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The Terahertz DNA Damage Response


The prime objective for every life-form is to deliver its genetic material, intact and unchanged, to the next generation. This must be achieved despite constant assaults by endogenous and environmental agents on the DNA.


To counter this threat, life has evolved several systems to detect DNA damage, signal its presence and mediate its repair. Such responses, which impact a wide range of cellular events, are biologically significant because they prevent diverse human diseases.


Studies show that terahertz frequency waves enhance hydrogen bonds vibrations leading to openings between the DNA strands.


This then triggers the DNA Damage Response (DDR).


This is a good thing because it triggers a reaction that upregulates genes and pathways that actually guard your genome, such as the gene called P53.


P53 plays a central role in DNA damage response and is considered a “Guardian of the Genome”.


As I’ll discuss later, many viruses use hydrogen bonding to attach to DNA to initiate viral assembly.


Utilizing the iTeraCare Quantum Terahertz Device may prove to be a useful tool to break the hydrogen bond that initiates viral attachment and assembly.


Unwinding the double helix of the DNA molecule is the basis of gene duplication and gene editing, and the acceleration of this unwinding process is crucial to the rapid detection of genetic information.


Terahertz stimulus can serve as an efficient method to accelerate the unwinding process of DNA duplexes. The average speed of the unwinding process increased by 20 times at least with the terahertz stimulus.


How does this work?


Water is well known as a substance of the highest importance for the stability and functioning of biological macromolecules. Deoxyribonucleic acid (DNA) is not an exception.


Terahertz stimulus allows for breaks in the hydrogen bonds on DNA inducing the DNA Damage Response.


Here’s the thing…Water is LIFE. You are Water.


The terahertz frequency lies in the energy range of hydrogen bonds which means that even simple molecules absorb terahertz well, ESPECIALLY WATER.


In the case of large biomolecules such as proteins, DNA, RNA, lipids, and even polysaccharides, with their multiple and unique vibrational modes and complex intramolecular interactions (e.g. protein folding and DNA double-strands) and associated counter-ion aura, terahertz is expected to be a good functional affecter.


Proof of this can be found in the ever-growing body of studies showing the terahertz spectral signatures of different biomolecules such as biotin, DNA, albumin, collagen, carbamazepine, glucose, lactose anhydrate, indomethacin, lactose, and many others.


The DNA Damage Response


Each of the 10 trillion cells in the human body receives tens of thousands of DNA lesions per day. These lesions can block genome replication and transcription, and if they are not repaired or are repaired incorrectly, they lead to mutations or wider-scale genome aberrations that threaten our health.


Aging is a complex process that results in loss of the ability to retain homeostasis following stress, leading, thereby, to increased risk of morbidity and mortality.


Many factors contribute to aging, such as the time-dependent accumulation of macromolecular damage, including DNA damage. The integrity of the nuclear genome is essential for cellular, tissue, and organismal health.


DNA damage is a constant threat because nucleic acids are chemically unstable under physiological conditions and vulnerable to attack by endogenous and environmental factors.


To combat this, all organisms possess highly conserved mechanisms to detect and repair DNA damage. Persistent DNA damage (genotoxic stress) triggers signaling cascades that drive cells into apoptosis or senescence to avoid replicating a damaged genome.


DNA Damage Response Pathway


Key DDR-signaling components in cells are the protein kinases ATM and ATR. Two of the best studied ATM/ATR targets are the protein kinases CHK1 and CHK2 which, together with ATM and ATR, act to reduce cyclin-dependent kinase (CDK) activity. Another important gene is PARP1, involved in the recovery of cell from DNA damage.


In response to DNA damage, the level of p53 protein increases.


Essentially, terahertz physiotherapy induces the guardian of the genome p53 through the DNA Damage Response.


The majority of the human cancer cells exhibit the inactivation of the P53 pathway.


The P53 pathway controls several genes that play a role in the arrest of the cell cycle, cellular senescence, DNA repair system, and apoptosis. P53 plays a crucial role in supporting DNA repair by arresting the cell cycle to purchase time for the repair system to restore genome stability.


Apoptosis is essential for maintaining tissue homeostasis and tumor suppression. P53 can induce apoptosis in a genetically unstable cell by interacting with many pro-apoptotic and anti-apoptotic factors.


Furthermore, P53 can activate autophagy, which also plays a role in tumor suppression. P53 also regulates many metabolic pathways of glucose, lipid, and amino acid metabolism. Thus under mild metabolic stress, P53 contributes to the cell’s ability to adapt to and survive the stress.


Numerous studies have demonstrated that viruses interact with DDR pathways. Whereas many viruses evade DDR, others appear to benefit from it.


Viruses and the DNA Damage Response


Approximately, 20% of all cases of human cancer have an infectious etiology, with ∼80% of those being viral. A link between viral infection, disruption of DNA damage response (DDR) pathways and cellular transformation/tumorigenesis has been established for a variety of oncogenic human DNA viruses.


Viruses must interact with their hosts in order to replicate; these interactions often provoke the evolutionarily conserved response to DNA damage, known as the DNA damage response (DDR). The DDR can be activated by incoming viral DNA, during the integration of retroviruses, or in response to the aberrant DNA structures generated upon replication of DNA viruses. Furthermore, DNA and RNA viral proteins can induce the DDR by promoting inappropriate S phase entry, by modifying cellular DDR factors directly, or by unintentionally targeting host DNA. The DDR may be antiviral, although viruses often require proximal DDR activation of repair and recombination factors to facilitate replication as well as downstream DDR signaling suppression to ensure cell survival. An unintended consequence of DDR attenuation during infection is the long-term survival and proliferation of precancerous cells.


Viral hijacking of the DNA Damage Response


For example, EBV infection of human B cells in vitro transiently activates an ATM-dependant DDR. EBV immortalizes primary human B cells in culture mimicking physiological activation and survival signals, which when constitutively active is capable of driving B-cell lymphomas in vivo in the immune-suppressed.


In other words, VIRAL PROTEINS SUPPRESS THE DDR TO PROMOTE TUMOURIGENESIS.


Viral Modulation of the DNA Damage Response and Innate Immunity: Two Sides of the Same Coin


Both the DDR and the innate immune system are signaling cascades that function to sense, signal, and respond to aberrant nucleic acids. Once considered to be independent cellular functions, evidence now suggests that they may not be mutually exclusive processes, and there is more crosstalk than previously considered.


In addition to maintaining genomic integrity, the DDR is exquisitely poised to regulate viral infection, since to the cell, viruses are essentially aberrant nucleic acids. In support of this, the connection between viral replication and the DDR has emerged in two primary roles: (1) viruses modulate the DDR proteins and pathways required for viral replication; (2) there is significant crosstalk between the DDR and the innate immune response against viruses. These connections have been observed extensively across viral classifications and are relevant to a variety of both DNA and RNA viruses, including single-stranded DNA (ssDNA) and double-stranded DNA (dsDNA) viruses, positive (+) and negative (−) stranded RNA viruses, and retroviruses (a (+) RNA virus that relies on a dsDNA intermediate).


Engagement and modulation of the DDR are central to the life cycles of a range of diverse viruses and are a phenotype that is broadly conserved beyond the viruses which we have discussed in this review. Despite the diversity in viral genomes, mechanisms of replication, and subcellular localization, the commonality of DDR engagement collectively highlights the importance of engaging ATM, ATR, and DNA-PK signaling pathways as well as the individual proteins in these pathways to promote the viral lifecycle. Converse to the benefits of utilizing the DDR, many of these factors themselves have antiviral activity as well as connections to innate immunity. As such, it is evolutionarily imperative for viruses to overcome this, and further demonstrates the convergence of these two important cellular functions which reflect two sides of the same coin that functions to sense, signal, and respond to aberrant nucleic acid – whether this be self or non-self.


Disrupting Hydrogen Bonds as Anti-Viral


Viral Capsids use hydrogen bonding for viral assembly.


The assembly of a virus is a complicated macromolecular dance. Tens or hundreds of proteins—each several hundred amino acids in length—must organize by way of salt bridges, hydrogen bonds, and other chemical linkages to form a protective shell known as a capsid, which encases the virus’s genetic material.


Example:


“We have identified the CP−RNA interactions in the MS2 phage by using ab initio quantum mechanical calculations, demonstrating the vital role of HBs at the interface between RNA and protein for virus assembly.”


In relation to the “current virus”, this study shows the same information which reveals enhanced receptor binding of the virus through networks of hydrogen-bonding and hydrophobic interactions.


Another study shows that Hydrogen Bonds Fight HIV Mutations.


P53 and the Viral Connection


P53 regulation was found to play a crucial role in different infection stages of various viruses. Therefore, it is rational to believe that novel treatments, based on targeting and reactivating p53, may lead to beneficial therapeutic outcomes not only for cancer therapy but also for infectious diseases at large.


p53 may serve as a therapeutic target for viral infections. For example, p53 activation and induction of p53-dependent apoptosis may function as such antiviral therapy.


P53 also inhibits the replication of THE CURRENT VIRUS.


Another study reveals p53 Triggers Viral Mimicry Response Thereby Abolishing Tumor Immune Evasion and Promoting Antitumor Immunity.


The tumor-suppressing protein p53 has earned the nickname “guardian of the genome” because of its well-studied arsenal of techniques for responding to genetic damage. When it binds to damaged DNA, it can activate DNA repair proteins, pause the cell division process until repairs are complete, or trigger programmed cell death if the damage is irreversible.


Now, new research suggests p53 has another trick up its sleeve: it can force cancer cells out of hiding by making them go viral.


Virtually all viruses have evolved molecular instruments to circumvent cell mechanisms that may hamper their replication, dissemination, or persistence. Among these is p53, a key gatekeeper for cell division and survival that also regulates innate immune responses.


In summary, here are the highlights:


  • Terahertz frequency enhances hydrogen bonds vibrations leading to openings between the DNA strands.


  • This triggers the DNA Damage Response.


  • The DNA Damage Response induces the expression of the “Guardian of the Genome” P53.


  • Altering hydrogen bonds and inducing the DDR via terahertz waves may be anti-viral.


* These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.



Sources:

https://pubs.acs.org/doi/abs/10.1021/acs.jpclett.0c01850

https://ieeexplore.ieee.org/document/7102290

https://www.nature.com/articles/s41598-020-67179-z

http://www.mathnet.ru/links/c2185c459f62205b6f1b97595f0a669e/nano658.pdf

https://www.mdpi.com/1422-0067/22/20/11089/pdf

https://figshare.com/collections/Terahertz_Wave_Accelerates_DNA_Unwinding_A_Molecular_Dynamics_Simulation_Study/5090783

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2906700/

https://royalsocietypublishing.org/doi/10.1098/rsif.2017.0585

https://europepmc.org/article/pmc/pmc3080051

https://letstalkscience.ca/educational-resources/backgrounders/dna-damage-and-repair

https://elifesciences.org/articles/62852

https://www.rndsystems.com/resources/articles/dna-damage-response

https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/dna-damage-response

https://jmhg.springeropen.com/articles/10.1186/s43042-020-00089-x

https://pubmed.ncbi.nlm.nih.gov/26958736/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3273341/

https://www.sciencedirect.com/science/article/pii/S0022283621005647#f0015

https://www.pnas.org/doi/pdf/10.1073/pnas.2008209117

https://journals.asm.org/doi/10.1128/JVI.01803-09

https://www.pnas.org/doi/10.1073/pnas.1018104108

https://search.bvsalud.org/global-literature-on-novel-coronavirus-2019-ncov/resource/en/covidwho-1367799

https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0019268

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6024945/

https://journals.lww.com/co-oncology/Abstract/2021/03000/Viral_strategies_for_circumventing_p53__the_case.10.aspx

https://physicstoday.scitation.org/do/10.1063/PT.4.0404/full/



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