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March 17, 2026Open Access

Analysis of the Sting Rs11554776 (C/T) Polymorphism and Its Association With Plasma TNF-Α and Ifn-Α Levels in Covid-19 Patients

EREduarda Jullianne de Almeida RamosUniversidade Federal do Pará MQMaria Alice Freitas QueirozUniversidade Federal do Pará WBWandrey Roberto dos Santos BritoUniversidade Federal do Pará

Key Points

To evaluate the association between the STING rs11554776 (C/T) polymorphism and plasma TNF-α and IFN-α levels in COVID-19 patients.
Analyzed blood samples from 127 COVID-19 individuals (67 severe, 60 non-severe)
Identified STING rs11554776 genotypes using real-time PCR
Quantified TNF-α and IFN-α levels using flow cytometry and ELISA
Employed Mann-Whitney and Kruskal-Wallis tests for statistical analysis
No significant difference in TNF-α levels between severe and non-severe cases (p = 0.5036)
IFN-α levels were significantly higher in severe COVID-19 cases (p = 0.0020)
Genotype analysis showed no significant association with TNF-α (p = 0.5792) or IFN-α levels (p = 0.0884)

Abstract

COVID-19 encompasses a wide range of clinical manifestations, from asymptomatic or mild illness to severe and potentially fatal forms. The host immune response plays a central role in determining disease severity. Among the inflammatory mediators involved, tumor necrosis factor alpha (TNF-α) and interferon alpha (IFN-α) stand out; they are synthesized following activation of the STING pathway (Stimulator of Interferon Genes), a cytoplasmic sensor that detects viral genetic material in the cytoplasm and triggers an antiviral response. Balanced production of these cytokines is essential to prevent progression to severe COVID-19. Objectives: To evaluate the association between the STING rs11554776 (C/T) polymorphism and plasma TNF-α and IFN-α levels and their relationship with COVID-19 severity. Blood samples from 127 individuals with COVID-19 (67 severe and 60 non-severe) were analyzed. Genotypes for the STING rs11554776 (C/T) polymorphism were identified by real-time PCR, and cytokine levels were quantified by flow cytometry and ELISA. Mann-Whitney and Kruskal-Wallis tests were used for statistical analyses. There was no significant difference in TNF-α levels between severe and non-severe cases (p = 0.5036). However, IFN-α levels were higher in individuals with severe disease (p = 0.0020). Genotype evaluation (CC, CT, and TT) showed no significant association with TNF-α (p = 0.5792) or IFN-α (p = 0.0884). The results indicate that changes in TNF-α levels are not influenced by COVID-19 severity nor by the STING rs11554776 (C/T) polymorphism. Elevated IFN-α levels were associated with severe COVID-19, possibly reflecting an attempt to control viral infection, but potentially also contributing to the intensification of systemic inflammation. However, the STING rs11554776 (C/T) polymorphism is not related to variations in cytokine levels in the context of SARS-CoV-2 infection.

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