What Is The Coronavirus
The Coronavirus is technically called the SARS-CoV-2 virus and is a single stranded RNA virus, same as the SARS-CoV and Middle East respiratory syndrome coronavirus called MERS-CoV. It spreads by droplets when someone with COVID-19 (what the syndrome is called) sneezes or coughs. They also spread as aerosols through the air. You might have noticed it spreads as easily as the common cold. This is no surprise as common human coronaviruses, including types 229E, NL63, OC43, and HKU1, usually cause mild to moderate upper-respiratory tract illnesses, like the common cold. There are about 120 different coommon viruses that cause cold-like syndromes we call the common cold. Whereas the cold affects only the upper respiratory system, the SARS-CoV-2 affects the lower respiratory system and multiple organ systems.
Where Did It Come From
There are two ideas, one is that this came from a bat at a seafood market in Wuhan, China in December 2019. However, a study came out in January 25th 2020, noting the individual first diagnosed had no connections to the market. The other idea is that it may have escaped from the biohazard laboratory in Wuhan, China. The Wuhan Institute of Virology (WIV) has come under special scrutiny because it hosts China’s only biosafety level 4 lab facilities. There is circumstantial evidence that this happened but not absolute proof although a scientist claims to have been working in the lab who took refuge in the USA in early 2020 that claimes this is true.
How The Virus Gets Into Our Cells
The SARs-CoV-2 infects a cell by attaching to the receptor on the cell called angiotensin converting enzyme 2 receptors (ACE2). This receptor is found in the oral mucosa, kidney, liver, intestine and heart as well as at the protein level in alveolar epithelial cells in the lungs. Various reports have shown expression of ACE2 receptors in the intestinal epithelium leads to viral shedding in the feces making the fecal oral route (one wipes their butt and does not wash hands and puts their dirty hands on food fed to others is what is meant by fecal oral route) of infection an issue. ACE2 has not been found to be expressed in the cells of our immune system.
The ACE2 receptors are the door by which SARS-Co-V-2 appears to enter the cell. Methylation is important for gene encoding for angiotensin-converting enzyme 2. Studies show the angiotensin-converting enzyme 2 receptor to be the virus receptor in the lung epithelial cells that is the most important receptor for SARS-CoV-2 entry into cells. The production and rate of the ACE2 enzyme by its gene is under epigenetic control (this means it can be altered by the environment, food you eat, life-style habits, stress etc.) and that activity is specifically based on methylation control. (To learn more about methylation see this article) The methylation rate in the lung epithelial cells was shown to be the lowest in relation to other tissues, which suggests the ACE2 enzyme is probably highest expressed in the lungs. The extensive surface of alveolar epithelial cells might also explain the vulnerability of this organ to the consequences of virus invasion.
Methylation May Be A Key Factor For SARS-CoV-2 Entry Into Cells
It turns out that methylation and perhaps enhancement of methylation may be protective from invasion of the SARS-CoV-2 virus. For a virus to invade our cells, it needs to fuse to the cell membrane and/or move through the membrane to get inside of our cells. This allows the virus to invade our cells and hide from our immune system. When it is inside our cells, the immune system can not get to it. This viral-cell membrane fusion is called a syncytium. Syncytium formation is normal for coronaviruses and seen in SARS-CoV-2 specifically. It has also been noted in some other viruses. Methylation of the syncytin genes is necessary to prevent expression of syncytium-forming proteins. (Leading researchers to believe that lack of adequate methylation would increase virulence and symptoms of viruses using this method to invade cells.) Some people are inadequate methylators due to genetics and we should investigate if this makes a difference and if so we need to support their methylation capabilities. If you are concerned about your methylation capabilities contact a local naturopath or functional medicine (MDs that practice somewhat like a naturopath) practitioner. They should know how to assist you. You also might want to read the article called COVID-19, Methylation and Prevention.
The Viral Path After It Enters The Cell
After entering the cell through the ACE2 receptor the virus is recognized by the immune system (Toll-like receptors 3, 7, 8 and 9 and viral-infection sensors RIG-I and MDA5). Recognition of the virus stimulates the immune system to release Type 1 interferon (IFN) response program and IFN-stimulated genes. It is interesting to note that the neutralizing autoantibodies to type I IFN were much more abundant in men than in women and men usually react stronger in the acute phase while women are more likely to have "long COVID". The TLR3 response causes NLR family pyrin domain containing 3 (NLRP3) gene as well as other cellular activities that includes release of oxidation species, calcium flux from cytoplasmic storages, protein aggregation and release of danger-associated patterns. This involves a release of NLRP3 inflammasome and subsequent release of proinflammatory cytokines. The severity of the COVID-19 process increases with the increased activation of NLRP3. This ultimately causes cell death that releases lactate dehydrogenase (LDH). More LDH is seen in the blood of patients with COVID-19 with increased severity and this is something commonly available for measure at a lab.
SARS-CoV-2 is able to inhibit the type I IFN responses that take place in infected cells. This leads to delayed or suppressed type I IFN responses allowing the virus to replicate and cause more tissue damage. The immune system revs up its system to fight harder when this happens and may possibly lead to increased symptoms.
More Body Responses
Seroconversion appears to happen in greater than 90% of people a few weeks after the initial infection and presence of anti-spike IgG antibodies are associated with protection from reinfection in a study of UK health-care workers who were highly exposed to COVID-19. T cell responses to SARS-CoV-2 spike protein correlate with the B cell responses to the protein and are seen in almost all patients in the recovery phase. T-cell reactions can also be found to SARS-CoV-2 in unexposed individuals. This is thought to be due to cross-reactive immunity to the common-cold cornoaviruses or other antigens.
Severity of COVID-19 is associated with neutrophil-to-lymphocyte ratio (NLR). This is a marker of systemic inflammation and it correlates with advancing age, the amount of obesity (especially in metabolic syndrome and diabetes type 2). It is an indicator of poor prognosis in COVID-19 and can be tested. It is not known if these individuals lack ability to develop the appropriate antiviral responses or if they might be likely to develop too exuberant of a response to the infection causing the well known hyperinflammation and acute respiratory distress syndrome seen clinically in COVID-19.
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