Int J Curr Pharm Res, Vol 18, Issue 1, 8-9Review Article

THYMOSINE, A T CELL MODULATOR IN COVID-19

OMKAR KALIDASRAO CHOUDHARI1*, AMOL ANBHULE2, VIKRANT3, DISHA SATYA1

1Department of Clinical Hematology, Mahatma Gandhi Medical College and Hospital, Jaipur, Rajasthan, India. 2Department of Biochemistry, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India. 3Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India
*Corresponding author: Omkar Kalidasrao Choudhari; *Email: omkarchoudhari@yahoo.com

Received: 07 Oct 2025, Revised and Accepted: 26 Nov 2025

ABSTRACT

The pandemic of Coronavirus Disease (COVID-19) has resulted in millions of deaths worldwide, and many big cities worldwide were under lockdown to contain the infection. Though the effectiveness of vaccines varies, people were getting infected with the Virus; however, the severity of clinical manifestations was variable. Many drugs used in the treatment of COVID-19 were being redirected from their original use and were used in COVID-19. Thymosineis involved in amplifying T cell maturation and enhances the specificity. Thymosineuse could potentiate the T cell response and naturally resist infections, and could help to contain infections

Keywords: COVID-19, Thymosine, T Cell, Lymphopenia, T cell polymorphism

© 2026 The Authors. Published by Innovare Academic Sciences Pvt Ltd. This is an open access article under the CC BY license (https://creativecommons.org/licenses/by/4.0/)
DOI: https://dx.doi.org/10.22159/ijcpr.2026v18i1.8039 Journal homepage: https://innovareacademics.in/journals/index.php/ijcpr

INTRODUCTION

The pandemic of Coronavirus Disease (COVID-19) has resulted in millions of deaths worldwide, and many big cities worldwide were under lockdown to contain the infection. It's been more than 5 y since the first case was reported in Wuhan Province of the Republic of China [1]. Recently, there has been an upsurge in COVID-19 cases worldwide. Thoughthe effectiveness of vaccines varies, people were getting infected with the Virus; however, the severity of clinical manifestations were variable. Many drugs were used in the treatment of COVID-19, including antibiotics like azithromycin and doxycycline, antivirals such as Remdesivir, along corticosteroids [2]. These drugs werebeing redirected from their original use and were used in COVID-19.

Remdesivir, primarily used for treating RNA viruses, did show promising results during the earlier SARS and MERS pandemics caused by the same coronavirus [3]. Benefits were limited to cases with early presentation, where the drug is assumed to inhibit viral replication, integration into cells, and utilisation of the host machinery. The problem with the immune system in COVID-19 is that innate immunity fails to remove the virus due to faulty interferons and dysregulation of T cells [4, 5].

The inability of T cells to act, due to invasion of the cellular machinery, which leads to T cells being unable to detect the cells as foreign antigens, similar to what happens in cancerous cells in the organism. After evading immune surveillance, thetumour cells grow and metastasize, just as the COVID-19 virus [6]. Spontaneous resolutionhas been documented in some cancers, including renal cell carcinoma, Hodgkin's lymphoma, and multiple myeloma [7]. Their spontaneous resolution is attributed to T cell modulation and their regained ability to recognisetumour cells as foreign, leading to the subsequent destruction of these cells [8].

Thymosine is a hormone derived from the thymus gland, which undergoes a size reduction and is only present in rudimentary form in adults. The development of T cells and B cells occurs in haematopoietic cells, and further maturation requires the thymus and bone marrow, respectively, for them to reach maturity and effectively combat infections. Thymosine is a 38 kDa peptide hormone that is regularly synthesized by the thymus. Its concentration diminishes with age in the blood. It is involved in amplifying T cell maturation and enhances the specificity [9]. Therefore, the use of these agents could potentiate the T cell response and naturally resist infections. Moreover, it will increase the lymphocyte count and contribute to immune strength, as lymphopenia is a common finding in COVID-19 and is associated with severe infection [10, 11].

Many COVID-19 patients experience mild symptoms or no symptoms at all, while a few develop moderate to severe illness. In a family, one person may suffer from severe disease, whereas others are asymptomatic but still test positive for COVID-19 via RT-PCR. The variability in disease expression is attributed to T cell function. Numerous T cell polymorphisms are known and may contribute to the differing immune responses. Therefore, enhancing T cell activity through Thymosine might help develop a sufficient immune response to the invading pathogen and contain the infection [12].

The safety concern regarding the use of Thymosine may arise; however, these hormones do not cause any significant side effects. The serum Thymosine level correlates with the size of the Thymus, and a high level of Thymosine induces negative feedback inhibition on the Thymus gland, further reducing its size. Therefore, it can be safely used as an immune modulator to combat COVID-19 infection naturally.

CONCLUSION

Thymosine can be used as an immune booster to fight COVID-19 infection

ETHICAL CONSIDERATION

Research was carried out according to the Declaration of Helsinki

FUNDING

Nil

AUTHORS CONTRIBUTIONS

All authors have contributed equally

CONFLICT OF INTERESTS

Declared none

REFERENCES

  1. Le Page M. First known covid case was Wuhan market trader after all. New Sci. 2021 Nov 27;252(3362):18. doi: 10.1016/S0262-4079(21)02107-2, PMID 34866733.

  2. Ticinesi A, Tuttolomondo D, Nouvenne A, Parise A, Cerundolo N, Prati B. Co-administration of remdesivir and azithromycin may protect against intensive care unit admission in COVID-19 pneumonia requiring hospitalization: a real-life observational study. Antibiotics (Basel). 2022;11(7):941. doi: 10.3390/antibiotics11070941, PMID 35884195.

  3. Singh AK, Singh A, Singh R, Misra A. Remdesivir in COVID-19: a critical review of pharmacology, pre-clinical and clinical studies. Diabetes Metab Syndr. 2020;14(4):641-8. doi: 10.1016/j.dsx.2020.05.018, PMID 32428865.

  4. Silva MJ, Rodrigues YC, Lima KV, Lima LN. Innate immunity to SARS-CoV-2 infection: a review. Epidemiol Infect. 2022;150:e142. doi: 10.1017/S095026882200125X, PMID 35843719.

  5. Kalfaoglu B, Almeida Santos J, Tye CA, Satou Y, Ono M. T-cell dysregulation in COVID-19. Biochem Biophys Res Commun. 2021;538:204-10. doi: 10.1016/j.bbrc.2020.10.079, PMID 33220925.

  6. Thachil J, Khorana A, Carrier M. Similarities and perspectives on the two C's-cancer and COVID-19. J Thromb Haemost. 2021;19(5):1161-7. doi: 10.1111/jth.15294, PMID 33725410.

  7. Teixeira Ferreira R, Cardoso Ferreira I, Carmona S, Montalvao A, Santos AI. Spontaneous remission of high-grade non-Hodgkin lymphoma after SARS-CoV-2 infection: a case report. Clin Nucl Med. 2024;49(2):e77-9. doi: 10.1097/RLU.0000000000004973, PMID 38048523.

  8. Potts DA, Fromm JR, Gopal AK, Cassaday RD. Spontaneous remission of an untreated MYC and BCL2 coexpressing high-grade B-cell lymphoma: a case report and literature review. Case Rep Hematol. 2017;2017:2676254. doi: 10.1155/2017/2676254, PMID 28321348.

  9. Dominari A, Hathaway D, Pandav K, Matos W, Biswas S, Reddy G, Thevuthasan S, Khan MA, Mathew A, Makkar SS, Zaidi M, Fahem MMM, Beas R, Castaneda V, Paul T, Halpern J, Baralt D. Thymosin alpha 1: a comprehensive review of the literature. World J Virol. 2020;9(5):67-78. doi: 10.5501/wjv.v9.i5.67.

  10. Janeway CA JR, Travers P, Walport M, Shlomchik MJ. Immunobiology: the immune system in health and disease. 5th ed. New York: Garland Science; 2001. Chapter: Generation of lymphocytes in bone marrow and thymus. Available from: https://www.ncbi.nlm.nih.gov/books/NBK27123.

  11. Zhao Q, Meng M, Kumar R, Wu Y, Huang J, Deng Y. Lymphopenia is associated with severe coronavirus disease 2019 (COVID-19) infections: a systemic review and meta-analysis. Int J Infect Dis. 2020 Jul;96:131-5. doi: 10.1016/j.ijid.2020.04.086, PMID 32376308.

  12. Sookaromdee P, Wiwanitkit V. Polymorphisms and severity of COVID-19. Am J Respir Crit Care Med. 2023;207(1):112. doi: 10.1164/rccm.202208-1494LE, PMID 36041212.