theatlantic.com/science/archive/2020/03/ and find the article called biographynewcoronavirus.
Your can access this article by going to the above site and type biography (dash) new (dash) coronavirus. My computer's dash is broken so I cannot type that in here. Otherwise you can google Science of Coronavirus and pick The Atlantic article.
I would like to just summarize some of this scientific information here in case you do not want to delve deeply.
The Coronaviruses are a widespread group of RNA viruses. Most are spherical and have spikes on the spherical surface that have what look like small crowns on the end of the spikes; hence the name Coronavirus. Coronaviruses exist rampantly in bats, pangolins, and have been found in civets and camels. Four of the Coronaviruses are human viruses only and cause relatively mild colds much like the common Rhinoviruses. It is thought that they cause up to 1/3 of common colds. They have been named OC43, HKU1, NL63, and 229E. Research on these viruses, both the cold viruses, and the animal Coronaviruses in the past has been few and far between. Such research has been regarded as sort of boring and backward. But we have faced two other Coronaviruses in the past which are nothing like the common cold virus. The first of these was called COV1 and caused the first epidemic of SARS Cov in 2003. SARS stands for Severe Acute Respiratory Syndrome. This Coronavirus also rose in China again from animals and then moved to humans. This particular Coronavirus did not transfer very effectively from human to human but it did do this well enough to move to 26 different countries. Fortunately it was not so communicable because its death rate was very high at 15% overall and 50% for those over 64 years old. The second famous Coronavirus to cross into humans was the MERS Cov 2 virus which caused as the name implies, Middle Eastern Respiratory Syndrome which broke out in Saudi Arabia. But again this virus did not transfer well between humans and stayed mostly in the Middle East. The camel was thought to be at least an intermediary vector. However, this virus also had quite a high death rate. So now we have reached the feared point where a deadly Coronavirus has gained the ability to rapidly and easily transfer from person to person. It is also thought that its origin was in bats in China but it is suspected that there was some intermediary animal between bats and humans, possibly an animal that was sold at the wild animal bushmeat markets of China. This virus is fortunately not as deadly as either SARS COV, or MERS COV, but on the other hand it has very effectively evolved to be able to infect humans very easily.
Just to clear up some confusions, this virus has several names. Some people in the beginning it called it a novel Coronavirus. Then people began to call it COVID 19 based on its origin in ;ate 2019. The Chinese scientists were able to sequence its RNA very early and did indeed supply that information to the world research community. Since this virus acts very much like the original SARS COV1, it is technically now called SARS COV2. But still the acronym COVID 19 is used both to refer to the disease it causes and to the virus itself.
Microscopically the crown at the end of the spike is really a couple of pincers held together by a lipid and protein bridge. In order for it to hook onto human cells and hold on long enough to break through the cell wall, this bridge has to break letting the pincer action allow the virus to stick to the cell. This virus has accomplished this mechanism. Actually it has adopted to use a small enzyme that the human cells themselves produce called furin. This protein is readily available throughout the human body and it accomplishes that break of the bond between claws on the crown allowing the grabbing of the human cell by a pincer like action.
Apparently it has evolved to utilize the ACE 2 receptor which is found on many cells in the human body. It seems that pincer actually grabs the ACE 2 receptor protein. The lungs have a particularly high concentration of these receptors as do the walls of blood vessels, and the gut. You may recognize the acronym, ACE. It stands for Angiotensin Converting Enzyme. Some of those of you with hypertension may recognize that you are on a drug called an ACE inhibitor. Such drugs block the protein, angiotensin and its tendency to raise blood pressure in our bodies. So does being on such a drug have any bad or good effects on this virus or the disease that it causes? Well we don't really know. There are anecdotal ideas, some held even among doctors, that one of the reasons that older individuals with underlying conditions often die from the disease is because they are on ACE inhibitors for their high blood pressure, or heart disease. Doctors have noticed this fact among their ICU patients on ventilators. But there are no studies that would prove this or disprove this idea. Since ACE inhibitors are so commonly used in these conditions that affect older people, it is more probable that this is just a coincidental presence of severe COVID 19 disease and the use of these drugs, and there is not a cause and effect relationship. In fact there is one small study that seems to postulate that being on ACE inhibitors may actually protect against the severe disease. We just don't know at this time. At any rate, we know that the virus uses the ACE2 receptor to stick to the cell wall and eventually get into the cell.
Many respiratory viruses tend to either cause mostly an upper respiratory illness or an infection of the lower respiratory tract. This virus seems to be able to do both. It first enters human cells probably in the upper respiratory tract and is able to infect cells there and proliferate without a lot of symptoms. This may be why people can seem almost or totally asymptomatic. But then once the virus has multiplied more it seems to in some people move down to the lower respiratory system and cause a viral pneumonia. At this stage several mechanisms can lead to worsening of the patient's condition. One problem seems to be that the secretions are very dry and hard to clear with coughing and this leads to portions of the lungs being closed off to good air movement for proper oxygenation. The body tries to mount an inflammatory response to kill this virus but sometimes that response seems to go berserk especially in compromised people such as the old, or those with other severe underlying conditions. This inflammatory over response does a couple things. First there is something called a cytokine storm where the inflammatory response produces a lot of these inflammatory proteins which in smaller amounts attract the white blood cells that produce killing antibodies and help fight off the invader. But if too much of these proteins are produced they make the blood vessels leaky and lots of fluid leaks out of the blood vessels into the lungs adding more difficulty to the breathing and oxygenation, essentially drowning the person microscopically. Also all of these conditions make the lungs open for invasion by bacteria as well and a bacterial pneumonia may occur. Sepsis is the cause of death in many of these patients which causes shut down of many other organs, such as the kidneys and liver.
There are a number of ways to attack this virus. Corticosteroids are used to suppress this immune over reaction called the cytokine storm. Now plasma from persons that have been infected and now recovered is being used in the very ill. There is one study from France with a relatively small group of patients who were given the antimalarial drug, hydroxychloroquine, and there seemed to be a good response that was statistically significant. But this was just one study. Currently studies are being done and this drug along with zithromycin are being used actively in the field against this virus, as long as the results are part of an organized study. Antivirals that have been used for influenza, HIV and other diseases are being tried. Various labs around the country now have live virus and are using those live virus to infect cell colonies and then measuring what various drugs do when added to these small human cell colonies. All of this work is done by robots and is observed microscopically. One drug seems to hold some promise so far, called remdesivir. This drug has been used to fight another very lethal respiratory virus called the Nipah virus which has caused outbreaks in Bangladesh and in Kerala, Inda. Studies are ongoing for this drug. There maybe new drugs that could be effective and perhaps are being safely used for totally different diseases. If any of these drugs have benefit in the lab, they could be introduced to human populations with COVID 19 fairly quickly because their general safety is already known. Such is the case for hydroxychloroquine and thus it is already being employed to some degree.
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