How COVID-19 Infection Attacks the Immune System & Differs from HIV (Lecture 55)
Welcome to another MedCram COVID-19 update. Let’s go to Worldometer and take a look at the individual numbers at this point. It looks like the daily new cases in the United States are starting to level off and maybe even reduce a bit. Here we can see a graph of daily new deaths in the United States, and that seems to be going down as well.
[It’s] a kind of a disturbing Nature article that was just published recently looking at the SARS-CoV-2 infection pattern, and it seems to indicate that SARS-CoV-2 may have another target in the human body, and that is the T lymphocyte, which is very important in the immune system.
This article goes through a number of molecular techniques in its communication. It’s open communication with nature.com, and it talks about how we know that the SARS-CoV-2 virus is interacting with the ACE2 receptor on the Type II pneumocytes.
But they also show that in patients with Covid-19, some studies reported that there was lymphocytopenia, basically meaning low white blood cell counts, and part of that white blood cell counts are the lymphocytes, specifically the CD4 and CD8 lymphocytes.
They also mention that this was also a finding in MERS. MERS was the Middle East Respiratory Syndrome that was seen back in 2012. In this article, they talked about their molecular techniques that tried to set out and to see whether or not SARS-CoV-2 also infects T cells, resulting in lymphocytopenia.
What they were able to show here is with SARS-CoV, which, remember, is the SARS virus of 2002, and the SARS-CoV-2, which of course is the recent one 2019 and now 2020. They were able to see whether or not these viruses, which appear as these bright dots in the fluorescence field, were able to infect these cells and fuse with them.
As you can see SARS-CoV, there was no fusion cells. In other words, there weren’t these big blobs of cells that were kind of lighting up. You can see that nothing here of the sort. But when they did it with SARS-CoV-2, they were able to see these blobs of cells where the virus was able to get in. Therefore, they were able to show that the virus was able to fuse with these T lymphocyte type cells and show that the SARS-CoV-2 virus through a spike protein was able to infect and go into these T lymphocytes.
The good news though is when the SARS-CoV-2 virus infects the T Cell via the CD 147 protein, the infection is a dead end, and it’s known as abortive. On the other hand, when the virus infects the Type II pneumocytes via the ACE 2 receptor, that infection of that cell does lead to replication of the virus. And the protein that the SARS-CoV-2 uses to enter into the T-cell is the CD 147, that is present on the surface of the T lymphocytes.
好消息是，当SARS-CoV-2病毒通过CD 147蛋白感染T细胞时，这种感染是死胡同，被称为流产。另一方面，当病毒通过ACE 2受体感染II型肺细胞时，该细胞的感染确实导致病毒复制。SARS-CoV-2用于进入T细胞的蛋白质是CD 147，它存在于T淋巴细胞的表面。
So some have compared SARS-CoV-2 with HIV in this sense because there are some similarities. SARS-CoV-2 is an RNA virus, so that’s RNA inside SARS-CoV-2 here on the left, and it’s also an RNA virus in HIV.
But let’s take a look at the differences between those. Let’s first look at HIV. So with HIV, you have an RNA virus and in this case, it docks with the docking protein CD4, which targets the T-cell specifically, in fact the helper T cells. But in this case, when the virus docks with the protein and comes into the cell, what is released is the RNA.
Now, the RNA and a couple of other enzymes are used in this infection without getting into too much detail, but there are two proteins that are very important to understand. The first one is something called reverse transcriptase (RT), and another one is called integrase or I. And what reverse transcriptase does in HIV is it uses the RNA as a template to make a DNA molecule and then very quickly it will make the other double strand of that DNA molecule.
Then what happens is integrase takes this molecule, this double-stranded DNA molecule, which is a copy essentially of the RNA from the original HIV, and what does it do is it actually integrates it into the host cell’s DNA, and it stays there permanently so that when the cell divides and divides, a copy of the HIV RNA will now be incorporated into its very nucleus. So every single time it divides, the progenitor T cells, or the daughter T cells of this division, will have that HIV genome in it.
So what can happen is when you have RNA polymerase coming by and reading this off, it will read this area off and it will make new copies of the HIV virus in terms of RNA, which can then be packaged and new virus can be made, so you can see how a HIV infection is going to be incorporated into the very cell. That’s different with SARS-CoV-2.
With SARS-CoV-2, when there is an infection of the RNA virus, it will dock with a different protein. In this case, it is the CD 147 and what will happen here is that the RNA will come into the cell and it will stay there and if there is another CD 147, there will be another virus with a genome and it will dock and another virion will come in and there will be another one. And so what happens is this cell will build up with a bunch of RNA genomes from the SARS-CoV-2.
对于SARS-CoV-2来说，当感染RNA病毒时，它将与另一种蛋白质对接。在这种情况下，它是CD 147，此时将发生的是RNA进入细胞并停留在细胞中，如果存在另一CD 147，将存在另一个带有基因组的病毒，它将进行对接，另一种病毒中病毒粒子会进来，还会有另外一个。因此，发生的情况是该细胞将由SARS-CoV-2的一堆RNA基因组构建。
So you can see interestingly this cell here is just filled with the virions, that shows fusion. So this article shows again how important it is to have a functional and good immune system, especially since this virus seems to be doing a one-two punch on it.
We’ve already shown a couple of times this article from nature medicine. This was a patient that was hospitalized in Australia. And they did a very good job looking specifically at the lymphocytes in this patient and we can see here that in terms of CD8 and CD4 cells if you look at what is normal in a healthy subject. These were actually a little bit higher and lower respectively in that category, but that this patient seemed to recover and there was a large increase in the number in this case of 8 cells and a large increase here in the number of CD4 cells. That may be the determining factor in whether a patient recovers or not.
The other interesting thing I found about this article was it showed when anti IgG and IgM were increasing in this patient, you can see here that it was by day 9 that the anti-IgM was two plus to three plus and anti-IgG was already starting to come up by day 7 and day 8. So that’s an important thing to keep in mind, especially as we enter into a season of antibody testing.
And speaking of improving your immune system, I also wanted to sort of clear up a number of comments and things that I’ve seen. There seems to be a theory at least that sauna baths or hot air can kill the virus and I don’t believe that anyone is making that claim at least here at MedCram. The claim or the interesting aspect is that heat followed by cold can actually improve immunity, which in turn can help potentially kill viruses, perhaps even Covid-19.
There seems to be some discussion of that. Even going back a number of years, I found this article for those who are really interested in this type of research to be a good clearing house and discussion of that. This is from The Business Insider, the article titled taking regular sauna seems to transform your health—more evidence that there could be a 3rd pillar of physical fitness be on diet and exercise.
对此似乎有一些讨论。甚至追溯到几年前，我觉得对于那些对此类研究非常感兴趣的人来说这篇文章是一个很好的讨论依据。这来自《商业内幕》（The Business Insider），标题为定期洗桑拿似乎可以改变你的健康–更多证据表明，饮食和运动可能是身体健康的第三大支柱。
And you can see here that they list off that people in Finland regular take saunas, where they go into extremely hot dry rooms for short periods of time. The more saunas people take, the healthier they seem to be. According to a new medical review, health benefits include improved heart health, mental health, immune system function.
And there’s also significant evidence that exposing yourself to cold temperatures improves health as well. And there’s actually a number of important and interesting medical articles and their links all through this article and I encourage you to take a look. We’ll leave a link to this in the description below.
I also wanted you to be aware of some news that’s breaking. We talked about ventilators and using one ventilator to ventilate multiple patients and we talked about how there was a letter from the AARC and a number of other societies that are involved with ventilation. They were concerned that this would not be a good idea because patients would have different sized lungs and different compliance.
Well, there was a press release today showing that there is a new device that would allow control over the amount of tidal volume going to specific patients, even though they’re hooked up to one ventilator, and that’s called a vent multiplexer. And apparently it was successfully deployed at Yale New Haven Hospital for Crisis Care Co-Ventilation during this pandemic. And apparently according to this press release, it was successful. They are still working with the FDA for full approval.
But that that work is going through right now as we speak. So we’ll see what happens. I think that’s interesting.