Effect of Chemokine Gene Variants on Covid-19 Disease Severity
IMMUNOLOGICAL INVESTIGATIONS, cilt.51, sa.7, ss.1965-1974, 2022 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 51 Sayı: 7
- Basım Tarihi: 2022
- Doi Numarası: 10.1080/08820139.2022.2088383
- Dergi Adı: IMMUNOLOGICAL INVESTIGATIONS
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, BIOSIS, CAB Abstracts, EMBASE, MEDLINE, Veterinary Science Database
- Sayfa Sayıları: ss.1965-1974
- Anahtar Kelimeler: Chemokines, COVID-19 severity, MCP-1, POLYMORPHISM, RECEPTOR
- İstanbul Üniversitesi Adresli: Evet
Özet
Patients immune phenotype/genotype data may be useful to understand the molecular mechanisms involved in SARS-CoV-2 infection and can contribute to the identify the different levels of disease severity. The roles of chemokines have been reported in the coronavirus-related diseases SARS and MERS and they may likewise play a critical role in the development of the symptoms of COVID-19 disease. We analyzed the association of the MCP-1-A2518 G, SDF-1-3'A, CCR5-delta32, CCR5-A55029 G, CXCR4-C138T and CCR2-V64I gene polymorphisms with COVID-19 severity to further unveil the immunological pathways leading to disease severity and death. Polymerase chain reaction(PCR)/Sanger sequencing analysis was performed for detection of the variations in 60 asymptomatic and 119 severe COVID-19 patients. In our study, we found that the frequencies of MCP-1 of GA genotype and G allele carriers were significantly higher in severe COVID-19 patients than the asymptomatic COVID-19 patients (p < .0001 and p: .005, respectively). However, no significant association was found for any of the other polymorphisms with the severity of COVID-19. Our findings suggest that there is a positive association between MCP-1-A2518 G gene variants with the severity of COVID-19. However, larger studies in different population which will focus on gene expression levels will help us to understand the capability of the mechanism role.