu
Scopus İndeksli Yayınlar Koleksiyonu