Coronaviruses (CoVs) & COVID-19
Coronaviruses (CoVs) including COVID-19 are by far the largest group of known positive‐sense RNA viruses having an extensive range of natural hosts. In the past few decades, newly evolved Coronaviruses, especially hot topic COVID-19, have posed a global threat to public health. The immune response is essential to control and eliminate CoV COVID-19 infections, however, maladjusted immune responses may result in immunopathology and impaired pulmonary gas exchange. Gaining a deeper understanding of the interaction between Coronaviruses and the innate immune systems of the hosts may shed light on the development and persistence of inflammation in the lungs and hopefully can reduce the risk of lung inflammation caused by CoVs.
Current research has connected Epigenetics to the immune system as scientists continue to learn more about the interaction between our bodies, our epigenetics, and our environment. For instance, research suggests a certain sugar could epigenetically reactivate a compromised immune system and that eating zinc might influence the immune system via DNA methylation.
This highlights the importance of immune responses under coronavirus COVID-19 infection and improves the understanding of Coronaviruses (CoV)‐induced inflammatory response by Epigenetics Cleaning Protocol.
How to boost Epigenetics response to the immune system?
About 80% of our immune tissue lies within our digestive tract, acting as a protective barrier between our bloodstream and potential pathogens, including viruses from the outside world, and the microbiome (the millions of micro-organisms and bacteria that live in our guts) is now a key area of scientific research; it has been shown to play a key role in immune response and overall health and fitness.
Diet plays an essential part in normal immune function, by ensuring that we have the necessary nutrients to allow the immune cells to work normally. Supplements, like Vitamins, Minerals can be helpful, but only if the person has an obvious deficiency or methylation issues, like polymorphism on MTHFR, BHMT, CBS, MTR and MTRR genes and probiotics might be helpful to restore a normal population of bacteria in the gut if the population has been altered by antibiotics or any mentioned above polymorphisms (researches confirms that more than 50% of population have confirmed polymorphism on these groups of genes).
Vitamins B6, B12, folic acid and methionine
Vitamins B6, B12, folic acid and methionine play the key role in the methylation process. The body should obtain all these elements from food but not always is possible due to the quality of food and how the genes are dirty already.
Methylation disorders are very often caused by an improper diet that causes nutritional deficiencies and can lead to the formation of cancer cells, increase oxidative stress, also disrupt amino acid metabolism and slow down energy production and of course compromise immune response to viruses.
To increase the efficiency of methylation processes, it is worth supplementing their level and, above all, ensuring a proper, balanced diet. Healthy immune system warriors need good, regular nourishment.
As we age, our immune response capability becomes reduced, which in turn contributes to more infections. While some people age healthily, the conclusion of many studies is that, compared with younger people with not working well the Methylation Cycle, the elderly are more likely to contract infectious diseases and, even more importantly, more likely to die from them. Respiratory infections, coronavirus, and particularly pneumonia are a leading cause of death in people over 60 worldwide. The scientists observe that this increased risk correlates with a decrease in T cells, possibly from the thymus atrophying with age and producing fewer T cells to fight off infection, especially with not working well Methylation Cycle. Whether this decrease in the Methylation Cycle explains the drop in T cells. A reduction in the immune response to infections has been demonstrated by older people’s response to coronavirus. There appears to be a connection between proper care of the Methylation Cycle, nutrition, properly selected exercises, moderate constructive stress, sleeping quality enough hours, reduced oxidative stress and immunity in the elderly.
It seems clear that exercise, stress, especially oxidative stress, healthy sex life and adequate sleep also affect the efficiency of the immune response.
When we’re stressed, the hormone corticosteroid is released: this can suppress the effectiveness of the immune system by lowering the number of lymphocytes.
Lack of sleep
has also been proven to affect the immune system – research shows that someone sleeping five to six hours a night has a far greater risk of virus infection than someone who sleeps for seven-eight hours. Sleep is an area of interest in immunology and Epigenetics. There’s an increasing number of papers looking at circadian rhythms – the immune system seems to tune to what time of day it is. There was an interesting study a while back showing that if you infected in the morning you would get better immune responses than later in the day, and suggesting that your immune system is heightened in the morning and starts to wane later on.
It can be down to the usual suspects – lifestyle factors such as obesity, smoking, lack of exercise, excess alcohol and poor diet.
The answer may lie in your genes
If you’re easily prone to frequent viral infections, yet all tests prove normal and you’re living a healthy lifestyle, it might be down to your dirty genes (Epigenetics Cleaning Protocol).
It is very hard to analyse in detail why some people get ill more often than others, as so many factors are involved, but undoubtedly your genome influences your adaptive immune response.
Inheritance plays a strong part in determining the type and power of the immune response. The particular genes that you carry determine how efficiently you will recognise each virus and your risk of coronavirus COVID-19 diseases. It is now known that variation between people in these genes is the main reason why some become ill with a certain infectious agent, while others don’t.
How you can check your issues and clean your genes?
Epigenetics Cleaning Protocol addressing the following lifestyle areas:
- Mother care and early life experience
- Diet, nutrition, hydration
- Addictions: smoking, alcohol, drugs, fast food, smartphones, social media
- Relaxation, meditation
- Relations – family, social, work
- Oxidative stress
- Toxins, drugs,
- Chemicals, Pesticides, Herbicides
Epigenetics Cleaning Protocol
The Epigenetics Cleaning Protocol, depending on the problem, lasts from a few to several months. It is primarily aimed at achieving a result that is the answer to the main problem of the client. It involves setting main goals and a strategic plan that is developed together with the client. The client commits to achieve the planned goal and adhere to the established principles of the coaching program. Every week the client receives a detailed goal for a given week and sends the report in the set format at the end of the week. On this basis, further specific objectives are developed for the following week. The customer always commits the adoption of a specific goal. The solution we check results in the real realization of assumed goals, solution of previously identified problems and as a result a real transformation of the client’s life.
For deeper understanding the issue of Coronavirus vs Immune response vs Epigenetics:
The innate immune response and adaptive immune responses of Coronaviruses (CoV) infection during an infection. A CoV infects macrophages, and then macrophages present CoV antigens to T cells. This process leads to T cell activation and differentiation, including the production of cytokines associated with the different T cell subsets (ie, Th17), followed by a massive release of cytokines for immune response amplification. The continued production of these mediators due to viral persistence has a negative effect on NK and CD8 T cell activation. However, CD8 T cells produce very effective mediators to clear CoV. B, Attachment of CoV to DPP4R on the host cell through S protein leads to the appearance of genomic RNA in the cytoplasm. An immune response to dsRNA can be partially generated during CoV replication. TLR‐3 sensitized by dsRNA and cascades of signalling pathways (IRFs and NF‐κB activation, respectively) are activated to produce type I IFNs and proinflammatory cytokines. The production of type I IFNs is important to enhance the release of antiviral proteins for the protection of uninfected cells. Sometimes, accessory proteins of CoV can interfere with TLR‐3 signalling and bind the dsRNA of CoV during replication to prevent TLR‐3 activation and evade the immune response. TLR‐4 might recognize S protein and lead to the activation of proinflammatory cytokines through the MyD88‐dependent signalling pathway. Virus‐cell interactions lead to the strong production of immune mediators. The secretion of large quantities of chemokines and cytokines (IL‐1, IL‐6, IL‐8, IL‐21, TNF‐β, and MCP‐1) is promoted in infected cells in response to CoV infection. These chemokines and cytokines, in turn, recruit lymphocytes and leukocytes to the site of infection. Red lines refer to inhibitory effects. Green lines refer to activating effects.
Host innate immune system
The host innate immune system detects viral infections by using pattern recognition receptors (PRRs) to recognize pathogen‐associated molecular patterns (PAMPs). At present, the known PRRs mainly include toll‐like receptor (TLR), RIG‐I‐like receptor (RLR), NOD‐like receptor (NLR), C‐type lectin‐like receptors (CLmin), and free‐molecule receptors in the cytoplasm, such as cGAS, IFI16, STING, DAI, and so on.
Dendritic cells (DCs) play a key role in innate immune and adaptive immune responses. As the strongest antigen‐presenting cells in the organism, they effectively stimulate the activation of T‐lymphocytes and B‐lymphocytes, thus combining innate and adaptive immunity.
Immune response – conclusions
Since the emergence of SARS‐CoV in 2002 and its spread throughout 32 countries and areas, the world has experienced the outbreak of MERS‐CoV and now, the COVID-19. All these viruses belong to the subfamily Coronavirinae in the family Coronaviridae. Since CoVs emerge periodically and unpredictably, spread rapidly, and induce serious infectious diseases, they become a continuous threat to human health. This is especially true when there are no approved vaccines or drugs for the treatment of CoV infections and there exists a range of animal reservoirs for CoVs and recombinant CoVs. In recent years, profound understandings of the innate immune response to viruses have been made.
This type of immune response inhibits virus replication, promotes virus clearance, induces tissue repair, and triggers a prolonged adaptive immune response against the viruses. In most cases, pulmonary and systemic inflammatory responses associated with CoVs are triggered by the innate immune system when it recognizes the viruses.
Although a broadly protective, universal vaccine is considered the ultimate protection against the virus spread, vaccine development can be time‐consuming. To fulfil the pressing need, we should propose effective therapeutic measures using the accumulated knowledge of the innate immune response system. Targeted immunotherapy by Epigenetics Cleaning Protocol, to boost the immune system, is a good alternative to some antivirals that have narrow treatment windows and meet with drug resistance easily.
Coronavirus vs Epigenetics
The molecular mechanisms regulating emerging coronavirus pathogenesis are complex and include virus-host interactions associated with the entry, replication, egress and innate immune control. Epigenetics research investigates the genetic and non-genetic factors that regulate phenotypic variation, usually caused by external and environmental factors that alter host expression patterns and performance without any change in the underlying genotype. Epigenetic modifications, such as histone modifications, DNA methylation, chromatin remodelling, and non-coding RNAs, function as important regulators that remodel host chromatin, altering host expression patterns and networks in a highly flexible manner.
Induction of the host innate immune
For most of the past two and a half decades, research has focused on the molecular mechanisms by which RNA viruses antagonize the signalling and sensing components that regulate the induction of the host innate immune and antiviral defence programs upon infection. More recently, a growing body of evidence supports the hypothesis that viruses, even lytic RNA viruses that replicate in the cytoplasm, have developed intricate, highly evolved, and well-coordinated processes that are designed to regulate the host epigenome, and control host innate immune antiviral defence processes, thereby promoting robust virus replication and pathogenesis. There are strategies that are used to evaluate the mechanisms by which viruses regulate the host epigenome, especially focusing on highly pathogenic respiratory RNA virus infections, like coronavirus COVID-19. By combining measures of epigenome reorganization with RNA and proteomic datasets, we address a spatial-temporal data integration approach to identify regulatory genomic clusters and regions that play a crucial role in the host’s innate immune response, thereby defining a new viral antagonism mechanism following emerging coronavirus infection.
Innate immunity is one of the earliest barriers to coronavirus infection. Following infection, pathogen recognition receptors (PRRs) such as retinoic acid-inducible gene I (RIG-I), melanoma differentiation-associated gene 5 (MDA5), Toll-like receptors (e.g., TLR 3, 4 and 7) and other sensing molecules recognize pathogen-associated molecular patterns (PAMPs) in viral components, such as viral structure proteins or viral nucleic acid. Successful recognition initiates a signalling cascade that activates an antiviral state in the host. Several main players of innate immunity, such as signal transducer and activator of transcription 1 (STAT1), myeloid differentiation primary response gene 88 (MyD88), TLR4, TLR7 and TLR3/TIR-domain-containing adapter-inducing interferon-β (TRIF), function to dampen infection severity during coronavirus infection in vivo.
Epigenetic regulation bridges genotype and phenotype by changing the function of the gene locus without changing the sequence of the underlying DNA. Over the last decade, research efforts have revealed a dynamic range of epigenetic factors that shape and regulate chromatin status, leading to changes in host gene expression patterns, and therefore to alterations in phenotypes. Epigenetic modifications are significant in regulating cellular mechanisms and pathways during embryonic development, in memory function, in immunity and in disease. While mutations directly affect the genetic material by changing the genetic code, epigenetic modifications change the chromatin structure or modify the nucleic acid without altering the genetic code. This makes epigenetic modifications reversible, flexible, and quickly responsive to changes in the environment and other exposures. Based on this ability, the study of epigenetic modifications is an important interface between the environment and the genome. Over the last decade, epigenetics research has made rapid progress in understanding developmental biology, memory, and inheritability functions. More recently, it has become increasingly important in studies of oncology, adaptive and innate immunity, and infectious diseases.
Two cell types
Two cell types of the innate immune system, dendritic cells and macrophages, are the primary sensors of ‘danger’ signals. Once these cells are activated, it is especially important that their signals are both cell-specific and stimulus-specific to ensure the initiation of a temporal and spatial response. These cell-specific signals can be mediated through cell-cell contact or by secretion of IFN and TNF. Thus, the ability of their epigenome to change within minutes after a stimulus is not just essential for initiating a rapid antiviral host response but is also essential to ensure a persistent and specific defence response. This way, epigenetic mechanisms are responsible for the priming and the memory of these responses and for guaranteeing a functional and highly regulated host response beyond the initial activation wave.
Epigenetics vs immune system
Current research has connected epigenetics to the immune system as scientists continue to learn more about the interaction between our bodies, our epigenetics, and our environment. For instance, research suggests a certain sugar could epigenetically reactivate a compromised immune system and that eating zinc might influence the immune system via DNA methylation.
DNA hydroxymethylation remains a mysterious epigenetic mechanism that’s still not completely understood by scientists. The function of 5-hydroxymethylcytosine (5-hmC), termed the “sixth base”, is still being revealed, but research has discovered that hydroxymethylation is a part of oxidative DNA demethylation pathways. 5-hydroxymethylcytosine (5-hmC) is a modified form of cytosine believed to play a vital role in switching genes on and off. Ten-eleven translocation (TET) enzymes oxidize the methyl group of 5-methylcytosine (5-mC) and convert it to 5-hmC. TET enzymes are often deactivated or mutated in coronavirus.
No content on this article should ever be used as a substitute for direct medical advice from your doctor or another qualified clinician.
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