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Let’s talk SARS CoV2. It is a very simple RNA virus, that is a capsid of proteins that contains a single strand of RNA. Your body uses RNA to direct cells to build proteins. It’s like a hard-coded program, directions, that organize cell function for growth and repair. SARS CoV2 attaches to certain cells in the body that play a part in a feedback loop that monitors and controls blood pressure. Unfortunately, this includes lung, heart, kidney, fat and even nervous system tissues.
When you are exposed to the virus, it travels into your eyes, nose, lungs or mouth and literally, by happenstance, may come in contact with its favorite cell (ACE 2) receptor. The more viruses you inhale (initial exposure) the higher the probability that a virus will bind with a receptor. The virus capsid itself is a spiky little sphere. When one of about ninety spikes touches a receptor, it binds. Within ten minutes, instead of receiving chemical signals from your body, the receptor opens and becomes an entry way for the viral RNA. The viral RNA enters the cell, reprograms the cell’s normal RNA directed functions and turns the cell into a SARS CoV2 factory. Within 7-8 hours, some 7000 newly created SARS CoV2 viruses begin exiting the infected cell. The infected cell does not “burst” at the end of its reproductive cycle spilling a massive dose of viruses and toxic byproducts as is characteristic with a cold or the flu. Hence, a COVID 19 infection lacks the characteristic fever/chill reproductive cycle that accompanies other common viral infections.
The infection is exponential, within days creating multiple billions of cloned viruses. The sheer number of viruses created increases the likelihood that a mutation in the viral RNA will occur, potentially creating a new form of the virus. However, study of the SARS CoV2 genome has led scientist to believe that SARS CoV2 contains genetic material that protects against random deleterious mutation. The virus is already a very efficient one. And it is not like influenza viruses, which are multi-RNA strand (8) viruses and prone to genetic material swapping in a host infected by more than one flu strain. Flu reproduction can much more easily result in a viable “new” viral infection.
We know that SARS CoV2 infections (COVID 19) are disproportionately more dangerous and lethal in those over 65. Of course, those with significant health concerns are more susceptible to any infection, not just COVID 19. But more specifically, there are two issues that have been suggested that may be the primary contributors to age-related risk. Many older people suffer from hypertension and have been prescribed medications that inhibit ACE 2 reception, which results in the creation of more ACE 2 receptors, especially in the lungs. This availability of receptors would in turn provide the virus easier entry, hence a larger initial dose of virus at the time of initial infection. In addition, researchers also speculate that prior coronavirus infections (not SARS CoV2 but common “cold” type coronaviruses which make up about 20% of all colds) are more likely present in older patients. The related antibodies for these “lesser” coronaviruses may contribute to an over-reaction to COVID 19, especially in the lungs, causing a destructive, sometimes fatal, auto-immune response.
The suggested ACE 2 inhibition mechanism would also at least partially explain the susceptibility of certain populations. Hypertension disproportionately affects people of African and Native American descent and type 2 diabetes and hypertension nearly always flock together and are also disproportionately reflected among those same groups.
A destructive autoimmune response to a new viral infection attributed to the existence of anti-bodies from other similar earlier infections has been noted with other viruses, like the flu. That would explain why the elderly would be more susceptible to that aspect of COVID 19. They are far more likely to have been exposed to other nominal coronaviruses. Younger people, on the other hand, would not suffer this immune over-reaction as their immune-historical exposure to coronaviruses would be far more limited.
Obesity, some medical researchers suggest, is likely itself a contributing factor to SARS CoV2 infection irrespective of hypertension and type 2 diabetes. Fat cells also have ACE 2 receptors and obesity seems to increase the number of ACE 2 receptors in the body, so the obese may provide the virus with a more receptive host. Also, obesity in general comes with other health issues that could exacerbate an auto-immune over-reaction to the virus.
New studies are, in addition to looking at existing anti-virals and other possible treatments, looking at vitamin D deficiency as a potential risk factor that could be easily remedied. We know that the virus can persist on some surfaces for a very long time, that it is susceptible to ultra-violet light, that thrives in certain environments where relative humidity is low and temperatures are moderate and that it is most likely shed with exhalation. The virus itself is quite small, however, N95 masks can do a decent job filtering out the virus and any mask will significantly slow the velocity of any virus expelled by an infected individual. Of course, the handling of potentially contaminated masks posits another potential problem.
Researchers also believe that initial exposure, that is how much virus an individual was exposed to, either at one time or over a number of days before the immune system could initiate a significant response, strongly correlates with the severity of COVID 19 and its lethality, especially for people under the age of 65. This would explain why certain otherwise young and healthy people, especially health care workers, have succumbed to the disease. So while wearing a mask, washing hands and social distancing might not provide great protection from infection, these steps will likely lessen potential initial exposure and lead to a lesser, even asymptomatic result should one be infected.
Unfortunately, since so many cells in the body play a part in the internal blood pressure monitoring loop, all receptor tissues are susceptible to COVID 19. While COVID related pneumonia may be the most difficult and common problem associated with the disease, we now know that kidney, heart, and even nervous tissue damage (encephalitis) can occur. COVID 19 has even been associated with clotting disorders leading to strokes. These complications are not common or unique to COVID 19, but they are worth noting.
There are several notable immunization efforts underway and some have shown early promise. However, it should be noted that previous attempts to produce any sort of coronavirus vaccine have all failed.
The initial US response to the SARS CoV2 was mixed. States that took steps to protect the elderly and most vulnerable fared the best. Those who mixed COVID 19 patients with at-risk patients in the same facilities fared the worst.
Initial responses may have been effective in keeping the health delivery system from being overwhelmed by infection, however, this strategy may have only delayed the achievement of exposure-related herd immunity, prolonging the crisis. The response did overestimate the severity of infection in most people and the virus’s negligible effect on those under 20. The delay did, however, allow the medical profession some time to learn about the infection and develop tests, protocols and treatments for dealing with it. These treatments have significantly decreased the severity and lethality of the disease and hospital stays for those with more severe infections have declined.
For all the effort put into attempts to control the spread of COVID 19, we have seen an increase in deaths from all other factors throughout the country. Suicides, overdoses, alcohol-related deaths, murders as well as deaths related to heart disease, cancer, strokes, and other chronic conditions have all reportedly increased. People at risk with chronic issues have obviously not sought care for fear of contracting COVID 19 or for lack of insurance brought on by job loss. As for the other categories, financial uncertainty and job losses caused by the COVID 19 response have likely contributed significantly to reported increases in death in those categories.Published in