New Insights Into the Basic Science of SARS CoV-2

You. It's great to be with everybody once again. In this video I would like to talk about the basic science behind the SARS CoV2 virus. What we've learned so far, what we know, what we don't know. And one thing I can't talk about is what we don't know that we don't know. And there's way more that we don't know than that we do know. And so after this video, hopefully you'll know a little more. But we have to realize that what we know now is, will probably change and be different. That's how science works. Science is a continuing thesis, antithesis and synthesis. That's what happens in science. You have a competing views and we learn. Sometimes they're both false, sometimes they both have a partial truth. And then you learn and you move on. That's how science progresses. Science is not absolute. There's not an absolute truth in science because we can't know everything. We actually are in the test tube of the scientific experiment. In order to be 100% objective, you have to go outside of the experimental box. For us, the experimental box is the universe. And there's really no way for us to go outside the box. We actually take part in experiments. We are part of the experiment. There's no way for us to ever be 100% objective with any scientific research because we are subjected to senses, sights, sounds, gravity, the electromagnetic fields of the Earth's force, gravity. All these things that affect the experiments themselves, affect us, affect how we interpret data. Our language affects how we interpret data. And so what that means is we ourselves are part of our own experiments subjectively and objectively. And what that means is our findings can later be found to be false. And we see that with about half of all scientific research defines later found to be false. So that's my short snippet about what I'm saying right now. May letter be found to be false. It's what we know that as of July 19, this is the state of science between in the SARS COV2 world. So hopefully this is helpful. First thing we need to think about is that the first coronaviruses came to existence on Earth about 10,000 years ago. Even later, some, some suggest, you know, potentially millions of years before that. That's not quite. No, but it's at least 10,000 years ago was the first coronavirus and there's seven strains that affect humans. Four strains cause common infections that we see all the time. About 15% of head colds, respiratory tract infections or some type of coronavirus. And about 30% of infections during acute flu season are coronavirus. The other three coronaviruses that are serious are SARS CoV1, which is the original SARS SARS CoV2, which we're dealing with now. And then MERS. Now SARS CoV1 2 and MERS. I'm sorry, sorry. MERS and SARS1 both originate in bats. And so there's a lot of these viruses actually start either in bats. The SARS CoV2, which is what we're dealing with now, started in a horseshoe bat. And what happens is this virus starts in some animal like a bat, and then has an intermediate animal it goes to. And the intermediate animal is some kind of mutation that then allows it to be transferred to us. This is how the flu works. Flu typically starts in animals, pigs in China, it's transmitted to duck or geese. They bring it to the United States. Eventually humans get exposed. And that's kind of how the flu works. And so that's the reason why we have to start making our flu virus about a year in advance. Based on what's going on in China, we figured out with the H1N1 that started actually in pigs or swine in Mexico. Totally different, caused by surprise. But this is a very typical way, these viruses, this interaction between humans and the animals around us. So the intermediate. So with the sars, there's actually civet cats, where the intermediate. And these are these cute little cats, the. And they're eaten for food in China, sometimes slaughtered, eaten at the space. So whoever's eating that animal is getting this, exposed to this. So in these wet markets, there's a very, very close contact between animals and the humans. Most people in America today don't have a close contact with an animal outside of a cat or a dog in their home. In these situations, you go to these markets and there's hundreds or thousands of different species with interaction with people. When with the mers, the intermediate was a camel. Okay, so it went from a bat to camel. Humans ride camels in the Middle east, and that's how that spread. Fortunately, that was not very transmissible between humans. And then. So the viral origins. Now, the thing about the current. The current coronavirus is that there's about 96% of its genetic material has been shared with the virus bat that's been found in the cave and the Yuan China, we think that's where this originated. And that's where some of the controversy comes from, because this area where it originated. Do you think it's about 500 miles away from the wet market, where eventually the spread occurred. As far as we know now, that 90%, 6% change in genetic material, it's still not 100%. And it takes sometimes a decade or so to get that much variation in a coronavirus. So we have found some other. The Malayan pangolins is another animal we think it may have been genomic origin for the SARS CoV2. However, the virus in these Malayan pangolins, which is these cute little critters, they kind of look like an aardvark, kind of, sort of. They only share 92% similarity with what's going around right now. So that's unlikely. The source is probably. These civets. So the thing about it is that the virus in the bat initially does not infect people, but it's this intermediary that that gets a mutation or change that can infect people. But the big thing about it, I think what this means for me is that because it takes such a long time to get this genetic change, we're probably not seeing a huge variation or genetic variation. We're not going to see one in the current virus. There has been some reported change, maybe two or three strains going around, but there's not enough genetic difference for it to be a totally different viral infection. The degree of severity of this infection, which is a big issue and has more to do with the amount of exposure of the virus than the strain per se itself. And we'll talk about that here in a second. So, yeah, so what we need to do is we need to find an animal host version that's about 99% similar to find the SARS CoV2 to know what we're dealing with. And unfortunately we're not really getting in. We're not being allowed to go research and find that right now. So we're kind of going on the knowledge information we have. There's also some question about the information we have just due the fact that there was just some mishandling with information. There was some misinissionally, we were told it wasn't infectious by Chinese researchers and the World Health Organization spread that information. So there's been also some misinformation throughout this time. So I tend to like when I find research articles talking about this originally in China, I tend to like to find a European counterpart to verify it, just because of the degree of misinformation. So why do people, okay, this is a big question. Why do people respond differently? You know, there's different factors, there's Genetic factors. We do know some genes associated with severity of SARS COV2 like an APOE gene. If you're APOE4, you're more prone to inflammation. You can clear the virus quicker if you have the APOE4 gene, but if you're already inflamed, you're also more prone to an inflammatory response. So the gene can either be typically is beneficial but if you're someone who's obese, diabetic, who's already inflamed, then you that's going to cause a low lying inflammation. This APOE4 gene is also associated with an increased risk for cardiovascular disease as well as Alzheimer's, dementia and certain cancers. So it's an interesting gene. There's also some data about blood types being more susceptible to. These are interesting points. But the biggest factor related to severity of disease is actually the two factors are the exposure, degree of exposure and the person's underlying immunologic status. So what do I mean by degree of exposure? So it takes about. If you get about 10 viral particles exposed into your respiratory tract, which is not a lot, it's not going to make it down to the base of your lungs. So the infection will most likely stay in your upper respiratory tract. You'll sneezing, coughing, maybe a loss of smell and taste might be your only symptom, which we've known that since March, April time frame. And you'll be better, you'll be fine. It takes about 100 plus viral particles to be exposed to, to get it down to your lungs and that's where you might get the viral pneumonia. If you get a huge, huge exposure from a COVID 19 party, which is a terrible idea if you're actually working in the hospital and someone is being nebulized. If you're. There's a. In my area there's a skilled nursing facility where people were being nebulized with nebulizers to treat asthma and they were getting nebulized with large amounts of viral particles, probably getting millions and millions of these viral particles that almost assuredly will lead to an acute respiratory pneumonia type infection. And so the first thing is the degree of how much you get exposed, hence the utility of wearing masks and social distancing. If you're far away from someone and you wear a mask when you get exposed, you just won't get exposed to quite as much. The other thing is your underlying immunologic status. If you're someone who's already inflamed, you already have elevated inflammatory markers like IL1IL6, your CRP is already high. We actually use HSCRP, which is a high sensitivity CRP as a marker for heart disease or risk for heart disease. If yours is already up a little bit and you expose this, you'll probably have very robust inflammatory response. And that's what we're seeing is we're seeing a different and expression of this inflammation when people exposed. The other thing is your nutritional status. We know very clearly that if you have a low vitamin D status, you're exposed to this, you're more prone to have an inflammatory response as well. Why Vitamin D is required to make antibodies. If you have a high vitamin D level, you make antibodies more robustly. Your body controls inflammation much better. If it's low, it's going to take your body a while to make antibodies. Hence vitamin D status is a huge, huge fact factor. There's also some gene variants, stuff we talked about neutralizing, neutralizing antibodies. So yeah, so we've learned a lot of things about neutralizing antibodies. The first IgM antibody, which is your antibody for fighting off an acute infection, hits its peak in about 23 days. The IGG goes up in about 49 days and you tend to have the IGM go down. And after four to six weeks, the IGG may go down in about three to four months. For more severe infections, these antibody levels can stay up for much, much longer. What we're learning about the underlying biology of this infection is that some people will have a quick infection and their antibodies will be gone pretty quickly. Some people will get infected and antibodies will be gone so quickly that we can't even pick them up. A lot depends on how robust of immune response a person has, how long they are around the environment, how much they're exposed to. But the antibodies do not correlate with the person's underlying immunity status. It's a surrogate marker. It's the best we have. It's what we're using. The best marker for immunity is actually neutralizing antibodies or B memory cells, which we can't really measure clinically today. What would be great to know is actually IgA antibodies, which are most of IgA, represent the vast majority of all antibodies made in our body. And these are actually secreted along respiratory tract, GI tract, lungs. You want these levels to be high. And actually right now most testing is not for secretory iga, it's for IGG antibodies. So we're actually not even testing for what represent respiratory tract and GI tract having immunity. So virus mutations. We mentioned Reinfrington Vaccination your vaccination again, when we get vaccines, the vaccines are actually, the point is to produce antibodies to the spike protein. And that's how we've learned how this thing actually enters our body is through a spike protein. The spike protein attaches to the angiotensin II receptor, which is mostly in our lungs, it's also in our GI tract, it's in our arteries, it's in our vasculature, in our kidneys, which are some of the places we see severe disease happening. And this is how it gets into our body. If you have a lot of an elevation of these receptors, you tend to get more infection and certain ethnic groups have this elevated. Certain disease states will see this elevated and some will see it lower. So if you actually are taking an inhaled steroid for asthma, you actually have that's actually protective against upregulating the angiotensin II receptor. So you actually will get less severe infection. As far as current trials, vaccine Trials, there's over 200 trials in development right now. In development, there's two that are actively working on phase two and phase three and we're waiting the placebo controlled trials. My research group actually is going to be involved with a phase three with the vaccine, with Pfizer and we actually are starting that in the next week or two. Moderna's hit most of the media, most people are familiar with that, but there's other 20 other companies right now doing studies. So and the vaccine, the big thing with the vaccine I think is that is to find out, you know, when it's deployed, we'll find out how it works. But vaccines, typically when you deploy them, you create a vaccine, antibodies, like the flu vaccine, like there's actually a vaccine in development right now for C. Difficolitis. And these are, these create antibodies, that's what vaccines do, they create antibodies and that's how they confer immunity. So hopefully that was helpful. That's some basic science we understand behind what's going with COVID Its origin. This is changing, it's in flux, it's in motion. So hopefully, as new updates come, we'll be making you all aware. Please continue to follow us on social media, YouTube, Facebook, if this is helpful, share it with your family, friends. If you have questions, please post them. And we can, as time allows, answer your questions. We're here for you to help, kind of guide you all through, lead you through, answer your questions, concerns and queries from hopefully evidence based, middle of the road kind of stance to help us all get through this. Take care, be blessed and stay safe.