Discussion in 'Biology & Genetics' started by KUMAR5, Jan 8, 2022.
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What can make Omicron not reach to Lungs or other tissues where ACE 2 receptors are there throug which its origibal counterparts take entry? Is it intrinsically different to COVID 19 in this characteristic?
Good question. I don't know. I'll try to find out.
It does reach the lungs. But compared to Delta, it grows much faster in the bronchi and much slower in the lungs (alveoli.)
Sort of. It evolves to be more contagious. That can be via changes to the structure of the virus, or it could be due to worsening symptoms (which spread the disease) or it could be due to letting that sick guy walk around for years spreading it.
So about all you can say is that it will evolve to kill people less quickly. Which is better than more quickly. But keep in mind that almost everyone survives HIV infection now. Is that something we want COVID to evolve towards? I mean, imagine HIV but spread through the air.
OK from an expert elsewhere I gather all variants use ACE2 to dock with the cell. What happens next is there has to be a way to gain entry. Here it seems there is evidence that Omicron may use a different method of entry from previous variants and this method does not favour lung cells. But it seems to be work still in progress, i.e. we don't know for sure yet.
Don't harmful virus evolve to become harmless virus to us...healthy human virome? It is also in their survival interest.
Thanks. However it is very important point, need full attention. I think in many cases of Covid, it also happen that their lungs are not infected. But yhere, it is due to some interference of immune response. But in Omicron it appear to be a different reason because every patient infected with it experisnce this type of outcome. Either omicron is wéaker variant than Delta so unable to reach in lungs or use some different route for entry.
We need to know it if it us due to difference in nature of Omicron variant or of our tissues or our immune response at these two sites.
We will know soon enough. But give it a few months.
Not really. A virus that cannot spread is a failure. Thus it is to its advantage to make us sick enough to spread, but not sick enough to kill us quickly.
?? It is, of course, due to both. Almost every virus in the world will kill someone with no immune system.
We need to be clear, that isn't friendly. Moreover, it's complete balderdash. Covid 19 is a virus; it isn't alive and cannot select itself as such.
The virus does not necessarily favor humans. Like I said, coronavirus has a wicked history:
In 1912, German veterinarians puzzled over the case of a feverish cat with an enormously swollen belly. That is now thought to be the first reported example of the debilitating power of a coronavirus. Veterinarians didn’t know it at the time, but coronaviruses were also giving chickens bronchitis, and pigs an intestinal disease that killed almost every piglet under two weeks old.
The link between these pathogens remained hidden until the 1960s, when researchers in the United Kingdom and the United States isolated two viruses with crown-like structures causing common colds in humans. Scientists soon noticed that the viruses identified in sick animals had the same bristly structure, studded with spiky protein protrusions. Under electron microscopes, these viruses resembled the solar corona, which led researchers in 1968 to coin the term coronaviruses for the entire group.
It was a family of dynamic killers: dog coronaviruses could harm cats, the cat coronavirus could ravage pig intestines. Researchers thought that coronaviruses caused only mild symptoms in humans, until the outbreak of severe acute respiratory syndrome (SARS) in 2003 revealed how easily these versatile viruses could kill people.
The question of humans as some sort of "favoured race" just does not work; not only do viruses not choose in such a manner, the notion still fails to make sense in any colloquial context. Coronavirus, in general, finds Chiroptera an excellent host, and relationship that seems to continue as we track the history of SARS-CoV-2. Covid 19 in particular is a variation disruptive of a long general relationship between coronavirus and humans, escalating the viral threat to the host species.
There is no manner of calling Covid 19 Omicron a friend that does not require an extraordinary definition of friendship. The idea that the question would even be structured as such very nearly seems to be its own question.
Cyranoski, David. "Profile of a killer: the complex biology powering the coronavirus pandemic". Nature. 4 May 2020. Nature.com. 10 January 2022. https://go.nature.com/3padQ5J
I feel I am able tohttps://www.nature.com/articles/d41586-022-00039-0 find some here:.
Probably it is due to variatiion in exoression of TMPRSS2 expression. Somewhat indicated here;
It changes due to age,gender, diseases, smóking, lifestyke etc.
I can not say, whether demostration of Omricron variant suggest if Covid virus is gaining power or losing oower if gaining then it us foe if losing them friend or at least not foe. Not so?
Again, I disagree there. It's an improvement. It does not make omicron "a friend."
If a serial killer who was killing 10 women a year cut back to 5 a year, would you call him a friend? Because fewer are dying?
Is it not true that by bringing Omicron, Covid Virus has increased its presence(spread) but at the cost of reducing its vitality? It it not in our favor?
To be alive or not is a vouge subject. There may not be any absolute definition to these unless one can agree on basic level that whatever matter is without any energy is dead and with enery is live. All other are just definition for convenience or convincing. Things show life factors by their chemical, structural and physical make ups and I these all these factors virus does possess. Even many time so taken as non-live are also shown to show behavior of natural selection. A more robust mountain will survive more. Whao has selected it. It is nature.
Like friendly bacteria are there few virus which can also be friendly to us?
However I am just comparing Omicron with Covid 19 or with Delta. If it is less harmful to us than its previous variants and is setting a trend toward making Covid less or non harmful by decreasing severity to us and reducing its own vitality then we can consider it is favouring us...so a friend. Not so?
Yes I know but this is all preliminary. Need to wait for more studies.
Most unsettling is the persistent need for a "friendly" context:
No, not so.
It's hard to count the ways it's not so. The lack of an EF-3 fire tornado in the Marshall Fire that swept through Boulder County, Colorado, recently, and its low death toll, do not imply any favor or friendliness. The way that fire went is the way it went, entirely subject to its driving natural factors, and cannot be taken to imply we won't be seeing EF-3 fire tornadoes in the future. Similarly, what passses for lesser severity about Omicron cannot be taken to suggest any good news about the future of SARS-CoV-2 Covid-19.
Nurse practitioner Erin C. Sanders↱ explains, in a Twitter thread:
The fact that #Omicron doesn't replicate as much in the lung doesn't make me feel better. Why? #COVID19 was never just a respiratory disease, that's its primary mode of transmission. I'm increasingly concerned about what this means for vasculature/clot presentation in particular.
The highly credentialed scientist from MIT continues↱:
It's also concerning to me that frontline healthcare workers are *already* reporting seeing increased rates of MI, stroke, and PE with #Omicron wave despite decreased ARDS.
To be clear: Less acute respiratory distress, but more heart attack, stroke, and pulmonary embolism. The neurological implications are nightmarish, including retrograde transport and dissemination to the central nervous system, and pathways to autoimmune complications. We've also discussed risks to pancreas and kidney.
Psychologist Emma Kavanagh↱, meanwhile, recalls her "mild" covid: "I have never recovered", she says, even two years later. Narratives that "we just have to get on with it" are "terrifying", she explains: "How many more of me will there be — illnesses that simply never end."
The fact of long Covid is observed, and will be among the costs of seeking friendship about Omicron. Kavanagh notes a lack of any substantial plans for dealing with long Covid, and for our part, we might also note the appeal to Omicron as friend does not really seem to account for that.
@EmmaLK. "Look, let me be frank. My initial covid infection did not require hospitalisation. Ergo it was 'mild'. However, I have never recovered. 2 years later & I am nowhere near who I once was. My body & brain have sustained long term damage. THAT is what Living With Covid looks like." (thread) Twitter. 9 January 2022. Twitter.com. 11 January 2022. https://bit.ly/33mvlqU
@ErinSandersNP. "The fact that #Omicron doesn't replicate as much in the lung doesn't make me feel better. Why? #COVID19 was never just a respiratory disease, that's its primary mode of transmission. I'm increasingly concerned about what this means for vasculature/clot presentation in particular.". (thread) Twitter. 3 January 2022. Twitter.com. 11 January 2022. https://bit.ly/3GkzxGn
Also this one:.
-Location within human body :
...Despite the fact that the respiratory system is the primary route of SARS-CoV-2 infection, very limited expression is seen, both at protein and mRNA level. The expression within the respiratory system is mainly restricted to the upper bronchial and nasal epithelia, especially in the ciliated cells."
Separate names with a comma.