Frequency of interleukin-6 rs1800795 (-174G/C) and rs1800797 (-597G/A) polymorphisms in COVID-19 patients in Turkey who develop macrophage activation syndrome.


Kerget F., Kerget B.

Japanese journal of infectious diseases, cilt.74, ss.543-548, 2021 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 74
  • Basım Tarihi: 2021
  • Doi Numarası: 10.7883/yoken.jjid.2021.046
  • Dergi Adı: Japanese journal of infectious diseases
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, CAB Abstracts, EMBASE, MEDLINE, Veterinary Science Database
  • Sayfa Sayıları: ss.543-548
  • Atatürk Üniversitesi Adresli: Evet

Özet

Severe acute respiratory syndrome coronavirus 2 has infected over 100 million people since it appeared in Wuhan, China, just one year ago. This study aimed to evaluate the relationship between interleukin-6 (IL-6) gene polymorphisms -174G/C and -597G/A and coronavirus disease 2019 (COVID-19) course. The study included 70 patients aged 18-45 years who were diagnosed with COVID-19 in Turkey between March and November 2020 and hospitalized in our hospital. Of these, 40 patients required intensive care admission due to macrophage activation syndrome (MAS), and 30 patients did not develop MAS or acute respiratory distress syndrome. The frequencies of the IL-6-174G/C and -597G/A polymorphisms were determined. There were significant differences between the groups in terms of the -174G/C allele and genotype frequency according to the Hardy-Weinberg equilibrium (chi(2) = 10.029, df = 1, P = 0.002 and chi(2) = 9.998, df = 1, P = 0.002, respectively). The frequency of the GG genotype was significantly higher in the MAS group than in the non-MAS group (P = 0.002). The G allele was also significantly more frequent in the MAS group than in the non-MAS group (P = 0.032). Analysis of the -174G/C polymorphism in patients with MAS showed that the G allele may be a risk factor for increased serum IL-6 levels and progression to MAS.