Volume 21, Issue 4 (Winter 2024)
Sci J Iran Blood Transfus Organ 2024, 21(4): 273-280 |
Back to browse issues page
Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
Sharifi Z, Yadgari A, Paz Z. The level of expression of programmed death type 1 during the natural course of hepatitis B virus infection in asymptomatic carriers of hepatitis B. Sci J Iran Blood Transfus Organ 2024; 21 (4) :273-280
URL: http://bloodjournal.ir/article-1-1559-en.html
URL: http://bloodjournal.ir/article-1-1559-en.html
Abstract: (317 Views)
Abstract
Background and Objectives
During chronic hepatitis B virus infection, the dynamic balance between virus replication and the host immune response is crucial in developing liver disease. In this study, the level of expression of programmed death type 1 in asymptomatic donors infected with hepatitis B during the natural course of the infection was investigated.
Materials and Methods
In this case-control study, 120 blood donors were divided into two groups. The first control group included 60 healthy individuals who tested negative for HBsAg and anti-HBc. The second group, known as the case group, comprised 60 asymptomatic HBV-infected blood donors who tested positive for HBsAg and anti-HBc. All participants were entered from the Tehran Blood Center in 2018. To check gene expression after RNA extraction and cDNA synthesis, a Real-Time PCR test was performed for the PD-1 gene and β-actin reference gene, then using REST software, gene expression changes compared to the healthy group were checked.
Results
All the samples of asymptomatic HBV-infected blood donors were 100% positive for total anti-HBc, anti-HBe, and negative for HBe Ag. The gene expression levels were analyzed using REST software, utilizing Cycle Threshold values obtained from Real-Time PCR tests for the PD-1 gene and a reference gene. The analysis revealed 1.5 times increase in PD-1 gene expression in asymptomatic HBV-infected donors compared to healthy donors. However, this increase was not found to be statistically significant.
Conclusions
PD-1 gene expression does not change during the normal course of chronic HBV infection in asymptomatic HBV-infected donors and is similar to healthy individuals.
Background and Objectives
During chronic hepatitis B virus infection, the dynamic balance between virus replication and the host immune response is crucial in developing liver disease. In this study, the level of expression of programmed death type 1 in asymptomatic donors infected with hepatitis B during the natural course of the infection was investigated.
Materials and Methods
In this case-control study, 120 blood donors were divided into two groups. The first control group included 60 healthy individuals who tested negative for HBsAg and anti-HBc. The second group, known as the case group, comprised 60 asymptomatic HBV-infected blood donors who tested positive for HBsAg and anti-HBc. All participants were entered from the Tehran Blood Center in 2018. To check gene expression after RNA extraction and cDNA synthesis, a Real-Time PCR test was performed for the PD-1 gene and β-actin reference gene, then using REST software, gene expression changes compared to the healthy group were checked.
Results
All the samples of asymptomatic HBV-infected blood donors were 100% positive for total anti-HBc, anti-HBe, and negative for HBe Ag. The gene expression levels were analyzed using REST software, utilizing Cycle Threshold values obtained from Real-Time PCR tests for the PD-1 gene and a reference gene. The analysis revealed 1.5 times increase in PD-1 gene expression in asymptomatic HBV-infected donors compared to healthy donors. However, this increase was not found to be statistically significant.
Conclusions
PD-1 gene expression does not change during the normal course of chronic HBV infection in asymptomatic HBV-infected donors and is similar to healthy individuals.
References
1. Ganem D, Prince AM. Hepatitis B virus infection--natural history and clinical consequences. N Engl J Med 2004 ; 350(11): 1118-29. [DOI:10.1056/NEJMra031087] [PMID]
2. Lai CL, Ratziu V, Yuen MF, Poynard T. Viral hepatitis B. Lancet 2003; 20; 362(9401): 2089-94. [DOI:10.1016/S0140-6736(03)15108-2] [PMID]
3. Bertoletti A, Maini M, Williams R. Role of hepatitis B virus-specific cytotoxic T cells in liver damage and viral control. Antiviral Res 2003; 60(2): 61-6. [DOI:10.1016/j.antiviral.2003.08.012] [PMID]
4. Chisari FV, Ferrari C. Hepatitis B Virus Immunopathogenesis. Annu Rev Immunol 1995 13: 29-60. [DOI:10.1146/annurev.iy.13.040195.000333] [PMID]
5. Maini MK, Boni C, Ogg GS, King AS, Reignat S, Lee CK, et al. Direct ex vivo analysis of hepatitis B virus-specific CD8(+) T cells associated with the control of infection. Gastroenterology 1999; 117(6): 1386-96. [DOI:10.1016/S0016-5085(99)70289-1] [PMID]
6. Yuen MF, Chen DS, Dusheiko GM, Janssen HLA, Lau DTY, Locarnini SA, et al. Hepatitis B virus infection. Nat Rev Dis Primers 2018; 4: 18035. [DOI:10.1038/nrdp.2018.35] [PMID]
7. Boni C, Fisicaro P, Valdatta C, Amadei B, Di Vincenzo P, Giuberti T, et al. Characterization of hepatitis B Virus (HBV)-Specific T-Cell Dysfunction in Chronic HBV Infection. J Virol 2007; 81(42): 15-25. [DOI:10.1128/JVI.02844-06] [PMID] []
8. Ai L, Chen J, Yan H, He Q, Luo P, Xu Z, et al. Research status and outlook of pd-1/pd-l1 inhibitors for cancer therapy. Drug Des Devel Ther 2020; 14: 3625-49. [DOI:10.2147/DDDT.S267433] [PMID] []
9. Chen Y, Pei Y, Luo J, Huang Z, Yu J, Meng X. Looking for the optimal PD-1/PD-L1 inhibitor in cancer treatment: A comparison in basic structure, function, and clinical practice. Front Immunol 2020; 11:1088. [DOI:10.3389/fimmu.2020.01088] [PMID] []
10. Bengsch B, Martin B, Thimme R. Restoration of HBV-specific CD8+ T cell function by PD-1 blockade in inactive carrier patients is linked to T cell differentiation. J Hepatol 2014; 61: 1212-9. [DOI:10.1016/j.jhep.2014.07.005] [PMID]
11. Singh V, Khurana A, Allawadhi P, Banothu AK, Bharani KK, Weiskirchen R. Emerging role of PD-1/PD-L1 inhibitors in chronic liver diseases. Front Pharmacol 2021; 12: 790963. [DOI:10.3389/fphar.2021.790963] [PMID] []
12. Wieland S, Thimme R, Purcell RH, Chisari FV. Genomic analysis of the host response to hepatitis B virus infection. Proc Natl Acad Sci U S A 2004; 101(17): 6669-74. [DOI:10.1073/pnas.0401771101] [PMID] []
13. Wykes MN, Lewin SR. Immune checkpoint blockade in infectious diseases. Nat Rev Immunol 2018; 18(2): 91-104. [DOI:10.1038/nri.2017.112] [PMID] []
14. Cox MA, Nechanitzky R, Mak TW. Check point inhibitors as therapies for infectious diseases. Curr Opin Immunol 2017; 48: 61-7. [DOI:10.1016/j.coi.2017.07.016] [PMID]
15. Schönrich G, Raftery MJ. The PD-1/PD-L 1axis and virus infections: a delicate balance. Front Cell Infect Microbiol 2019; 9: 207. [DOI:10.3389/fcimb.2019.00207] [PMID] []
16. Ortega-Prieto AM, Dorner M. Immune Evasion Strategies during Chronic Hepatitis B and C Virus Infection. Vaccines (Basel) 2017; 5(3): 24. [DOI:10.3390/vaccines5030024] [PMID] []
17. Ye P, Weng ZH, Zhang SL, Zhang JA, Zhao L, Dong JH, et al. Programmed death-1 expression is associated with the disease status in hepatitis B virus infection. World J Gastroenterol 2008; 14: 4551-7. [DOI:10.3748/wjg.14.4551] [PMID] []
18. Liang XS, Zhou Y, Li CZ, Wan MB. Natural course of chronic hepatitis B is characterized by changing patterns of programmed death type-1 of CD8-positive T cells. World J Gastroenterol 2010; 16(5): 618-24. [DOI:10.3748/wjg.v16.i5.618] [PMID] []
19. Day CL, Kaufmann DE, Kiepiela P, Brown JA, Moodley ES, Reddy S, et al. PD-1 expression on HIV-specific T cells is associated with T-cell exhaustion and disease progression. Nature 2006; 443: 350-4. [DOI:10.1038/nature05115] [PMID]
20. Petrovas C, Casazza JP, Brenchley JM, Price DA, Gostick E, Adams WC, et al. PD-1 is a regulator of virus-specific CD8+ T cell survival in HIV infection. J Exp Med 2006; 203: 2281-92. [DOI:10.1084/jem.20061496] [PMID] []
21. Zhang JY, Zhang Z, Wang X, Fu JL, Yao J, Jiao Y, et al. PD-1 up-regulation is correlated with HIV-specific memory CD8+ T-cell exhaustion in typical progressors but not in long-term nonprogressors. Blood 2007; 109: 4671-8. [DOI:10.1182/blood-2006-09-044826] [PMID]
22. Golden-Mason L, Palmer B, Klarquist J, Mengshol JA, Castelblanco N, Rosen HR. Upregulation of PD-1 expression on circulating and intrahepatic hepatitis C virus-specific CD8+ T cells associated with reversible immune dysfunction. J Virol 2007; 81: 9249-58. [DOI:10.1128/JVI.00409-07] [PMID] []
23. Urbani S, Amadei B, Tola D, Massari M, Schivazappa S, Missale G, et al. PD-1 expression in acute hepatitis C virus (HCV) infection is associated with HCV-specific CD8 exhaustion. J Virol 2006; 80: 11398-403. [DOI:10.1128/JVI.01177-06] [PMID] []
24. Boni C, Fisicaro P, Valdatta C, Amadei B, Di Vincenzo P, Giuberti T, et al. Characterization of hepatitis B virus (HBV)-specific T-cell dysfunction in chronic HBV infection. J Virol 2007; 81: 4215-25. [DOI:10.1128/JVI.02844-06] [PMID] []
25. Zhou JY, Zhou DF, Li JQ. PD-1 expression in HBcAg-specific CD8+ T cells of adolescents with chronic HBV infection. Zhonghua Gan Zang Bing Za Zhi 2013; 21(1): 27-32. [Article in Chinese]
26. Cui D , Jiang D , Yan C , Liu X , Lv Y , Xie J, Chen Y. Immune Checkpoint Molecules Expressed on CD4+ T Cell Subsets in Chronic Asymptomatic Hepatitis B Virus Carriers With Hepatitis B e Antigen-Negative. Front Microbiol 2022; 13: 887408. [DOI:10.3389/fmicb.2022.887408] [PMID] []
Send email to the article author
| Rights and permissions | |
 |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |
