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RNA Interference: Antiviral Defense Mechanism and Immune Memory

Received: 14 July 2020    Accepted: 5 August 2020    Published: 7 September 2020
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Abstract

A review of the mechanisms of the generation of antiviral immunity in bacteria, plants, invertebrates, and vertebrates directly indicates the leading role of innate immunity. Bornovirus infections in mammals have been proven to be inhibited by the RNA interference mechanism. Authors propose a possible role of innate human immunity in combating viral infections, including SARS-Cov2. This hypothesis is based on the notion that antiviral response involves a molecular mechanism of RNA interference stemming from the specific viral patterns incorporated into host cells’ DNA. Innate immunity plays an important role not only at the first encounter with a viral infection, but also fully participates in the formation of specific immune memory. RNA-interference along with interferon system is integral parts of human anti-viral defense system. The joint work of these systems is considered. Caution is warranted in both PCR testing interpretation and in assessing prospective vaccines. False positive result without any clinical presentation of the disease in some people might mean that PCR test was picking up any specific SARS-Cov2 sequences that already had incorporated into asymptomatic person’s cellular DNA due to the possible RNA-interference based anti-viral immunity. Future vaccines aimed at producing specific antibodies can cause the phenomenon of antibody-dependent enhancement (ADE) of the infection. In ADE virus not only infects susceptible cells through appropriate receptor, but is able to highjack virus-specific antibodies to easily traffic virus bodies inside the monocytes/macrophages, granulocytes, platelets, mast and many more host cells through interaction with Fc and/or complement receptors. It is necessary to draw the attention of medical community, especially practitioners to the role of innate immunity, which is especially important in the current COVID-19 pandemic.

Published in Advances in Applied Physiology (Volume 5, Issue 2)
DOI 10.11648/j.aap.20200502.13
Page(s) 24-29
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

RNA-Interference, Innate Immune Memory, Antiviral Immunity, COVID-19, ADE

References
[1] Reimer-Michalski EM, Conrath U. Innate immune memory in plants. Semin Immunol (2016) 28: 319–27. doi: 10.1016/j.smim.2016.05.006.
[2] Zhang T, Qiu L, Sun Z, Wang L, Zhou Z, Liu R, et al. The specifically enhanced cellular immune responses in Pacific oyster (Crassostreagigas) against secondary challenge with Vibrio splendidus. Dev Comp Immunol (2014) 45: 141–50. doi: 10.1016/j.dci.2014.02.015.
[3] Pope EC, Powell A, Roberts EC, Shields RJ, Wardle R, Rowley AF. Enhanced cellular immunity in shrimp (Litopenaeusvannamei) after “vaccination”. PLoS One (2011) 6: e20960. doi: 10.1371/journal.pone.0020960.
[4] Wu G, Li M, Liu Y, Ding Y, Yi Y. The specificity of immune priming in silkworm, Bombyxmori, is mediated by the phagocytic ability of granular cells. J Insect Physiol (2015) 81: 60–8. doi: 10.1016/j.jinsphys.2015.07.004.
[5] Kurtz J. Specific memory within innate immune systems. Trends Immunol (2005) 26: 186–92. doi: 10.1016/j.it.2005.02.001.
[6] Chester KS. The problem of acquired physiological immunity in plants. Q Rev Biol. 1933; 8: 275–324.
[7] Ross AF. Localized acquired resistance to plant virus infection in hypersensitive hosts. Virology. 1961; 14: 329–339.
[8] Diana Boraschi and Paola Italiani. Innate Immune Memory: Time for Adopting a Correct Terminology. Front. Immunol., 19 April 2018 | https: //doi.org/10.3389/fimmu.2018.00799.
[9] Agrawal AA, Laforsch C, Tollrian R. Transgenerational induction of defences in animals and plants. Nature (1999) 401: 60–3. doi: 10.1038/43425.
[10] Mackaness G. B. The immunological basis of acquired cellular resistance. J. Exp. Med. 1964; 120: 105-120.
[11] Cynthia Castro-Vargas et al. Potential Mechanism Related to Immune Priming within But Not across Generations. Front. Microbiol., 28 March 2017. doi.org/10.3389/fmicb.2017.00473.
[12] Mihai G. Netea, Jessica Quintin, Jos W. M. van der Meer. Trained Immunity: A Memory for Innate Host Defense. PERSPECTIVE| VOLUME 9, ISSUE 5, P355-361, MAY 19, 2011 doi.org/10.1016/j.chom.2011.04.006.
[13] RodolpheBarrangou. The Roles of CRISPR-Cas Systems in Adaptive Immunity and Beyond. Current Opinion in Immunology. 32: 36–41. doi: 10.1016/j.coi.2014.12.008.
[14] Eugene V. Koonin, Kira S. Makarova. Mobile Genetic Elements and Evolution of CRISPR-Cas Systems: All the Way There and Back. Genome Biology and Evolution, Volume 9, Issue 10, October 2017, Pages 2812–2825, doi.org/10.1093/gbe/evx192.
[15] Fire A., Xu S., Montgomery M., Kostas S., Driver S., Mello C. Potent and specific genetic interference by double-stranded RNA in Caenorhabditiselegans. Nature. 1998. Vol. 391, 6669. P. 806—811. doi: 10.1038/35888.
[16] Byung-Chun Yoo et al. A Systemic Small RNA Signaling System in Plants. Plant Cell. 2004 Aug; 16 (8): 1979–2000. doi: 10.1105/tpc.104.023614.
[17] Shou-Wei Dingand Olivier Voinnet. Antiviral Immunity Directed by Small RNAs. Cell. 2007 Aug 10; 130 (3): 413–426. doi: 10.1016/j.cell.2007.07.039.
[18] Cordula Kemp and Jean-Luc Imler. Antiviral immunity in drosophila. CurrOpinImmunol. 2009 Feb; 21 (1): 3–9. Published online 2009 Feb 14. doi: 10.1016/j.coi.2009.01.007.
[19] Peter Sarkies, Eric A Miska. RNAi Pathways in the Recognition of Foreign RNA: Antiviral Responses and Host-Parasite Interactions in Nematodes. BiochemSoc Trans. 2013 Aug; 41 (4): 876-80. doi: 10.1042/BST20130021.
[20] RoghiyhAliyari and Shou-Wei Ding. RNA-based viral immunity initiated by the Dicer family of host immune receptors. Immunol Rev. 2009 Jan; 227 (1): 176–188. doi: 10.1111/j.1600-065X.2008.00722.
[21] Pierre V Maillard, Annemarthe G van der Veen, Enzo Z Poirier, Caetano Reis e Sousa. Slicing and dicing viruses: antiviral RNA interference in mammals. EMBO J.2019. 38: e100941 doi.org/10.15252/embj.2018100941.
[22] Zhang Y, Li Y. Regulation of innate receptor pathways by microRNAs. Sci China Life Sci. 2013 Jan; 56 (1): 13-8. doi: 10.1007/s11427-012-4428-2. Epub 2012 Dec 27.
[23] Yingke Li, Xueyin Shi. Micro RNAs in the Regulation of TLR and RIG-I Pathways. Cell MolImmunol. 2013 Jan; 10 (1): 65-71. doi: 10.1038/cmi.2012.55.
[24] Jiaxi Wu, Zhijian J Chen. Innate Immune Sensing and Signaling of Cytosolic Nucleic Acids. Annu Rev Immunol. 2014; 32: 461-88. doi: 10.1146 /annurev-immunol-032713-120156.
[25] Annemarthe G van der Veen et al. The RIG-I-like receptor LGP2 inhibits Dicer-dependent processing of long double-stranded RNA and blocks RNA interference in mammalian cells. EMBO J. 2018 Feb 15; 37 (4): e97479. doi: 10.15252/embj.201797479.
[26] Ian G. Cannell, Yi Wen Kong, Martin Bushell. How do microRNAs regulate gene expression? Biochem Soc Trans (2008) 36 (6): 1224–1231. https://doi.org/10.1042/BST0361224.
[27] LalehHabibi and HamzehSalmani. Pivotal Impacts of Retrotransposon Based Invasive RNAs on Evolution. Front. Microbiol., 10 October 2017 | doi.org/10.3389/fmicb.2017.01957.
[28] W Wei, T A Morrish, R S Alisch, J V Moran. A Transient Assay Reveals That Cultured Human Cells Can Accommodate Multiple LINE-1 Retrotransposition Events. Anal Biochem. 2000 Sep 10; 284 (2): 435-8. doi: 10.1006/abio.2000.4675.
[29] Lander ES, Linton LM, Birren B, Nusbaum C, Zody MC, Baldwin J, et al. (February 2001). "Initial sequencing and analysis of the human genome". Nature. 409 (6822): 860–921. doi: 10.1038/35057062.
[30] Wicker T, Sabot F, Hua-Van A, Bennetzen JL, Capy P, Chalhoub B, Flavell A, Leroy P, Morgante M, Panaud O, Paux E, San Miguel P, Schulman AH (December 2007). "A unified classification system for eukaryotic transposable elements". Nature Reviews. Genetics. 8 (12): 973–82. doi: 10.1038/nrg2165.
[31] Song, Ji-Joon, Stephanie K. Smith, Gregory J. Hannon, Leemor Joshua-Tor. 2004. Crystal Structure of Argonaute and Its Implications for RISC Slicer Activity. Science 305: 1434-1437.
[32] Meister, Gunter, and Thomas Tuschi. 2004. Mechanisms of Gene Silencing by Double Stranded RNA. Nature 431: 343-349.
[33] K Onomoto, M Yoneyama, T Fujita. Regulation of Antiviral Innate Immune Responses by RIG-I Family of RNA Helicases. Curr Top MicrobiolImmunol. 2007; 316: 193-205. doi: 10.1007/978-3-540-71329-6_10.
[34] Agnieszka Jabłońska, Edyta Paradowska. Role of the RIG-I-like Receptors in Antiviral Response. Postepy Hig Med Dosw (Online). 2014 Jan 2; 68: 541-56. DOI: 10.5604/17322693.1102281.
[35] Amir Apelbaum, GanitYarden, ShiraWarszawski, Daniel Harari, and Gideon Schreiber. Type I Interferons Induce Apoptosis by Balancing cFLIP and Caspase-8 Independent of Death Ligands. Mol Cell Biol. 2013 Feb; 33 (4): 800–814. doi: 10.1128/MCB.01430-12.
[36] Kevin P. Kotredes and Ana M. Gamero. Interferons as Inducers of Apoptosis in Malignant Cells. J Interferon Cytokine Res. 2013 Apr; 33 (4): 162–170. doi: 10.1089/jir.2012.0110.
[37] David E. Levy. Whence Interferon? Variety in the Production of Interferon in Response to Viral Infection. J Exp Med. 2002 Feb 18; 195 (4): f15–f18. doi: 10.1084/jem.20020075.
[38] Daniel B. Stetson and RuslanMedzhitov. Type IInterferons in Host Defense. Immunity. Volume 25, Issue 3, September 2006, Pages 373-381. doi.org/10.1016/j.immuni.2006.08.007.
[39] Julie Eggenberger, Daniel Blanco-Melo, MarylinePanis, Kristen J. Brennand, and Benjamin R. tenOever. Type I interferon response impairs differentiation potential of pluripotent stem cells. PNAS January 22, 2019 116 (4) 1384-1393; doi.org/10.1073/pnas.1812449116.
[40] RuslanMedzhitov. Approaching the Asymptote: 20 Years Later. Immunity. 2009 Jun 19; 30 (6): 766-75. doi: 10.1016/j.immuni.2009.06.004.
[41] KanFujino, Masayuki Horie, Tomoyuki Honda, Dana K. Merriman, and KeizoTomonaga. Inhibition of Borna disease virus replication by an endogenous bornavirus-like element in the ground squirrel genome. PNAS September 9, 2014 111 (36) 13175-1318, doi.org/10.1073/pnas.1407046111.
[42] Tomoyuki HondaandKeizoTomonaga. Endogenous Non-Retroviral RNA Virus Elements Evidence a Novel Type of Antiviral Immunity. Comment Mob Genet Elements. 2016 Mar 22; 6 (3): e1165785. doi: 10.1080/2159256X.2016.1165785.
[43] NICHOLAS F. PARRISH et al. piRNAs derived from ancient viral processed pseudogenesas transgenerational sequence-specific immune memory in mammals. RNA. 2015. (10): 1691-703. doi: 10.1261/rna.052092.115.
[44] Horie M, Kobayashi Y, Suzuki Y, Tomonaga K. Comprehensive analysis of endogenous bornavirus-like elements in eukaryote genomes. Philos Trans R SocLond B Biol Sci. 2013; 368 (1626): 20120499. Published 2013 Aug 12. doi: 10.1098/rstb.2012.0499.
[45] Daniel Gebert, Hans Zischler, David Rosenkranz. Primate piRNA Cluster Evolution Suggests Limited Relevance of Pseudogenes in piRNA-Mediated Gene Regulation. Genome Biology and Evolution, Volume 11, Issue 4, April 2019, Pages 1088–1104, https://doi.org/10.1093/gbe/evz060.
[46] Gebert D, Rosenkranz D. RNA-based regulation of transposon expression. Wiley Interdiscip Rev RNA. 2015; 6 (6): 687-708. doi: 10.1002/wrna.1310.
[47] Holtzman, J., Lee, H. Emerging role of extracellular vesicles in the respiratory system. Exp Mol Med (2020). https://doi.org/10.1038/s12276-020-0450-9.
[48] Irun R. Cohen and Douglas B. Youngb. Autoimmunity, microbial immunity and the immunological homunculus. Immunology Today. Volume 12, Issue 4, April 1991, Pages 105-110. doi.org/10.1016/0167-5699(91)90093-9.
[49] А. М. Зайчик, А. Б. Полетаев, Л. П. Чурилов. РАСПОЗНАВАНИЕ «СВОЕГО» И ВЗАИМОДЕЙСТВИЕ СО «СВОИМ» КАК ОСНОВНАЯ ФОРМА АКТИВНОСТИ АДАПТИВНОЙ ИММУННОЙ СИСТЕМЫ. (Self recognition and self interaction as the main form of immune system activity). ВестникСПбГУ. Сер. 11. 2013. Вып. 1 УДК 612.017.1+616.097+576.8.
[50] Галактионов В. Г. Проблемыэволюционнойбиологии. Медицинскаяиммунология. 2004, том 6, №3-5.
[51] HawkesR. A. Enhancementoftheinfectivityofarbovirusesbyspecificantiseraproducedindomesticfowls. Aust. J. Exp. Biol. Med. Sci. 42, 465–482. DOI: 10.1038/icb.1964.44.
[52] Maria K. Smatti, Asmaa A. Al Thani, and Hadi M. Yassine. Viral-Induced Enhanced Disease Illness. Front Microbiol. 2018; 9: 2991. doi: 10.3389/fmicb.2018.02991.
[53] Vennema Harry; Poland Amy; Foley Janet; Pedersen NielsC."Feline Infectious Peritonitis Viruses Arise by Mutation from Endemic Feline Enteric Coronaviruses". Virology. 1998. 243 (1): 150–157. doi: 10.1006/viro.1998.9045.
[54] Tirado S. M. andYoonK. J. "Antibody-dependent enhancement of virus infection and disease". Viral Immunology. 2003. 16 (1): 69–86. doi: 10.1089/088282403763635465.
[55] Khandia R.; Munjal A.; Dhama K.; Karthik K.; Tiwari R.; Malik Y. S.; Singh R. K.; Chaicumpa W. "Modulation of Dengue/Zika Virus Pathogenicity by Antibody-Dependent Enhancement and Strategies to Protect Against Enhancement in Zika Virus Infection". Frontiers in Immunology. 2018. 9: 597. doi: 10.3389/fimmu.2018.00597.
[56] Iwasaki Akiko; Yang Yexin. "The potential danger of suboptimal antibody responses in COVID-19". Nature Reviews Immunology. 2020-04-21. doi: 10.1038/s41577-020-0321-6.
[57] Tseng C. et al. "Immunization with SARS Coronavirus Vaccines Leads to Pulmonary Immunopathology on Challenge with the SARS Virus". PLOS ONE. 2012.7 (4): e35421. Bibcode: 2012PLoSO...735421T. doi: 10.1371/journal.pone.0035421.
[58] Liu L. et al. "Anti–spike IgG causes severe acute lung injury by skewing macrophage responses during acute SARS-CoV infection". JCI Insight. 2019.4 (4). doi: 10.1172/jci.insight.123158.
[59] Wan Y. et al. "Molecular Mechanism for Antibody-Dependent Enhancement of Coronavirus Entry". Journal of Virology. 2020. 94 (5). doi: 10.1128/JVI.02015-19.
[60] YipMing S; Cheung Chung Y; Li Ping H; Bruzzone Roberto; Peiris JS Malik; Jaume Martial. "Investigation of Antibody-Dependent Enhancement (ADE) of SARS coronavirus infection and its role in pathogenesis of SARS". BMC Proceedings. 2011-01-10. 5 (S1). doi: 10.1186/1753-6561-5-s1-p80.
[61] Lynne Peeples. News Feature: Avoiding pitfalls in the pursuit of a COVID-19 vaccine. ProcNatlAcadSci U S A. 2020 Apr 14; 117 (15): 8218–8221. doi: 10.1073/pnas.2005456117.
[62] Peter J. Hotez, David B. Corry and Maria Elena Bottazzi. COVID-19 vaccine design: the Janus face of immune enhancement. Nat Rev Immunol. 2020 Apr 28: 1–2. doi: 10.1038/s41577-020-0323-4.
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    Muratkhodjaev Javdat, Aripova Tamara. (2020). RNA Interference: Antiviral Defense Mechanism and Immune Memory. Advances in Applied Physiology, 5(2), 24-29. https://doi.org/10.11648/j.aap.20200502.13

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    Muratkhodjaev Javdat; Aripova Tamara. RNA Interference: Antiviral Defense Mechanism and Immune Memory. Adv. Appl. Physiol. 2020, 5(2), 24-29. doi: 10.11648/j.aap.20200502.13

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    Muratkhodjaev Javdat, Aripova Tamara. RNA Interference: Antiviral Defense Mechanism and Immune Memory. Adv Appl Physiol. 2020;5(2):24-29. doi: 10.11648/j.aap.20200502.13

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  • @article{10.11648/j.aap.20200502.13,
      author = {Muratkhodjaev Javdat and Aripova Tamara},
      title = {RNA Interference: Antiviral Defense Mechanism and Immune Memory},
      journal = {Advances in Applied Physiology},
      volume = {5},
      number = {2},
      pages = {24-29},
      doi = {10.11648/j.aap.20200502.13},
      url = {https://doi.org/10.11648/j.aap.20200502.13},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.aap.20200502.13},
      abstract = {A review of the mechanisms of the generation of antiviral immunity in bacteria, plants, invertebrates, and vertebrates directly indicates the leading role of innate immunity. Bornovirus infections in mammals have been proven to be inhibited by the RNA interference mechanism. Authors propose a possible role of innate human immunity in combating viral infections, including SARS-Cov2. This hypothesis is based on the notion that antiviral response involves a molecular mechanism of RNA interference stemming from the specific viral patterns incorporated into host cells’ DNA. Innate immunity plays an important role not only at the first encounter with a viral infection, but also fully participates in the formation of specific immune memory. RNA-interference along with interferon system is integral parts of human anti-viral defense system. The joint work of these systems is considered. Caution is warranted in both PCR testing interpretation and in assessing prospective vaccines. False positive result without any clinical presentation of the disease in some people might mean that PCR test was picking up any specific SARS-Cov2 sequences that already had incorporated into asymptomatic person’s cellular DNA due to the possible RNA-interference based anti-viral immunity. Future vaccines aimed at producing specific antibodies can cause the phenomenon of antibody-dependent enhancement (ADE) of the infection. In ADE virus not only infects susceptible cells through appropriate receptor, but is able to highjack virus-specific antibodies to easily traffic virus bodies inside the monocytes/macrophages, granulocytes, platelets, mast and many more host cells through interaction with Fc and/or complement receptors. It is necessary to draw the attention of medical community, especially practitioners to the role of innate immunity, which is especially important in the current COVID-19 pandemic.},
     year = {2020}
    }
    

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    AB  - A review of the mechanisms of the generation of antiviral immunity in bacteria, plants, invertebrates, and vertebrates directly indicates the leading role of innate immunity. Bornovirus infections in mammals have been proven to be inhibited by the RNA interference mechanism. Authors propose a possible role of innate human immunity in combating viral infections, including SARS-Cov2. This hypothesis is based on the notion that antiviral response involves a molecular mechanism of RNA interference stemming from the specific viral patterns incorporated into host cells’ DNA. Innate immunity plays an important role not only at the first encounter with a viral infection, but also fully participates in the formation of specific immune memory. RNA-interference along with interferon system is integral parts of human anti-viral defense system. The joint work of these systems is considered. Caution is warranted in both PCR testing interpretation and in assessing prospective vaccines. False positive result without any clinical presentation of the disease in some people might mean that PCR test was picking up any specific SARS-Cov2 sequences that already had incorporated into asymptomatic person’s cellular DNA due to the possible RNA-interference based anti-viral immunity. Future vaccines aimed at producing specific antibodies can cause the phenomenon of antibody-dependent enhancement (ADE) of the infection. In ADE virus not only infects susceptible cells through appropriate receptor, but is able to highjack virus-specific antibodies to easily traffic virus bodies inside the monocytes/macrophages, granulocytes, platelets, mast and many more host cells through interaction with Fc and/or complement receptors. It is necessary to draw the attention of medical community, especially practitioners to the role of innate immunity, which is especially important in the current COVID-19 pandemic.
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Author Information
  • Cellular Therapy Department, Institute of Immunology and Human Genomics, Tashkent, Uzbekistan

  • Cellular Therapy Department, Institute of Immunology and Human Genomics, Tashkent, Uzbekistan

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