Skip to content
2000
  1. Home
  2. A-Z Publications
  3. Infectious Disorders - Drug Targets (Formerly Current Drug Targets - Infectious Disorders)
  4. Volume 25, Issue 1
  5. Article
Volume 25, Issue 1
  • ISSN: 1871-5265
  • E-ISSN: 2212-3989

Abstract

Introduction

Bruton’s Tyrosine Kinase (BTK), an important element for the production of several inflammatory cytokines, may play a role in the pathogenesis of COVID-19. This study aimed to assess BTK gene expression levels in COVID-19 cases based on disease severity and outcome.

Methods

In this study, 33 hospitalized patients with COVID-19 were recruited and divided into two groups based on the severity of the disease: “mild to moderate” and “severe to critical”. A blood sample was taken from each patient, peripheral blood mononuclear cells (PBMCs) were extracted, and BTK gene expression was measured. The level of BTK gene expression was compared based on the demographic data, laboratory results, and the severity and outcome of the disease.

Results

Among the 33 patients, 22 (66.7%) were male, with nearly half having at least one underlying condition. The severity groups comprised 12 patients in the “mild to moderate” category and 21 in the “severe to critical” category, with eight (24.2%) experiencing fatal outcomes. Age, weight, and BMI showed no significant associations with BTK expression. BTK expression was notably lower in “severe to critical” and ICU-admitted cases, as well as in individuals with low O saturation. However, no significant difference in BTK expression was observed between cured and deceased patients ( = 0.117).

Conclusion

BTK gene expression in PBMCs exhibited an inverse correlation with COVID-19 severity. However, no difference was found between BTK expression and disease outcome.

© 2025 Bentham Science Publishers
Loading

Article metrics loading...

/content/journals/iddt/10.2174/0118715265301312240529044923
2024-06-27
2025-04-02

  • From This Site

    /content/journals/iddt/10.2174/0118715265301312240529044923
    dcterms_title,dcterms_subject,pub_keyword
    -contentType:Contributor -contentType:Concept -contentType:Institution
    10
    5
Loading full text...

Full text loading...

References

  1. TalS. SpectreG. KornowskiR. PerlL. Venous thromboembolism complicated with COVID-19: What do we know so far?Acta Haematol.2020143541742410.1159/000508233 32396903
     [Google Scholar]
  2. MahmoudiS. RezaeiM. MansouriN. MarjaniM. MansouriD. Immunologic features in coronavirus disease 2019: Functional exhaustion of T cells and cytokine storm.J. Clin. Immunol.202040797497610.1007/s10875‑020‑00824‑4 32648027
     [Google Scholar]
  3. MohammadpourH. ZiaiA. SadrM. RezaeiM. MarjaniM. TabarsiP. A novel coronavirus disease (COVID-19): A review of host cell signaling pathways.Tanaffos2020192108111 33262797
     [Google Scholar]
  4. Ghazizadeh EsslamiG. MamishiS. PourakbariB. MahmoudiS. Systematic review and meta‐analysis on the serological, immunological, and cardiac parameters of the multisystem inflammatory syndrome (MIS‐C) associated with SARS‐CoV‐2 infection.J. Med. Virol.2023957e2892710.1002/jmv.28927 37436781
     [Google Scholar]
  5. McDonaldC. XanthopoulosC. KostareliE. The role of Bruton’s tyrosine kinase in the immune system and disease.Immunology2021164472273610.1111/imm.13416 34534359
     [Google Scholar]
  6. López-Herrera G, Vargas-Hernández A, González-Serrano ME, et al. Bruton’s tyrosine kinase—an integral protein of B cell development that also has an essential role in the innate immune system.J Leukoc Biol20139522435010.1189/jlb.0513307 24249742
     [Google Scholar]
  7. WeberA.N.R. BittnerZ. LiuX. DangT.M. RadsakM.P. BrunnerC. Bruton’s tyrosine kinase: An emerging key player in innate immunity.Front. Immunol.20178145410.3389/fimmu.2017.01454 29167667
     [Google Scholar]
  8. YeB. ZhouC. GuoH. ZhengM. Effects of BTK signalling in pathogenic microorganism infections.J. Cell. Mol. Med.201923106522652910.1111/jcmm.14548 31397086
     [Google Scholar]
  9. RoschewskiM. LionakisM.S. SharmanJ.P. Inhibition of Bruton tyrosine kinase in patients with severe COVID-19.Sci. Immunol.2020548eabd011010.1126/sciimmunol.abd0110 32503877
     [Google Scholar]
  10. RezaeiM. BabamahmoodiA. MarjaniM. Bruton’s tyrosine kinase: A promising target for the treatment of COVID-19.Tanaffos20201928588 33262793
     [Google Scholar]
  11. RezaeiM. BaratiS. BabamahmoodiA. DastanF. MarjaniM. The possible role of bruton tyrosine kinase inhibitors in the treatment of COVID-19: A review.Curr. Ther. Res. Clin. Exp.20229610065810.1016/j.curtheres.2021.100658 34931090
     [Google Scholar]
  12. Coronavirus disease 2019 (COVID-19) treatment guidelines.2023 Available from: https://www.covid19treatmentguidelines.nih.gov/ cited March 31, 2023.
  13. McGonagleD. SharifK. O’ReganA. BridgewoodC. The role of cytokines including interleukin-6 in COVID-19 induced pneumonia and macrophage activation syndrome-like disease.Autoimmun. Rev.202019610253710.1016/j.autrev.2020.102537 32251717
     [Google Scholar]
  14. BorczukA.C. YantissR.K. The pathogenesis of coronavirus-19 disease.J. Biomed. Sci.20222918710.1186/s12929‑022‑00872‑5 36289507
     [Google Scholar]
  15. SamelsonL.E. Immunoreceptor signaling.Cold Spring Harb. Perspect. Biol.2011312a01151010.1101/cshperspect.a011510 22134888
     [Google Scholar]
  16. LiuY. Bruton’s Tyrosine Kinase: Structure and Functions.Expression and Mutations2013
     [Google Scholar]
  17. DuZ. LovlyC.M. Mechanisms of receptor tyrosine kinase activation in cancer.Mol. Cancer20181715810.1186/s12943‑018‑0782‑4 29455648
     [Google Scholar]
  18. MohamedAJ YuL Bäckesjö CM, et al. Bruton’s tyrosine kinase (Btk): Function, regulation, and transformation with special emphasis on the PH domain.Immunol. Rev.20092281587310.1111/j.1600‑065X.2008.00741.x 19290921
     [Google Scholar]
  19. TreonS.P. CastilloJ.J. SkarbnikA.P. The BTK inhibitor ibrutinib may protect against pulmonary injury in COVID-19–infected patients.Blood2020135211912191510.1182/blood.2020006288 32302379
     [Google Scholar]
  20. RedaG. NotoA. CassinR. Reply to “CLL and COVID-19 at the hospital clinic of Barcelona: An interim report” Analysis of six hematological centers in lombardy.Leukemia20203492531253210.1038/s41375‑020‑0966‑y 32753689
     [Google Scholar]
  21. Scarfò L, Chatzikonstantinou T, Rigolin GM, et al. COVID-19 severity and mortality in patients with chronic lymphocytic leukemia: A joint study by ERIC, the European Research Initiative on CLL, and CLL Campus.Leukemia 202034923546310.1038/s41375‑020‑0959‑x 32647324
     [Google Scholar]
  22. ThibaudS. TremblayD. BhallaS. ZimmermanB. SigelK. GabriloveJ. Protective role of Bruton tyrosine kinase inhibitors in patients with chronic lymphocytic leukaemia and COVID‐19.Br. J. Haematol.20201902e73e7610.1111/bjh.16863 32433778
     [Google Scholar]
  23. GomesA.M.C. FariasG.B. TrombettaA.C. Phenotype of BTK ‐lacking myeloid cells during prolonged COVID ‐19 and upon convalescent plasma.Eur. J. Haematol.2023110220921210.1111/ejh.13881 36208028
     [Google Scholar]
  24. SoresinaA. MorattoD. ChiariniM. Two X‐linked agammaglobulinemia patients develop pneumonia as COVID‐19 manifestation but recover.Pediatr. Allergy Immunol.202031556556910.1111/pai.13263 32319118
     [Google Scholar]
  25. AnS. LiY. LinY. Genome-wide profiling reveals alternative polyadenylation of innate immune-related mRNA in patients With COVID-19.Front. Immunol.20211275628810.3389/fimmu.2021.756288 34777369
     [Google Scholar]
  26. GandhiR.T. LynchJ.B. del RioC. Mild or moderate COVID-19.N. Engl. J. Med.2020383181757176610.1056/NEJMcp2009249 32329974
     [Google Scholar]
  27. BerlinD.A. GulickR.M. MartinezF.J. Severe Covid-19.N. Engl. J. Med.2020383252451246010.1056/NEJMcp2009575 32412710
     [Google Scholar]
  28. WangF. NieJ. WangH. Characteristics of peripheral lymphocyte subset alteration in COVID-19 pneumonia.J. Infect. Dis.2020221111762176910.1093/infdis/jiaa150 32227123
     [Google Scholar]
  29. ClaudeL. MartinoF. HermandP. Platelet caspase‐1 and Bruton tyrosine kinase activation in patients with COVID‐19 is associated with disease severity and reversed in vitro by ibrutinib.Res. Pract. Thromb. Haemost.202268e1281110.1002/rth2.12811 36514346
     [Google Scholar]
  30. ParkA. IwasakiA. Type I and type III interferons – Induction, signaling, evasion, and application to combat COVID-19.Cell Host Microbe202027687087810.1016/j.chom.2020.05.008 32464097
     [Google Scholar]
  31. FlorenceJ.M. KrupaA. BooshehriL.M. DavisS.A. MatthayM.A. KurdowskaA.K. Inhibiting Bruton’s tyrosine kinase rescues mice from lethal influenza-induced acute lung injury.Am. J. Physiol. Lung Cell. Mol. Physiol.20183151L52L5810.1152/ajplung.00047.2018 29516781
     [Google Scholar]
/content/journals/iddt/10.2174/0118715265301312240529044923
Loading
The Relationship between the Clinical Course of SARS-CoV-2 Infections and Expression of Bruton's Tyrosine Kinase
Infect. Disord. Drug Targets 25, E270624231361 (2025); https://doi.org/10.2174/0118715265301312240529044923
/content/journals/iddt/10.2174/0118715265301312240529044923
/content/journals/iddt/10.2174/0118715265301312240529044923
Loading

Data & Media loading...


  • Article Type:     Research Article
Keyword(s): BMI; Bruton’s Tyrosine Kinase; COVID-19; gene expression; potients; SARS-CoV-2

Most Cited Most Cited RSS feed

This is a required field
Please enter a valid email address
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error
Please enter a valid_number test