Selecting the Molecular Mechanisms of Neurodegenerative in COVID-19 Pandemic and No tropical Sprue

Laura Ailioaie^*
*Correspondence: Laura Ailioaie, Research Unit of Biomedical Engineering in Anesthesia and Intensive Care Medicine, Medical University of Graz, Auenbruggerplatz 39, 8036 Graz, Austria, Email:

Introduction

The extreme acute respiratory syndrome coronavirus two (SARS-CoV-2) is a brand-new coronavirus that was first identified in late 2019 in Wuhan, China. After the disease, it became known as Coronavirus Disease-2019 (COVID-19), which caused the current pandemic and the global health catastrophe that continues to have major global repercussions. In March 2020, the World Health Organization (WHO) declared COVID-19 a pandemic. Over 6 million deaths and 516 million confirmed cases of COVID-19 had been reported worldwide as of May 12, 2022; In the meantime, more than eleven billion vaccine doses have been given out. Even though the COVID-19 pandemic appears to be getting better and better under control, there is still a wealth of data and knowledge that has been gained over the past two years. These data and knowledge need to be analyzed in order to draw useful conclusions for the future in all fields, but especially in molecular medicine and drug discovery, virology, epidemiology, genetics, immunology, vaccinology, and medical fields like gastroenterology [1].

Description

Recent research into the molecular and cell pathophysiological mechanisms of numerous chronic inflammatory issues that cause serious clinical issues and burdens worldwide reaffirms the great understanding of Hippocrates Before Common Era, the father of modern medicine, who postulated that "all disease starts off evolved in the gut." The explanations for nearly all diseases, including cancer, were based solely on two factors—genetic susceptibility and stochastic events caused by surrounding circumstances—up until a few years ago, prior to the discovery of the human genome. However, modern epidemiology has rendered this model obsolete. The twenty-three thousand genes and the concept of "one gene, one protein, one disease" can't explain the fundamental puzzle of health and disease, let alone the actual explosion of power conditions caused by inflammatory processes, as revealed by complete human genome decryption [2].

The human small intestine is the largest and longest of the many adjoining surfaces or interfaces that our body and the environment use to manage this complicated mutual interaction. It is approximately 6.7 to 7.6 meters (22 to 25 feet) long and the absorptive floor place is just about 250 rectangular meters, or nearly 2700 rectangular feet, the size of a tennis court. The remaining interaction with the surrounding environment, i.e., the microscopic organisms that cause illness (bacteria, viruses, etc.), is controlled by the intestinal mucosa. nutritive substances, potentially contaminating waste, and so on. Intestinal permeability, which finely regulates the molecular transit between the tubular cavity of the small intestine and the layer of areolar connective tissue beneath the mucous membrane, is a 0.33-important player in autoimmunity or forbearance. Antigen transit is controlled by tight junctions (TJs) between cells, which are molecularly coordinated by zonulin, the only known modulator of intestinal permeability [3].

Even in the event of brief contact with a variety of bacteria, viruses, gluten (for celiac disease), and other substances, the zonulin pathway should be initiated. Multiple molecular and mobile physiological mechanisms for maintaining mucosal homeostasis rely on the zonulin pathway. Many (but not all) persistent inflammatory or autoimmune diseases, including celiac disease (CD), type 1 diabetes mellitus (T1DM), obesity, and others, are caused by disruptions in this pathway, functions of the epithelial and endothelial barriers, and changes in the elements or activities of the intestinal microbiome. The primary objective of this study was to investigate the likelihood of children with CD contracting SARS-CoV-2 and developing severe COVID-19 strains. The second goal was to gain a better understanding of the interactions and effects of SARS-CoV-2 infection in children and adolescents with CD. The 0.33 objective was to examine zonulin's role as a regulator of intestinal permeability in relation to the ambitious pathology known as multisystem inflammatory syndrome in adolescents (MIS-C), which occurs within a few weeks of viral contagion from contact or contamination with SARS-CoV-2 [4]. Additionally, the objective was to highlight the molecular mechanisms underlying CD.

This overview demonstrates how the COVID pandemic's CD served as a catalyst for the development of novel molecules and the testing of an adjuvant drug for the MIS-C fulminant structure. Due to the fact that SARS-CoV-2 remains and continues to have an impact on our lives, original posted works on COVID-19, CD, and new records and points of view have been analyzed. The scientific community continues to address the scientific ambiguities brought on by the SARS-CoV-2 contamination and its effects, such as in CD. By understanding the molecular mechanisms and how genes, proteins, and other molecules interact within our cells, it is possible to develop new methods for rapid and precise prognosis and quantified infectious disease management [5].

Conclusion

This study demonstrated that CD patients and the general population did not have a higher risk of contamination or death from COVID-19. Immunocompromised patients and those with dietary deficiencies, particularly CD patients who did not adhere to GFD, posed the greatest risks of contracting the infection. The number of intestinal biopsies has decreased, but the incidence of CD prognosis has increased, particularly in relation to T1DM. Problems have grown, resulting in life-threatening delays and lengthy waiting lists for GI endoscopies, particularly in younger children. Due to high shipping costs, grant issues, long travel distances to obtain GFD, lower household income, and reduced QOL during the lockdown, GFD adherence was affected by the COVID-19 pandemic. The pandemic resulted in psychological distress, insomnia, irritability, anxiety, persistent fatigue, depression, decreased quality of life, low GFD compliance, and metabolic issues like diabetes and obesity in CD patients.

Because none of the current vaccines contain gluten or prolamins, patients with CD can obtain any vaccine that is safe and effective in preventing COVID-19. A zonulin antagonist inspired by CD was proposed as a treatment for MIS-C after in-depth examination of the molecular pathophysiological mechanisms of SARS-CoV-2 contamination and the striking similarity between CD and the disruption of mucosal integrity. Since the pandemic is still going on and there are still cases of MIS-C, research is also needed to learn more about the pathophysiological mechanisms of this serious disease. New shipping structures and molecules as immunotherapies for balancing the response of the GI immune device as a multi-field sovereign system and treating immunerelated diseases are ongoing assignments. Zonulin is the subject of a lot of research in immunoengineering as a way to improve the absorption of new oral medications and vaccines. In the not-too-distant future, researchers will need to improve new treatments for autoimmune diseases.

References

1. Stewart, Martin P, Xiaoyun Ding, Robert Langer and Klavs F. Jensen. "In vitro and ex vivo strategies for intracellular delivery." Nat 538 (2016): 183-192.

Google Scholar, Crossref, Indexed at

2. Sarvari, Raana, Mohammad Nouri, Alexander M. Seifalian and Peyman Keyhanvar, et al. "A summary on non-viral systems for gene delivery based on natural and synthetic polymers." Int J Polym Mater Polym Biomater 71 (2022): 246-265.

Google Scholar, Crossref, Indexed at

3. Hadjizadeh, Afra, Farzaneh Ghasemkhah, and Niloofar Ghasemzaie. "Polymeric scaffold based gene delivery strategies to improve angiogenesis in tissue engineering: A review." Polym Rev 57 (2017): 505-556.

Google Scholar, Crossref, Indexed at

4. Rincon, Melvin Y, Thierry VandenDriessche and Marinee K. Chuah. "Gene therapy for cardiovascular disease: Advances in vector development, targeting, and delivery for clinical translation." Cardiovasc Res 108 (2015): 4-20.

Google Scholar, Crossref, Indexed at

5. Pan, Xiuhua, Hanitrarimalala Veroniaina, Nan Su and Xiaole Qi. "Applications and developments of gene therapy drug delivery systems for genetic diseases." Asian J Pharm (2021).

Google Scholar, Crossref, Indexed at