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.
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:
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,, 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.