Scientists Race To Successfully Dissect Coronavirus

It appears that evacuated passengers from the Sick Ship in Japan.  454 people on that ship got sick, so far.  The killer element in this disease is pneumonia.  Indeed, this is exactly what made the Hong Kong flu so dangerous, I took on significant lung damage from that disease and it took over a year to recover.  The virus is spreading but the ratio of deaths from it continue to be much lower than the infection rate.

 

Every hour we learn more about this virus.  This ability to study new viruses quickly is important.  At first, the dictators running China refused to share materials with other research centers but now naked fear has forced them to share, finally.  Here is a picture of the virus’s genetic structure:

What a tangled web if viral deceit doth this germ weave!  It isn’t a simple structure, it is quite complex.

 

Scientists are mobilizing their resources quickly, sharing information about the virus with unprecedented pace, and turning experiments into peer-reviewed research in a matter of weeks.

 

That’s the case for Jason McLellan, a structural biochemist, and his team at UT Austin who have been studying similar coronaviruses for years. Their latest study, published in the journal Science on Wednesday, took advantage of state-of-the-art technology at the university to map the molecular structure of the novel coronavirus, with a particular focus on the virus’ “spike protein.”

 

So, the coronavirus has been studied for years?  Interesting.  This is a mutation, this new virus. I found this article from 1996: 

David A.J. Tyrrell and Steven H. Myint.

General Concepts

Clinical Presentation

Coronaviruses cause acute, mild upper respiratory infection (common cold).

Structure

Spherical or pleomorphic enveloped particles containing single-stranded (positive-sense) RNA associated with a nucleoprotein within a capsid comprised of matrix protein. The envelope bears club-shaped glycoprotein projections.

Classification

Coronaviruses (and toroviruses) are classified together on the basis of the crown or halo-like appearance of the envelope glycoproteins, and on characteristic features of chemistry and replication. Most human coronaviruses fall into one of two serotypes: OC43-like and 229E-like.

Multiplication

The virus enters the host cell, and the uncoated genome is transcribed and translated. The mRNAs form a unique “nested set” sharing a common 3′ end. New virions form by budding from host cell membranes.

Pathogenesis

Transmission is usually via airborne droplets to the nasal mucosa. Virus replicates locally in cells of the ciliated epithelium, causing cell damage and inflammation.

Host Defenses

The appearance of antibody in serum and nasal secretions is followed by resolution of the infection. Immunity wanes within a year or two.

Epidemiology

Incidence peaks in the winter, taking the form of local epidemics lasting a few weeks or months. The same serotype may return to an area after several years.

 

I will note that this information has been ignored for the most part with media and governments pretending this form of coronavirus is something new now something very old and quite common and which generally happens in winters which is what this virus is doing and incidentally, is what other flu viruses like the Hong Kong flu works, too.

 

Back to the news story from this last three days:

 

The first 3D map of SARS-CoV-2, the coronavirus responsible for over 2,000 deaths since December 2019, has been produced by a collaboration of coronavirus researchers at the University of Texas at Austin and the National Institutes of Health. Heralded as a breakthrough, the map provides a stepping stone to the development of antivirals or vaccines to stymie the virus.

 

The question is, can this work?  According to the CDC (who studied my own blood samples, for example, back in the Hong Kong flu epidemic) this is a novel virus but it is in the family of the common cold viruses.  This is why it is not the fever killing people, it is the lung damage that is killing people.

 

The coronavirus is running riot now in South Korea and I assume, North Korea.  As I said in the past, the horses have long left the barn, we have to endure another epidemic and this means we have to keep on dealing with viruses and I hope an inoculation is created that will protect us but I will also note that though the disease is moving fast, it will probably weaken over time, all diseases that kill very fast, end fast.

 

The research team showed there are similarities between the spike protein in the coronavirus responsible for the 2002-2003 SARS outbreak and the new coronavirus, SARS-CoV-2. However, the latter appears to bind to human cells much more strongly than the SARS virus did and antibodies against the first SARS virus don’t seem to react to the new virus in the same way.

 

That is both bad news and good news.  The bad news is, the virus is even worse than the SARS virus event.  On the other hand, the unique antibodies of this virus may open the door to possible vaccination protection in the future?

 

Creating the 3D map of the spike protein in SARS-CoV-2 is the first step in speeding up vaccine design and development, but experiments to examine how successfully it elicits an immune response are ongoing, according to McLellan, but looking to previous viruses provides a little hope.

 

Yes, looking into the history of these viruses shows that they follow a track that usually follows a pattern of appearing when population levels are high and weakening as the population level drops to some degree.

 

“The spike proteins from other coronaviruses, such as MERS-CoV and SARS-CoV have been very immunogenic when used as a vaccine antigen,” McLellan says. “We expect the same to be true for this novel coronavirus.”

 

We must consider this good news, the possibility of a vaccine is hopeful.  I expect anti-vaccinationists to do their utmost to prevent this from happening.  This is why we still have measles in first world countries.

 

From the above CDC report from thirty years ago:

 

Colds caused by coronaviruses cannot be distinguished clinically from other colds in any one individual. Laboratory diagnosis may be made on the basis of antibody titers in paired sera. The virus is difficult to isolate. Nucleic acid hybridization tests (including PCR) are now being introduced.

The suggestion back then is ‘isolate patients and improve hygiene.’  This is why the disease first appeared in an ‘underground’ meat market which sold bats to eat (yuck).

 

Coronaviruses are found in avian and mammalian species. They resemble each other in morphology and chemical structure: for example, the coronaviruses of humans and cattle are antigenically related. There is no evidence, however, that human coronaviruses can be transmitted by animals. In animals, various coronaviruses invade many different tissues and cause a variety of diseases, but in humans they are only proved to cause mild upper respiratory infections, i.e. common colds. On rare occasions, gastrointestinal coronavirus infection has been associated with outbreaks of diarrhoea in children, but these enteric viruses are not well characterized and are not discussed in this chapter.

 

And this is what makes this disease so troubling: it is a mere common cold gone wild.  It is a change in the degree of impact, that is, it causes a collapse of the lungs.  I remember living in the shadow of lung damage from the flu.

 

For years, I wore face coverings in winter, I wore gloves everywhere. I was very paranoid of getting the common cold, it could kill me via messing up my lungs again which were damaged.  My lungs finally recovered by 1976, nearly a decade after the disease.

 

People die every winter from the ‘common cold.’  Nearly always, it is due to the lungs giving out mostly in the very elderly and very young.  This disease hits everyone hard and requires great care to prevent lung failure.

 

From the old CDC report:

 

Although mucociliary activity is designed to clear the airways of particulate material, coronaviruses can successfully infect the superficial cells of the ciliated epithelium. Only about one-third to one-half of infected individuals develop symptoms, however. Interferon can protect against infection, but its importance is not known. Because coronavirus infections are common, many individuals have specific antibodies in their nasal secretions, and these antibodies can protect against infection. Most of these antibodies are directed against the surface projections and neutralize the infectivity of the virus. Cell-mediated immunity and allergy have been little studied, but may play a role.

 

And this is the hope: common cold antibodies is probably why only 20% or fewer of the coronavirus victims are dying.  This isn’t a 100% death rate, it may be a 50% infection rate or less.  The fact that many people who get it don’t die or even get very ill is proof that something is at work here that is causing it to be highly fatal with certain populations.

 

This is another area scientists are examining, I would imagine.  By the way, I will note here that most people who are infected or around infected people in Asia are NOT WEARING GLOVES.  I noted way back in 1970 that wearing gloves was key to keeping from getting ill with the common cold which was a grave danger to my lungs due to damage done by the Hong Kong flu.

 

This inability to see the role hands play in disease transmission is very annoying.

5 Comments

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5 responses to “Scientists Race To Successfully Dissect Coronavirus

  1. Moe

    The virus is also airborne.

    One must train them-self to stop touching the face. (If you monitor this you will be surprised how often this occurs).

    I can’t find the source but one report stated the virus is small enough to penetrate latex gloves, but I have not found confirmation of this.

  2. Ken

    The latest medical reports indicate that the coronavirus does not just attack the lungs. It results in “multiple organ failure” due to it attacking the ACE2 receptors, which are throughout the body. Organs attacked in addition to the lungs include “heart, kidney, liver, intestine, testis (ouch!), etc.”

    “Abstract

    Angiotensin converting enzyme 2 (ACE2) in the lung has been recognized as the key receptor of the 2019 novel coronavirus (2019-nCoV) as people may get infected through the respiratory tract. However, the clinical features of other systems have not been addressed yet. More than the respiratory system, ACE2 also extensively expressed in the vascular endothelial cells of the heart, kidney, liver, intestine, and testis, etc. In other words, the new coronavirus may probably intrude on any tissues or organs as long as the needed number of ACE2 is available. Therefore, once exposed to the coronavirus (e.g. through the blood or other body fluid), these organs may also get affected especially for those the receptor has the direct-acting control. This paper aims to analyze the possibility of the association between 2019-nCoV infection and the multiple organ failure (MOF) other than pneumonia.”

    Source: Yang, Ming and Zhao, Jinming and Zhang, Zheng, More Than Pneumonia, The Potential Occurrence of Multiple Organ Failure in 2019 Novel Coronavirus Infection (February 5, 2020). Available at SSRN: https://ssrn.com/abstract=3532272 or http://dx.doi.org/10.2139/ssrn.3532272

    So this is quite a nasty bug. It goes after everything.

  3. Jim R

    The “authorities” seem to be doing everything they can to spread this virus. They coop up thousands of people on a cruise ship because of a couple of cases, and incubate them together for a couple weeks, and then decide to let them disperse to all over the planet. You are going to be exposed to it, just like you are exposed to the “common cold” every year. Cruise ships are not known for their BSL-4 isolation equipment, they are built to encourage people to mingle.

    And, this virus is airborne, as I have said before, and as everyone says. You do not need to touch anything to get it.

    The good news, of course, is that the faster a virus goes, the faster it mutates, and it is not exactly the same virus from one case to the next. Mutations pile up, and it will soon be this year’s version of the common cold. It is an RNA virus, which has no ‘repair’ mechanism at all for its genetic code, so each and every mutation propagates, and 99.999+% of the time, dilutes the effectiveness of the virus.

    It is unfortunate that you caught the Hong Kong flu in its first flush, Elaine. If you could have avoided it for a couple weeks, you would have had the flu but it probably would not have been so horrible.

  4. Jim R

    @Ken,

    I tend to doubt the importance of that paper. If they examine any tissue sample from someone who has had a bad case, or died, from this virus, guess what they will find? Viruses, duh!

    Another report I saw recently said that the victims who suffer multiple organ failures are experiencing a ‘cytokine storm’. This is the phenomenon that kills young adults with the flu. And it is the same, or similar, to the mechanism of an allergy to bee stings or peanuts. The immune system gets so hyped up that it starts attacking everything it can get to.

  5. All so true, thanks for the added information. Yes, viruses mutate easily. They are also the earliest replicant ‘life’ forms way back when the planet was very new and quite hot waters. Now, these germs need NO OXYGEN and I suspect, this is why they attack the lungs with such ferocity.

    They are from the early planet’s evolution, oxygen was created by plant life creatures which happen to be the hosts for these RNA strings and give them their ‘happy climate conditions’ inside other entities.

    I do hope they come up with something to inoculate us against these germs! I know first hand how terrifying it is to not be able to breathe easily.

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