Expression level of interferon-stimulated genes PKR, OAS1, MX1, and ISG15 in peripheral blood mononuclear cells of COVID-19 patients: A retrospective study

Elham Jafari Maskouni , Samaneh Abbasi , Elham Mousavi , Zahra Najafimemar , Ali Mohammad Arabzadeh , Mehrdad Farrokhnia , Saeedeh Ebrahimi

›› 2024, Vol. 13 ›› Issue (3) : 111 -115.

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›› 2024, Vol. 13 ›› Issue (3) :111 -115. DOI: 10.4103/jad.jad_64_24
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Expression level of interferon-stimulated genes PKR, OAS1, MX1, and ISG15 in peripheral blood mononuclear cells of COVID-19 patients: A retrospective study
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Abstract

Objective: To explore expression level of interferon-stimulated genes PKR, OAS1, MX1, and ISG15 in peripheral blood mononuclear cells of COVID-19 patients. Methods: In this study, changes in the expression of four interferon-stimulated genes (ISGs), including PKR, OAS1, MX1, and ISG15, in peripheral blood mononuclear cells of 45 COVID-19 patients with different severities were evaluated by real-time PCR method. Results: OAS1, MX1, PKR, and ISG15 were differently expressed in COVID-19 patients with different severity. The results showed that the expression of OAS1, MX1, PKR, and ISG15 genes was significantly (P=0.001) lower in severe patients. Conclusions: Weak and defective IFN response and subsequent disruption of ISGs may be associated with COVID-19 severity.

Keywords

COVID-19 / SARS-CoV-2 / Interferon / ISGs / Severe COVID-19 / Risk factors / Interferon signaling

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Elham Jafari Maskouni, Samaneh Abbasi, Elham Mousavi, Zahra Najafimemar, Ali Mohammad Arabzadeh, Mehrdad Farrokhnia, Saeedeh Ebrahimi. Expression level of interferon-stimulated genes PKR, OAS1, MX1, and ISG15 in peripheral blood mononuclear cells of COVID-19 patients: A retrospective study. , 2024, 13 (3) : 111-115 DOI:10.4103/jad.jad_64_24

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References

[1]

Rabi FA, Al Zoubi MS, Kasasbeh GA, Salameh DM, Al—Nasser AD. SARS—CoV—2 and Coronavirus Disease 2019: What we know so far. Pathogens 2020; 9(3). DOI: 10.3390/pathogens9030231.

[2]

Wang MY, Zhao R, Gao LJ, Gao XF, Wang DP, Cao JM. SARS—CoV—2: Structure, biology, and structure—based therapeutics development. Front Cell Infect Microbiol 2020; 10: 587269. DOI: 10.3389/fcimb.2020.587269.

[3]

Wu YC, Chen CS, Chan YJ. The outbreak of COVID—19: An overview. J Chin Med Assoc 2020; 83(3): 217-220. DOI: 10.1097/jcma.0000000000000270.

[4]

Jordan RE, Adab P, Cheng KK. Covid—19: Risk factors for severe disease and death. BMJ 2020; 368: m1198. DOI: 10.1136/bmj.m1198.

[5]

Yahya BA, Saad DN, Ali SH. The effect of age and gender on the severity of coronavirus infection. Mosul J Nurs 2022; 10(2): 169-174.

[6]

Zhang Q, Bastard P, Cobat A, Casanova JL. Human genetic and immunological determinants of critical COVID—19 pneumonia. Nature 2022; 603(7902): 587-598. DOI: 10.1038/s41586-022-04447-0.

[7]

Li S, Duan X, Li Y, Li M, Gao Y, Li T, et al. Differentially expressed immune response genes in COVID—19 patients based on disease severity. Aging 2021; 13(7): 9265-9276. DOI: 10.18632/aging.202877.

[8]

Park A, Iwasaki A. Type I and type III interferons — Induction, signaling, evasion, and application to combat COVID—19. Cell Host Microbe 2020; 27(6): 870-878. DOI: 10.1016/j.chom.2020.05.008.

[9]

Vincent JL, Taccone FS. Understanding pathways to death in patients with COVID—19. Lancet Respir Med 2020; 8(5): 430-432. DOI: 10.1016/s2213-2600(20)30165-x.

[10]

Zhou Z, Ren L, Zhang L, Zhong J, Xiao Y, Jia Z, et al. Heightened innate immune responses in the respiratory tract of COVID—19 patients. Cell Host Microbe 2020; 27(6): 883-890. DOI: 10.1016/j.chom.2020.04.017.

[11]

Combes AJ, Courau T, Kuhn NF, Hu KH, Ray A, Chen WS, et al. Global absence and targeting of protective immune states in severe COVID—19. Nature 2021; 591(7848): 124-130. DOI: 10.1038/s41586-021-03234-7.

[12]

Hadjadj J, Yatim N, Barnabei L, Corneau A, Boussier J, Smith N, et al. Impaired type I interferon activity and inflammatory responses in severe COVID—19 patients. Science 2020; 369(6504): 718-724. DOI: 10.1126/science.abc6027.

[13]

Munnur D, Teo Q, Eggermont D, Lee HH, Thery F, Ho J, et al. Altered ISGylation drives aberrant macrophage—dependent immune responses during SARS—CoV—2 infection. Nat Immunol 2021; 22(11): 1416-1427. DOI: 10.1038/s41590-021-01035-8.

[14]

Wang Z, Pan H, Jiang B. Type I IFN deficiency: An immunological characteristic of severe COVID—19 patients. Signal Transduct Target Ther 2020; 5(1): 198. DOI: 10.1038/s41392-020-00306-4.

[15]

Lv LL, Yang YX, Shi TD. Effect of haptoglobin on the treatment of chronic hepatitis B with interferon. Exp Ther Med 2019; 18(2): 1417-1425.

[16]

Chen M, Hu P, Ling N, Peng H, Lei Y, Hu H, et al. Enhanced functions of peripheral γδ T cells in chronic hepatitis B infection during interferon α treatment in vivo and in vitro. PloS One 2015; 10(3): e0120086.

[17]

Ranganath N, Sandstrom TS, Fadel S, Côté SC, Angel JB. Type I interferon responses are impaired in latently HIV infected cells. Retrovirology 2016; 13: 1-9.

[18]

Lechler P, Balakrishnan S, Schaumburger J, Grässel S, Baier C, Grifka J, et al. The oncofetal gene survivin is re—expressed in osteoarthritis and is required for chondrocyte proliferation in vitro. BMC Musculoskelet Disord 2011; 12: 1-8.

[19]

King C, Sprent J. Dual nature of type I Interferons in SARS—CoV—2—induced inflammation. Trends Immunol 2021; 42(4): 312-322. DOI: 10.1016/j.it.2021.02.003.

[20]

Zhang Q, Meng Y, Wang K, Zhang X, Chen W, Sheng J, et al. Inflammation and antiviral immune response associated with severe progression of COVID—19. Front Immunol 2021; 12: 631226. DOI: 10.3389/fimmu.2021.631226.

[21]

Clark LK, Green TJ, Petit CM. Structure of nonstructural protein 1 from SARS—CoV—2. J Virol 2021; 95(4). DOI: 10.1128/jvi.02019-20.

[22]

Niranjan V, Setlur AS, Karunakaran C, Uttarkaor A, Kumar KM, Skariyachan S. Scope of repurposed drugs against the potential targets of the latest variants of SARS—CoV—2. Struct Chem 2022; 33(5): 1585-608. doi: 10.1007/s11224-022-02020-z.

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