A) Improved Treatments.
Key in treatment is early recognition of those with hypoxemia and Xray change and quick treatment with plasma, anti-viral (Remdesivir), and high-dose steroids. In my experience and in the experience of my colleges, the early treatment with this combination really does seem to save lives. Prior to these therapies and back when COVID 19 first started, it was not unusual for me to have 10-12 ICU patients with COVID 19 on the ventilator. These days, for the last 2 months, I have averaged about 3 ventilated COVID 19 patients a week. That represents a tremendous improvement. Keeping the patient off the vent is key. If you don't go on the vent, you have a substantially higher survival rate. If you do go on the vent you have a 55-60% "survival" rate nationally. This mirrors my experience. I caution that "survival" simply means survival to discharge, but it doesn't quantify what shape you may be in at discharge.
How does this combination therapy work? Why is it such a game changer?
When you get COVID 19 infection your body has a natural immune response to the infection. In a small percentage of people, the immune system is hyper-responsive and attacks not just the virus but also the human body, most frequently in COVID, the lungs. This leads to Acute Respiratory Distress Syndrome (ARDS) which causes the Respiratory Failure through shunt physiology in the lung. This leads to severe hypoxemia (low oxygen levels) and eventual scaring of the lung. At its fullest expression, this leads to death due to suffocation.
So, the COVID IgG antibody, either from plasma from donors who have recovered from COVID or the new monoclonal IgG COVID AB soon to be on the market (the one the president received), binds to the Coronavirus preventing it or killing it before it infects more airway and lung cells thus preventing infection and the potential hyper-immune response. The more IgG AB you have to COVID, the less virus is left to worsen the infection. The anti-viral Remdesivir kills the Coronavirus that infects your body thereby reducing the number of virions left alive, something in medicine referred to as lowering your viral load. How well Remdesivir works remains unproven. The high dose Dexamethasone reduces your immune response (which is what Plaquenil does as well in theory, but not as effectively as steroids).
So, in summation, after exposure and infection, if you are treated with this "cocktail," the IgG binds to much of the Coronavirus in your body rendering it less infectious and eventually killing the virus. Most of the small percentage of virus that eludes the IgG will likely be killed by the Remdesivir. If there is still enough virus left (live or dead) to cause a hyper-immune response in the susceptible population, the dexamethasone greatly reduces the immune response. This combination seems extremely effective if given early. If given too late in the course (when they are already near 100% oxygen requirements or on the vent) it is seldom effective and often too late.
B) Reduced Viral Virulence.
Reduced viral virulence is the natural evolution of every viral plague or bacterial plague throughout history. The purpose of a virus is to reproduce its genetic code, which is an RNA code in this case. Therefore, it serves no purpose for the virus to kill its host which it is using to reproduce its genetic code to then be released by millions of viral particles through the host. The host in this case being us. If a virus mutates in such a way that it becomes more virulent, and kills off its host, then less of that virus is replicated and released. Those mutations therefore die out. The mutations that allow the virus to replicate with little-to-no damage to the host are replicated and released in much higher numbers and win out over time. This is a key reason why, historically, most viral and bacterial "plagues" weaken over time and you see a generally predicable decline in mortality rate within the first few years. There is no reason to suspect that COVID 19 will be any different, and we are—indeed—seeing lowering mortality rates. The key here is to realize the mortality rates are declining not just in the US (where we have all these amazing treatments at our fingertips as doctors) but also around the world, including many countries with little access to quality healthcare.
If you want further proof of how super-virulent viruses die out before they spread, well, ever wonder why all Ebola outbreaks are very time limited and geographically limited? They kill off the host too fast and at too high a percentage to spread.
C) Group Immunity.
Too much has been made of the term "herd immunity." It is being applied incorrectly here as it is not herd immunity that is lowering the mortality rate. Herd immunity usually refers to immunoglobulin immunity, which requires specific antibodies, which develop only after specific exposure to the infection or through immunization. In theory, once you reach a critical threshold for number of people in a society with immunoglobulins to the virus, you have reached "herd immunity." In that state, usually around 50-70% of the herd with IgG antibodies to COVID, less people can get infected, there are fewer host, and therefore the viral numbers drop because less virus is replicated which, in turn, protects the part of the herd that may not have enough IgG antibodies. But this is just one way in which a herd can show immunity or, more so in my meaning, protection from a viral infection.
In understanding this, I prefer the term “group immunity” because it allows for inclusion of all aspects of the human immune response, not just immunoglobulins. The human immune system has a vast armamentarium of weapons to fight invaders of which immunoglobulins are just one branch. The human immune system fights infections with numerous types of cells and other components including T-cells, B-cells, Natural Killer Cells, Polymorphonuclear Leukocytes (basophils, eosinophils, neutrophils), Lymphocytes, Monocytes, Cytokines, and the Complement System. It is through the combination of all of these responses that we attack and kill invaders to our body. In addition, the largest defense we have against invaders—the largest organ of our body—is the skin. It is my contention as a doctor that both the US and the World is developing a group immunity to COVID (or already had one to some extent), making us less susceptible to catching the virus and/or allowing us to fend it off better if we do catch it. Eventually, after enough have been exposed or vaccinated when available, there will then also be a more classic "herd immunity" at least temporarily for however long the IgG to COVID 19 is being produced by the herd (unknown at present).
It is also my contention that this group immunity did not just develop this year but was somewhat already in place. How is that possible? Because COVID 19 is not the first coronavirus to which our bodies have been exposed. Coronavirus as a cause for upper respiratory tract infection (URI, aka cold virus), has been around for a hundred years having first been discovered in the 1920s. There are several types of coronaviruses including, but not limited to, several common cold viruses, MERS, SARS, and COVID 19 (aka SARS2). As a species on this planet, Homo Sapiens Sapiens (aka humans) have been exposed to coronaviruses for a minimum of 100 years and likely for several thousands of years. As such, our body, in particular our immune system, has already evolved to be less susceptible to coronaviruses as a mechanism of survival and natural selection. So when a novel strain of coronavirus comes along, such a SARS and SARS2 (aka COVID 19) our bodies already are familiar enough with the new strain to prevent most of us from either catching it or catching a severe case of the new virus as a function of our combined immune system, not just antibodies. This is why most that are infected with COVID 19 get common cold like symptoms and nothing more. Occasionally, as with many URI viruses, more susceptible humans develop a viral pneumonia or a deeper infection termed a lower respiratory infection (LRI) which can be far more serious and can lead to hyper-immune responses, ARDS, and even death. Over time, through natural selection, the more susceptible Homo Sapiens Sapiens die off, the group immunity improves, and the virus becomes less virulent.
Much has been made of the phrase "common cold." Many have taken exception to referring to COVID as a "common cold virus." The definition of a common cold is a viral infection of the upper respiratory system, including the nose, throat, sinuses, eustachian tubes, trachea, larynx, and bronchial tubes. There are over 200 types of common cold viruses using this definition with rhinoviruses making up the majority. Almost all cold viruses clear up in less than two weeks with minimal complications. Many of these URI viruses can, on occasion, lead to LRI and viral pneumonias, which often get misdiagnoses as bacterial pneumonias and are, therefore, under reported. Some are more likely to lead to LRIs—such as COVID 19—but COVID 19 is a URI of which the vast majority of people that "catch" COVID 19 get either no symptoms or only mild "cold-like" symptoms. So—and really this is all semantics—does that not make COVID 19 just another version of the other Coronaviruses that cause a "cold," albeit a nastier version? Your response to this question is often more a reflection of your politics than a reflection of the medical facts.
