The suppressor of cytokine signaling-1 (SOCS1) gene polymorphism and promoter methylation correlate with the course of COVID-19

ABSTRACT

The suppressor of the cytokine signaling-1 (SOCS1) gene is a short sequence located on chromosome 16 that functions to induce an appropriate immune response and is an essential physiological regulator of interferon (IFN) signaling. In addition to comparing the global DNA and SOCS1 gene promoter methylation status between our patients with coronavirus disease 2019 (COVID-19) and healthy controls, this study demonstrates the effect of the SOCS1 rs33989964 polymorphism on patients with COVID-19. The study group included 139 patients diagnosed with COVID-19 in our hospital’s clinics between June and December 2020, and the control group included 78 healthy individuals. After comparing the initial gene polymorphisms of the patients with the healthy control group, three separate clinical subgroups were formed. The gene polymorphism distribution and the methylation status of SOCS1 were examined in these clinical subgroups. Hypomethylation of the SOCS1 gene was observed in the COVID-19 patient group compared to the healthy control group (p = 0.001). Between the patients divided into two separate clinical subgroups, those with severe and mild infections, the Del/Del genotype of the SOCS1 gene was more common in patients with severe infection than in patients with mild infection (p = 0.018). Patients with the CA/CA and CA/Del genotypes were 0.201 times more likely to have a severe infection (95% CI: 0.057–0.716, p = 0.007). Having a non-Del/Del genotype was a protective factor against severe infection. The effect of the SOCS1 rs33989964 polymorphism and methylation status of the SOCS1 gene throughout the COVID-19 pandemic could be significant contributions to the literature.

GRAPHICAL ABSTRACT

KEYWORDS:

• COVID-19
• SOCS1
• polymorphism
• methylation
• prognosis
• mortality

Acknowledgments

In memory of all our colleagues who have sacrificed their lives in the fight against COVID-19, we pay our respects. We would like to extend our sincere thanks to Ege Turen for their valuable contributions to the writing and editing of this article. We are grateful to Burak Gıroglu for creating the abstract graphic design.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Authors’ contributions

T.T., S.P., A.M., I.S., H.A., N.S., Y.O., and U.I.A. collected the data; M.P., I.S., and S.P. contributed data or analysis tools; M.P. performed the analysis; I.S. and S.P. wrote the paper.

Data availability statement

The authors declare that data supporting the findings of this study are available within the referenced articles.

Ethical approval and consent to participate

Ethical committee approval was received (xxx University, Faculty of Medicine, approval date and number: 29/05/2020–86529), and the patients and control subjects gave informed consent before the beginning of the study. The experimental procedures were based on the Declaration of Helsinki and relevant institutional regulations.

Patient consent for publication

Informed consent was obtained as written forms from all our patients to publish.

Additional information

Funding

The author(s) reported there is no funding associated with the work featured in this article.