Volume 8, Issue 2 (4-2020)                   JoMMID 2020, 8(2): 65-70 | Back to browse issues page

XML Print

Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
Teimouri H, Maali A. Single-Nucleotide Polymorphisms in Host Pattern-Recognition Receptors Show Association with Antiviral Responses against SARS-CoV-2, in-silico Trial. JoMMID 2020; 8 (2) :65-70
URL: http://jommid.pasteur.ac.ir/article-1-250-en.html
Single-Nucleotide Polymorphisms in Host Pattern-Recognition Receptors Show Association with Antiviral Responses against SARS-CoV-2, in-silico Trial
Hossein Teimouri , Amirhosein Maali *
Pasteur Institute of Iran
Abstract:   (3754 Views)
Introduction: Coronavirus infectious disease 2019 (COVID-19) is a viral infection caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Pathogen-associated molecular patterns (PAMPs) can be detected by host pattern-recognition receptors (PRRs) expressed in inherent immune cells. The polymorphisms in PRRs leads to different recognizing and immune responses against viral infections. Methods: Single-nucleotide polymorphisms of PRRs, minor allele frequency (MAF), and their geographical distribution were obtained from the Ensembl genome database. Interaction between the common polymorphic forms of PRRs (including TLR3, TLR7, RIG-1, and MDA-5) and SARS-CoV-2 virus genome (dsRNA) were predicted using the hybrid protein-RNA docking algorithm HDOCK server. Also, the global distribution of common SNPs and their MAFs were statistically analyzed using SPSS, ver.16. Results: The wild-type TLR3 and TLR3 SNP rs73873710 had the same docking energy score (-330.48 kcal/mol), and had lower docking energy scores compared to the other two SNPs, rs3775290 and rs3775291 (-301.42 and -295.81 kcal/mol, respectively). TLR7 SNP rs179008 had a higher docking energy score (-423.03 kcal/mol), comparing to the wild-type TLR7 (-445.46 kcal/mol). Also, there was a statistically significant direct relationship between MAF of TLR3 SNP rs3775290 and rs3775291 with SARS-CoV-2 prevalence (P=0.021 and P=0.023, respectively) and prevalence/population ratio of COVID-19 (P=0.026 and P<0.001, respectably). Conclusion: Wild-type TLR3 and TLR3 SNP rs73873710 can recognize the SARS-CoV-2 dsRNA genome through a better performance compared to TLR3 SNP rs3775290 and TLR3 SNP rs3775291. Therefore, our in-silico study established that PRRs SNPs are associated with antiviral responses against SARS-CoV-2.
Keywords: COVID-19, Severe Acute Respiratory Syndrome Coronavirus 2, Polymorphism, Single Nucleotide, Pathogen-Associated, Molecular Pattern Molecules
Full-Text [PDF 481 kb]   (1479 Downloads)    
Type of Study: Original article | Subject: Host-pathogen interactions and susceptibility factors
Received: 2020/06/5 | Accepted: 2020/04/13 | Published: 2020/08/16
References
1. 1. Li Q, Guan X, Wu P, Wang X, Zhou L, Tong Y, et al. Early Transmission Dynamics in Wuhan, China, of Novel Coronavirus-Infected Pneumonia. N Engl J Med. 2020;382(13):1199-207. [DOI:10.1056/NEJMoa2001316]
2. WHO. Coronavirus disease 2019 (COVID-19) Situation Report. Available on https://www.who.int/emergencies/diseases/novel-coronavirus-2019.
3. Chen Y, Liu Q, Guo D. Emerging coronaviruses: Genome structure, replication, and pathogenesis. J Med Virol. 2020;92(4):418-23. [DOI:10.1002/jmv.25681]
4. Kawai T, Akira S. Innate immune recognition of viral infection. Nat Immunol. 2006;7(2):131-7. [DOI:10.1038/ni1303]
5. Li G, Fan Y, Lai Y, Han T, Li Z, Zhou P, et al. Coronavirus infections and immune responses. J Med Virol. 2020;92(4):424-32. [DOI:10.1002/jmv.25685]
6. Lu X, Pan J, Tao J, Guo D. SARS-CoV nucleocapsid protein antagonizes IFN-beta response by targeting initial step of IFN-beta induction pathway, and its C-terminal region is critical for the antagonism. Virus Genes. 2011;42(1):37-45. [DOI:10.1007/s11262-010-0544-x]
7. Hu W, Yen YT, Singh S, Kao CL, Wu-Hsieh BA. SARS-CoV regulates immune function-related gene expression in human monocytic cells. Viral Immunol. 2012;25(4):277-88. [DOI:10.1089/vim.2011.0099]
8. Totura AL, Whitmore A, Agnihothram S, Schafer A, Katze MG, Heise MT, et al. Toll-Like Receptor 3 Signaling via TRIF Contributes to a Protective Innate Immune Response to Severe Acute Respiratory Syndrome Coronavirus Infection. mBio. 2015;6(3):e00638-15. [DOI:10.1128/mBio.00638-15]
9. E Christopher M, P Wong J. Use of toll-like receptor 3 agonists against respiratory viral infections. Anti-Inflammatory Anti-Allergy Agents in Medicinal Chemistry. 2011;10(5):327-38. [DOI:10.2174/1871523011109050327]
10. de Wilde AH, Snijder EJ, Kikkert M, van Hemert MJ. Host factors in coronavirus replication. Roles of Host Gene and Non-coding RNA Expression in Virus Infection: Springer; 2017. p. 1-42. [DOI:10.1007/82_2017_25]
11. Li Y, Chen M, Cao H, Zhu Y, Zheng J, Zhou HJ. Extraordinary GU-rich single-strand RNA identified from SARS coronavirus contributes an excessive innate immune response. Microbes infection. 2013;15(2):88-95. [DOI:10.1016/j.micinf.2012.10.008]
12. Zhao X, Chu H, Wong BH-Y, Chiu MC, Wang D, Li C, et al. Activation of C-Type Lectin Receptor and (RIG)-I-Like Receptors Contributes to Proinflammatory Response in Middle East Respiratory Syndrome Coronavirus-Infected Macrophages. The Journal of Infectious Diseases. 2020;221(4):647-59. [DOI:10.1093/infdis/jiz483]
13. Arpaia N, Barton GMJ. Toll-like receptors: key players in antiviral immunity. Current opinion in virology. 2011;1(6):447-54. [DOI:10.1016/j.coviro.2011.10.006]
14. Yu M, Levine SJJ. Toll-like receptor 3, RIG-I-like receptors and the NLRP3 inflammasome: key modulators of innate immune responses to double-stranded RNA viruses. Cytokine growth factor reviews. 2011;22(2):63-72. [DOI:10.1016/j.cytogfr.2011.02.001]
15. Tuvshinjargal N, Lee W, Park B, Han KJ. PRIdictor: protein-RNA interaction predictor. Biosystems. 2016;139:17-22. [DOI:10.1016/j.biosystems.2015.10.004]
16. Yan Y, Zhang D, Zhou P, Li B, Huang S-YJ. HDOCK: a web server for protein-protein and protein-DNA/RNA docking based on a hybrid strategy. Nucleic acids research. 2017;45(W1):W365-W73. [DOI:10.1093/nar/gkx407]
17. Yan Y, Huang S-YJ. Pushing the accuracy limit of shape complementarity for protein-protein docking. BMC bioinformatics. 2019;20(25):696. [DOI:10.1186/s12859-019-3270-y]
18. Rokni M, Ghasemi V, Tavakoli Z. Immune responses and pathogenesis of SARS-CoV-2 during an outbreak in Iran: Comparison with SARS and MERS. Rev Med Virol. 2020.
19. Sheahan T, Morrison TE, Funkhouser W, Uematsu S, Akira S, Baric RS, et al. MyD88 is required for protection from lethal infection with a mouse-adapted SARS-CoV. PLoS pathogens. 2008;4(12). [DOI:10.1371/journal.ppat.1000240]
20. Guillot L, Le Goffic R, Bloch S, Escriou N, Akira S, Chignard M, et al. Involvement of toll-like receptor 3 in the immune response of lung epithelial cells to double-stranded RNA and influenza A virus. Journal of Biological Chemistry. 2005;280(7):5571-80. [DOI:10.1074/jbc.M410592200]
21. Hewson CA, Jardine A, Edwards MR, Laza-Stanca V, Johnston SLJ. Toll-like receptor 3 is induced by and mediates antiviral activity against rhinovirus infection of human bronchial epithelial cells. Journal of virology. 2005;79(19):12273-9. [DOI:10.1128/JVI.79.19.12273-12279.2005]
22. Huang S, Wei W, Yun YJ. Upregulation of TLR7 and TLR3 gene expression in the lung of respiratory syncytial virus infected mice. Acta microbiologica Sinica. 2009;49(2):239-45.
23. Wong J, Christopher M, Viswanathan S, Dai X, Salazar A, Sun L-Q, et al. Antiviral role of toll-like receptor-3 agonists against seasonal and avian influenza viruses. Current pharmaceutical design. 2009;15(11):1269-74. [DOI:10.2174/138161209787846775]
24. Wang Q, Nagarkar DR, Bowman ER, Schneider D, Gosangi B, Lei J, et al. Role of double-stranded RNA pattern recognition receptors in rhinovirus-induced airway epithelial cell responses. The Journal of Immunology. 2009;183(11):6989-97. [DOI:10.4049/jimmunol.0901386]
25. Sironi M, Biasin M, Cagliani R, Forni D, De Luca M, Saulle I, et al. A common polymorphism in TLR3 confers natural resistance to HIV-1 infection. The Journal of Immunology. 2012;188(2):818-23. [DOI:10.4049/jimmunol.1102179]
26. Rong Y, Song H, You S, Zhu B, Zang H, Zhao Y, et al. Association of Toll-like receptor 3 polymorphisms with chronic hepatitis B and hepatitis B-related acute-on-chronic liver failure. Inflammation. 2013;36(2):413-8. [DOI:10.1007/s10753-012-9560-4]
27. Huang X, Li H, Wang J, Huang C, Lu Y, Qin X, et al. Genetic polymorphisms in Toll-like receptor 3 gene are associated with the risk of hepatitis B virus-related liver diseases in a Chinese population. Gene. 2015;569(2):218-24. [DOI:10.1016/j.gene.2015.05.054]
28. Barkhash AV, Voevoda MI, Romaschenko AGJ. Association of single nucleotide polymorphism rs3775291 in the coding region of the TLR3 gene with predisposition to tick-borne encephalitis in a Russian population. Antiviral research. 2013;99(2):136-8. [DOI:10.1016/j.antiviral.2013.05.008]
29. Ishizaki Y, Takemoto M, Kira R, Kusuhara K, Torisu H, Sakai Y, et al. Association of toll-like receptor 3 gene polymorphism with subacute sclerosing panencephalitis. Journal of neurovirology. 2008;14(6):486-91. [DOI:10.1080/13550280802298120]
30. Mukherjee S, Tripathi AJ. Contribution of Toll like receptor polymorphisms to dengue susceptibility and clinical outcome among eastern Indian patients. Immunobiology. 2019;224(6):774-85. [DOI:10.1016/j.imbio.2019.08.009]
31. Sghaier I, Zidi S, Mouelhi L, Ghazoueni E, Brochot E, Almawi W, et al. TLR3 and TLR4 SNP variants in the liver disease resulting from hepatitis B virus and hepatitis C virus infection. British journal of biomedical science. 2019;76(1):35-41. [DOI:10.1080/09674845.2018.1547179]
32. Mosaad YM, Metwally SS, Farag RE, Lotfy ZF, AbdelTwab HEJ. Association between toll-like receptor 3 (TLR3) rs3775290, TLR7 rs179008, TLR9 rs352140 and chronic HCV. Immunological investigations. 2019;48(3):321-32. [DOI:10.1080/08820139.2018.1527851]
33. Huang C, Wang Y, Li X, Ren L, Zhao J, Hu Y, et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. The Lancet. 2020;395(10223):497-506. [DOI:10.1016/S0140-6736(20)30183-5]
Add your comments about this article : Your username or Email:
CAPTCHA
Send email to the article author

Rights and permissions
Creative Commons License This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.