Functional and tissue enrichment analyses suggest that SARS-CoV-2 infection affects host metabolism

The article below describes the basic theoretical mechanisms of how

COVID-19 viral infections most severely affect older patients

with Fatty Liver, Obesity, Diabetes, High Blood Pressure,

High Triglycerides and other inflammatory (cytokine) issues.

The above metabolic disorders contribute to immune dysregulation

and exacerbate the inflammatory reaction causing homeostasis

breakdown during SARS-CoV-2 infection to eventual "cytokine

storm" instances. Sometimes in fatalities.

Our "Dibenorm - L" is the:

Anti-Inflammatory and Immuno-Modulating Therapeutic

to safely "methylate all genes, resultsing in the

eventual stabilisation of all metabolism of cells" and prevents

or shuts down the very dangerous instance of the "cytokine

storm" which is closely linked to the below severe inflammatory

underlying conditions, in which the COVID-19 virus interferes

with the expression of multiple host genes involved in the

metabolism and biosynthesis of glucose, lipid and amino acids.

Luciano Rodrigo Lopes

Severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), is phylogenetically close to SARS-CoV and Middle East respiratory syndrome-related coronavirus (MERS-CoV) and triggers similar symptoms as observed in SARS and MERS—high fever, cough, sputum production, pneumonia, dyspnea, and acute lung injury with high mortality. Although respiratory aspects of COVID-19 have been the main clinical concern, extra-pulmonary alterations frequently occur, including severe inflammatory reaction, kidney failure, acute cardiac injury, arrhythmias, sepsis, and others. Furthermore, central metabolic organs, such as the pancreas and liver, can also be affected by SARS- CoV-2 infection.

Despite the absence of pre-existing immunity against SARS-CoV-2, inflammatory immune reaction has been commonly observed in COVID-19. Inflammation is essential for host protection, but SARS-CoV-2 infection triggers an aggressive inflammatory response. Consequently a vast set of cytokines (including IL-2, IL-6, IL-7, and TNF) is produced resulting in a cytokine storm. Uncontrolled inflammation inflicts multi-organ damage. Metabolic disorders, such as obesity or diabetes, contribute to immune dysregulation and exacerbate the inflammatory reaction causing homeostasis breakdown during SARS-CoV-2 infection.

Moreover, the expression of ACE2 (the receptor for SARS-CoV-2) is enhanced in diabetic individuals in comparison with non- diabetic ones. Therefore, the control of the altered metabolism ameliorates the acute effects of SARS- CoV-2 and reduces the inflammatory response. Thus, diabetes might contribute to a more prolonged proinflammatory response and deficient control of SARS-CoV-2 replication.

Viruses can interfere with the expression of multiple host genes involved in metabolism and biosynthesis of glucose, lipid, and amino acids. The partial control of the host metabolism by viral evolved mechanisms, hijacking nutrient, and molecular building blocks from hosts favors the viral replication and persistence. For instance, while cytomegalovirus (CMV) and dengue virus induce the elevation of glucose consumption, MERS-CoV, human coronavirus 229E (HCoV-229E), and mouse hepatitis virus (MHV) pick up host lipids to increase replication.

Similar to other human viruses, coronaviruses establish molecular interactions with their hosts to take over the cellular mechanisms to support viral replication. Coronaviruses have adaptive benefits to take advantage from the host operating at different organs which disrupt a wide variety of biological processes and pathways.

Better understanding of the interference of SARS-CoV-2 on host biological processes and the viral impact on the tissue and organs can provide important insight into research and clinical aspects of COVID-19. Thus, the present study attempts to investigate and explore the most affected biological processes which involve host proteins interfered by SARS-CoV-2 combined with the tissue-specific differential expression.