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COVID-19 For Non-Premed Majors
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.
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Reticulator,
Because your Comment teaches us basic facts about this subject which are essential to any understanding of it, and is so clearly, concisely, and comprehensively written, I have to say thanks in a Comment, not just a Like.
I just love my Ricochet friends so much. :-) :-)
We will figure this virus out before anyone else, and we will laugh while we are doing it. :-)
Just to belabor the Prinivil point: :-)
I know that a huge number of people are on this medication or its alternative, the name of which I don’t remember offhand.
I’ve been wondering about two things for months now: (1) Why the disease particularly hard on old people and why kids don’t seem to exhibit symptoms (and the hypertension thing would explain it since it strikes older people, and sure enough, there was a story last week about that very thing–the ACE inhibitors and receptors and surprisingly genes play a role (but that didn’t make sense since genes would be a lifelong presence, not just a presence in kids). And (2) when the reporters write that people with hypertension are more likely to become symptomatic, I immediately wonder about all those people in nursing homes. It seems to me that it would be likely that most of them would be on Prinivil. I’ve seen it said that it is untreated hypertension that is the problem. Back to the nursing homes. Are they not on prinivil even though they have high blood pressure? Prinivil is really cheap.
The T-cell explanation–older people have trouble making effective T-cells to fight off the virus–makes more sense actually than the ACE inhibitor theory. I also read somewhere that people who take antacids become symptomatic, and again, that makes sense too. Kids don’t take antacids.
So we should stop taking blood-pressure-lowering medication and antacids. I wonder if that would help.
You can see why I am really curious this entire line of research and reporting. I honestly cannot figure out what is going on with hypertension, Prinivil, and the virus. Everything I read seems contradictory.
:-)
Got a link? All I found was a study that suggested a link between Pepcid and better outcomes. I ask because I have a Rolaids dependency.
Perhaps the answer lies in the epithelium, a very thin (one cell wide) ACE2 receptor rich barrier between lung tissue and the air you inhale. It serves many functions, in the exchange of O2 for CO2, and in keeping the lung tissue clean and free of all that other nasty stuff we breath in. We also know that hypertension increases the risk that blood and other bodily fluids will permeate this and other similar barriers in the heart and blood vessels. Similar barriers in the heart and blood vessels are also rich in ACE2 receptors and hence fertile points for SARS CoV2 infection. So imagine that these barriers are all infected with CoV2 and pocked with holes. Blood fluids permeate those barriers and fill the lungs (pneumonia), which is in turn, filled with debris inhaled through a compromised epithelium. The immune system over-reacts and you have SARS. Now imagine that same scenario among a population of elderly, former smokers, whose lungs are already compromised. Children with healthy lungs, a vibrant immune response and normal blood pressure would not present the conditions for this perfect storm of COVID 19. (OK, I’m done. I’m out of my league here.)
MedCram is paying great attention to the idea that covid-19 is a disease of the
epitheliumendothelium more than the lungs, and also to the mechanisms by which it causes clots in these locations where O2 exchange takes place. It causes clots elsewhere, too, which is probably related to the not so uncommon phenomenon of covid-19 resulting in strokes.This is all I have seen on this, but it makes sense since we know that stomach acid kills the AIDS virus. If we are inhibiting the production of stomach acid, and we know that this virus has a tiny piece of DNA that looks like HIV, we may be inhibiting one thing that might protect us against it:
So if it is normal and healthy to have ACE 2 receptors in this barrier, than blood pressure medication that inhibits ACE 2 receptors would be bad for a person battling a covid-19 assault.
I’m calling our resident cardiologist. :-)
@drbastiat
The hypertension aspect of the covid-19 story has been bugging me for another reason, which I think I have an answer to now, thanks to this discussion. The word “untreated” keeps appearing and disappearing from the coverage on this aspect of this virus. Sometimes I see “untreated,” sometimes I don’t. I don’t understand why. At first I read that they talking about people who weren’t being treated for it.
That’s probably part of it; one uncomfortable thing about SARS CoV2 is that it damages cells just under the vascular lining, the lung epithelium and IIRC the lining of the kidney tubules (but I’m not looking that up) whose function is supporting the function of the active membranes. I think that’s also true in the brain.
One of the best pieces of science copywriting ever was the coinage of the term Advanced Glycation End Products and giving it the acronym AGEs. Glycation is the process by which cell structures are sugar coated. Permanently. Among other things, it impairs their function. Hemoglobin A1c measures the glycation of hemoglobin in your blood cells. Some glycation is normal and helpful. But when your blood sugar is too high and especially if it stays high, you get excessive accumulation of AGES. Even with good blood sugar, AGEs accumulate with, yes, age, so one way to look at blood sugar problems is that they cause accelerated aging of your tissues. It has broad effects on immune cell response to infection, on the proper consistency of your tissues, on membrane function, on a bunch of things. It promotes a lot of the processes that underlie poor COVID outcome, but it’s not the only way those processes get underway.
I get my ‘theliums mixed up!
You should be tested. Could be conflatiotheliumosis.