Covid-19 - Background Science, etc.

Updated: Mar 16

Pro Tip: This is going to affect people who don't believe in it more than those who do.


What is it, who is most at risk, what tissues are affected and how, etc...


I am sure most of you are well aware of the precautions each of us should be taking to minimize the spread of Covid-19. Practicing these precautions will ultimately temper the burden on the hospital system and this is good for you and your fellow citizens! This is an opportunity to step back from our busy lives, rest, and re-evaluate what it means to be a member of a local, national, and global society. There is a silver lining if you look for it, I promise.


Basic Precautions (not an exhaustive list)

  • Prepare for the worst. Hope for the best.

  • The virus can stay alive on cardboard x 2 days, on plastic x 3 days and on conventional surfaces x 3 days.

  • The virus can be spread via the breath. Hence the social distancing of 6 feet is imperative. No fist bumps, handshakes, hugs... Not even elbow bumps as that puts a person in proximity to a potentially infectious person.


I highly recommend listening to the Joe Rogan/Michael Osterholm PhD, MPH interview. Dr. Osterholm is an infectious disease epidemiologist and has been tracking Coronaviruses for a long time and understands them. He is director of CIDRAP, Center for Infectious Disease Research and Policy in Minnesota and in 2017 predicted COVID-19 in his book Deadliest Enemy: Our War Against Killer Germs including a whole chapter on SARS/MERS - the other coronaviruses.


Background on SARS-CoV-2 virology and pathogenesis:


The virus, called SARS-CoV-2, is in the same family as the SARS virus from early 2002 (also called SARS-CoV). The spike proteins that the two viruses use to attach to human tissue are almost identical. They both use the ACE-2 (Angiotensin Converting Enzyme-2) receptor, mainly found in the lung, to attack our cells. After binding to the receptor, the virus uses a protease, a substance that breaks down proteins, to break through tissue and enter the host cell. This is where the infection begins.


Over-expression of (or extra) ACE-2 makes things worse, because there are more doors to choose from. Conditions such as hypertension and the use of ACE inhibiting blood pressure medications can increase the number of ACE-2 receptors in the lung. These drugs include: Lisinopril, Captopril, all of these drugs end in -pril). There is also a higher incidence genetically of ACE-2 receptors in men, and especially Asian men.

  • Note: I am NOT telling you to stop taking your medications! It wouldn't help in the short term anyway, but know that this is a risk factor for the infection.


As the infection advances, the virus downregulates the expression of ACE-2, thus increasing the susceptibility of the tissue to recover from the infection. This is potentially why it is so lethal. In cases where lung infection is significant, but the patient recovers we are seeing potential for permanent pulmonary fibrosis, or scar tissue in the lung.


The main tissues where ACE-2 is expressed is the testes, heart, and kidneys, lung, liver, intestine, and the brain. In the brain, it is a key regulator of cardiovascular function.


Lung: The lung is not the only tissue with the ACE-2 receptor, so why is the virus apparently targeting the lung? The lung has a great deal of surface area which increases the exposure. Alveolar type II cells (type II pneumocytes) are critical for proper lung function. One potential reason that Covid-19 is so deadly is that inside of these ACE-2 expressing cells, lies the tools for processing viral genetics, in greater numbers than the typical lung cell. These cells are like factories for the virus.


Cardiac: ACE-2 was found and confirmed to be a cardio-protective protein, after gene knockout studies in mice showed cardiac tissue that resembled that seen in long term hypoxia. ACE-2 plays a role in cardiac regeneration after injury such as a heart attack.


Kidney: A loss of ACE-2 is directly related to susceptibility to injury and hypertension. The expression of ACE-2 in the Kidneys is inversely proportional to the incidence of hypertension.


Intestine: The intestinal lining uses the ACE-2 receptor as a co-receptor in the absorption of amino acids. This also happens to be the most likely vector by which the virus entered the human population, from consuming meat containing the virus.



So this is a viral infection, how are people dying from it?


Two words: Cytokine Storm.


What does this mean? Cytokines are a diverse group of tiny signaling proteins that are secreted by cells to talk to other cells, like millions of text messages. Cytokines often trigger small amounts of inflammation, that is useful in healing tissue when used appropriately. Cytokines also happen to be what makes us feel sick when we're sick, it's not often the bug itself.


A cytokine storm is essentially the body responding to a virus inappropriately, causing incredible amounts of inflammation by uncontrollably dumping these messages into the body. The resulting cytokines dump triggers body-wide inflammation, and can have huge impact on certain organs. If a cytokine storm occurs in the lungs, for example, fluids and immune cells accumulate and eventually block off the airways, potentially resulting in death.


This all may sound terrible, but this is what we're dealing with. It's important to understand why this virus is absolutely worth paying attention to.


So what can we do about it?


Stay tuned for a lighter and more hopeful follow-up post regarding herbal medicine, prevention, and potential treatments of this nasty little bug!!



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