Author(s):
Nikhat Farhana, Thouheed Ansari, Moid Ansari
Email(s):
Email ID Not Available
DOI:
10.5958/0974-4150.2020.00057.7 
Address:
Nikhat Farhana1, Thouheed Ansari2, Moid Ansari3
1Anjuman-I-Islam's Kalsekar Technical Campus, Plot No. 2 and 3, Sector - 16, Near Thana Naka, Khandagao, New Panvel, Navi Mumbai, Maharashtra 410206.
2Dr. Noor Mohammed Khan General Hospital, Hafr Al-Batein, Saudi Arabia-31991.
3Sanofi Group of Pharmacies, Abha, Saudi Arabia.
*Corresponding Author
Published In:
Volume - 13,
Issue - 4,
Year - 2020
ABSTRACT:
Many viral and cellular mRNA species contain a leader sequence derived from a distant upstream site on the same gene by a process of RNA splicing. This process usually involves either nuclear functions or self-splicing of RNA molecules. Coronavirus, a cytoplasmic RNA virus, un- folds yet another mechanism of joining RNA, which involves the use of a free leader RNA molecule. This molecule is synthesized and dissociates from the template RNA, and subsequently re-associates with the template RNA at down- stream initiation sites of sub-genomic mRNAs to serve as the primer for transcription. This leader-primed transcriptional process thus generates viral mRNAs with a fused leader sequence. The purpose of the review to aggregate the anti-SARS drugs in the structural proteins from human SARS related coronavirus (SARS-CoV) while knowing little about the functional sites and possible mutations in these proteins. From a probabilistic viewpoint, we can theoretically select the amino acid pairs as potential candidates for anti-SARS drugs.
Cite this article:
Nikhat Farhana, Thouheed Ansari, Moid Ansari. Sars-CoV-2leader-RNA-primed Transcription and RNA-Splicing prevention, control and Treatment. Asian J. Research Chem. 2020; 13(4):291-298. doi: 10.5958/0974-4150.2020.00057.7
Cite(Electronic):
Nikhat Farhana, Thouheed Ansari, Moid Ansari. Sars-CoV-2leader-RNA-primed Transcription and RNA-Splicing prevention, control and Treatment. Asian J. Research Chem. 2020; 13(4):291-298. doi: 10.5958/0974-4150.2020.00057.7 Available on: https://ajrconline.org/AbstractView.aspx?PID=2020-13-4-11
REFERENCE:
1. Sturman, l. s. and Holmes, k. v. The molecular biology of coronaviruses. adv. in virus res. 28 (1983), 35-1 12
2. Lai, MM.C., Pattonc. D. andStohl- man, S. A. Replication of mouse hepatitis virus: negative-stranded RNA and replicative form RNA are of genome length. J. Virol. 44, 487492.1982
3. Massalski. A., Coulter-Mackie, M. and Dales, S. Assembly of mouse hepatitis virus strain JHM. In Biochemistry and Biology of Coronaviruses (ed. V. ter Meulen, S. Siddell and H. Wege), p. 111- 118. 1981
4. Lai, M. M. C., Brayton, P. R., Armen R. C. Patton, C. D., Pugh, C. and Stohl- Man, S. A. Mouse hepatitis virus A59: messenger RNA structure and genetic localization of the sequence divergence from the hepatotropic strain MHV 3. J. Virol. 39, 1981
5. Leibowitjz. L., Weiss, S R, Paavola, E. and Bondc W. Cell-free transla- tion of murine coronavirus RNA. J. Virol. 43,905-913.1982
6. Rottier, P. J. M., Spaan, W. J. M., Hor- Zinek, m. andVan der zeijst, B. A. M. 823. Translation of three mouse hepatitis virus (MHV-A59) subgenomic RNAs in Xenopus laevis oocytes. J. Virol. 38, 20-26.1981
7. Leibowitz, J. L., Wilhelmsen, K. C. and Bond, C. W. The virus-specific intracellular RNA species of two murine coronaviruses: MHV-A59 and MHV-JHM. Virology 114, 29-51.1981
8. Spaan, W, Delius H. Skinnerm, Armstronjg. Rottier P. Smeekens, S., Van Der Zeijst, B. A. M. and Siddell, S. G. Coronavirus mRNA synthesis in- volves fusion of noncontiguous sequences. 1983
9. Lai, M. M. C., Baric, R. S., Brayton, P. R. and Stohlman, S. A.. Character- ization of leader RNA sequences on the virion and mRNAs of mouse hepatitis virus, a cytoplasmic virus. Proc. Natl. Acad. Sci. USA 81, 3626-3630.1984
10. Lai, M. M. C., Patton, C. D. and Stohl- Man, S. A. Further characteriza- tion of mouse hepatitis virus: presence of common 5’-end nucleotides. J. Virol. 41,1982
11. Braytonp, R., Ganges, R. G. and Stohlman SA. Host cell nuclear function and murine hepatitis virus replica- tion. J. Gen. Virol. 56, 45740.1981
12. Wilhelmsenk, C., Leibowitz, J. L., Bond, C. W. and Robb, J.A. The replication of murine coronaviruses in enucleated cells. Virology 110, 225-230. 1981
13. Jacobs L, Spaan, W. J. M., Horzinek MC. and Vander Zeijst, Bam. The synthesis of the subgenomic mRNAs of mouse hepatitis virus is initiated independ- ently: evidence from UV transcriptional mapping. J. Virol. 39, 401406. 1981.
14. Baric RS, Stohlman SAand Lai MMC. Characterization of repli- cative intermediate RNA of mouse hepatitis virus: presence of leader RNA sequences on nascent chains. J. Virol. 48, 633440.1983.
15. Baric RS, Stohlman SA, Razavi MK and Lai MMC. Character- ization of leader-related small RNAs in coronavirus-infected cells: further evidence for leader-primed mechanism of transcrip- tion. Virus Res. 3, 19-33.1985
16. Makino S, StohlmanSAand Lai, MMC. Leader sequences of murine coronavirus mRNAs can be freely reassorted: evidence for the role of free leader RNA in transcription. Proc. Natl. Acad. Sci. USA. 83,4204-4208. 1986.
17. Shieh CK, SoeL, Makino S, Stohlman SA, and Lai MMC. The 5‘end sequence of murine coronavirus genome: implication for multiple fusion sites in leader-primed transcription. Virol- ogy (In press). 1986
18. Budzilowicz CJ, Wilczynski SP, and Weiss SR. Three intergenic regions of coronavirus mouse hepatitis virus strain A59 genomic RNA contain a common nucleotide sequence that is homo- logous to the 3’end of the viral mRNA leader sequence. J. Virol. 53, 834840.1985.
19. Rawlings ND, Tolle DP, Barrett AJ "Evolutionary families of peptidase inhibitors". Biochem. J. 378 (Pt 3): 705–16. 03,2004.
20. Parkin J, Cohen B "An overview of the immune system". Lancet. 357 (9270): 1777–89.06-2001.
21. Venkiteshwaran, Adith "Tocilizumab". mAbs. 1 (5): 432–438.2009.
22. Tse GM, To KF, Chan PK, et al. Pulmonary pathological features in coronavirusassociated severe acute respiratory syndrome (SARS). J Clin Pathol 2004; 57:260–5.
23. Haagmans BL, Kuiken T, Martina BE, et al. Pegulated interferon-a protects type Ipneumocytes against SARS coronavirus infection in macaques. Nat Med 2004; 10:290–3.
24. Peiris JS, Chu CM, Cheng VC, et al, HKU/UCH SARS Study Group. Clinical progressionand viral load in a community outbreak of coronavirus-associatedSARS pneumonia: a prospective study. Lancet 2003; 361:1767–72.
25. Sung JJ, Wu A, Joynt GM, et al. Severe acute respiratory syndrome: report oftreatment and outcome after a major outbreak. Thorax 2004; 59:414–20.
26. Chu CM, Cheng VC, Hung IF, et al, HKU/UCH SARS Study Group. Role of lopinavir/ritonavir in the treatment of SARS: initial virological and clinical findings. Thorax 2004;59:252–6.
27. Chan KS, Lai ST, Chu CM, et al. Treatment of severe acute respiratory syndromewith lopinavir/ritonavir: a multicenter retrospective matched cohort study. HongKong Med J 2003; 9:399–406.
28. Loutfy MR, Blatt LM, Siminovitch KA, et al. Interferon Alfacon-1 plus corticosteroidsin severe acute respiratory syndrome. A preliminary study. JAMA 2003; 290:3222–8.
29. Leung GM, Hedley AJ, Ho LM, et al. The epidemiology of severe acute respiratorysyndrome in the 2003 Hong Kong epidemic: an analysis of all 1755 patients. Ann Intern Med 2004;141:662–73.
30. Booth CM, Matukas LM, Tomlinson GA, et al. Clinical features and short-termoutcomes of 144 patients with SARS in the greater Toronto area. JAMA 2003; 289:2801–9.
31. Tan YJ, Fielding BC, Goh PY, et al. Overexpression of 7a, a protein specificallyencoded by the severe acute respiratory syndrome coronavirus, inducesapoptosis via a caspase-dependent pathway. J Virol 2004; 78:14043–7.
32. Nicholls JM, Poon LL, Lee KC, et al. Lung pathology of fatal severe acute respiratorysyndrome. Lancet 2003; 361:1773–8.
33. Fisman DN. Hemophagocytic syndrome and infection. Emerg Infect Dis 2000; 6:601–8.
34. Tsang OT, Chau TN, Choi KW, Coronavirus-positive nasopharyngeal aspirateas predictor for severe acute respiratory syndrome mortality. Emerg InfectDis 2003; 9:1381–7.
35. WHO. List of blue print priority diseases. Available at: https://www.who.int/blueprint/priority-diseases/en/. Accessed 01-7, 2019.
36. Tsang KW, Ho PL, Ooi GC, et al. A cluster of cases of severe acute respiratorysyndrome in Hong Kong. N Engl J Med 2003; 348:1977–85.
37. Ison MG, Gnann JW, Jr., Nagy-Agren S, et al. Safety and effi cacy of nebulized zanamivir in hospitalized patients with serious infl uenza. Antivir Ther 2003; 8: 183–90.
38. Duval X, van der WS, Blanchon T, et al. Effi cacy of oseltamivirzanamivir combination compared to each monotherapy for seasonal infl uenza: a randomized placebo-controlled trial. PLoS Med 2010; 7: e1000362.
39. Atiee G, Lasseter K, Baughman S, et al. Absence of pharmacokinetic interaction between intravenous peramivir and oral oseltamivir or rimantadine in humans. J Clin Pharmacol 2012; 52: 1410–19.
40. Pukrittayakamee S, Jittamala P, Stepniewska K, et al. An open-label crossover study to evaluate potential pharmacokinetic interactions between oral oseltamivir and intravenous zanamivir in healthy Thai adults. Antimicrob Agents Chemother 2011; 55: 4050–57.
41. Hung IF, To KK, Lee CK, et al. Convalescent plasma treatment reduced mortality in patients with severe pandemic infl uenza A (H1N1) 2009 virus infection. Clin Infect Dis 2011; 52: 447–56.
42. 122 Wang CH, Chung FT, Lin SM, et al. Adjuvant treatment with a mammalian target of rapamycin inhibitor, sirolimus, and steroids improves outcomes in patients with severe H1N1 pneumonia and acute respiratory failure. Crit Care Med 2014; 42: 313–21.