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The New Covid19 Virus
What property of the new variant makes it so much more transmittable ?
Is it a smaller particle that can remain airborne for longer distances?
Does it take fewer particles to cause an individual to become
infected because it is so much more virulent ?
Are there any additional precautions that people can take against it
Is it a smaller particle that can remain airborne for longer distances?
Does it take fewer particles to cause an individual to become
infected because it is so much more virulent ?
Are there any additional precautions that people can take against it
Answers
1 to 10 of 10
Yes, the Independent link provides a good overview of the current situation. PP, tightly bound does not mean bound for longer: it merely reflects the tenacity of the contact residue in the RBD. The binding affinity to human ACE2 is indeed increased because of mutation N501Y in the variant. It has been suggested that transmissibi
20:28 Sun 03rd Jan 2021
it's explained here
https:/
It doesn't sound as it you need to take different precautions, just more of the same.
https:/
It doesn't sound as it you need to take different precautions, just more of the same.
truth is they dont know
https:/
"One, called N501Y, has previously been shown to increase how tightly the protein binds to the angiotensin-converting enzyme 2 receptor, its entry point into human cells."
tightly bound also means bound for longer
It has long been recognised since 1665 and probably 1348 that as a epidemic goes on, the cases get worse
["passage thro the host increases virulence"]
and this has predictably happened here
so they have the 17 changes that happened at once in the virus,
and they know it is more aggressive
but still nowhere near: " you see that mutation at B15? well that twoingies the blong-blong, the dongles droop and the femta falls and turns it into a killer virus"
even saying - and the R number goes up by 0.5
all that means is that more peoplle get it from one person, around 50% more than before
https:/
"One, called N501Y, has previously been shown to increase how tightly the protein binds to the angiotensin-converting enzyme 2 receptor, its entry point into human cells."
tightly bound also means bound for longer
It has long been recognised since 1665 and probably 1348 that as a epidemic goes on, the cases get worse
["passage thro the host increases virulence"]
and this has predictably happened here
so they have the 17 changes that happened at once in the virus,
and they know it is more aggressive
but still nowhere near: " you see that mutation at B15? well that twoingies the blong-blong, the dongles droop and the femta falls and turns it into a killer virus"
even saying - and the R number goes up by 0.5
all that means is that more peoplle get it from one person, around 50% more than before
Yes, the Independent link provides a good overview of the current situation.
PP, tightly bound does not mean bound for longer: it merely reflects the tenacity of the contact residue in the RBD. The binding affinity to human ACE2 is indeed increased because of mutation N501Y in the variant.
It has been suggested that transmissibility of VOC-202012/01 (the variant) has increased by around 70% as a result of this change, but we're keeping an open mind at the moment for some technical reasons.
A number of other mutations have occurred but the one that's being looked at particularly closely is an amino acid deletion called 69-70del. Changes have happened here before and it's possible that the deletion when combined with mutation N501Y is enhancing the transmissibility of the variant. We know that this can happen. Some but not all of the other mutations are also significant, including P681H.
Funnily enough Peter, one discussion I had in the high containment lab yesterday morning went very much along the lines of your "you see that mutation at ...." although the key words were slightly different. We've even invented our own acronyms!
Still, let me reassure you it's onwards and upwards. Progress is being made and we'll beat this *** in the end. Further, expansive information on this matter is readily available on the web for those who wish to expand on the information I've provided.
Finally, no it's not a smaller particle. You can regard it as a structural change.
The number of individual virions needed to allow a person to become infected is immaterial as the human host cells manufacture the virus following infection. In slightly more detail, the spike protein binds with an enzyme receptor on the cell. The spike protein then cleaves and allows the virion to enter the cell where it releases its DNA and is translated into new viral proteins. Cell proteins then package the lot into new virus particles and can release up to around a thousand per day.
There are no additional precautions to follow - government advice on these measures is first rate.
PP, tightly bound does not mean bound for longer: it merely reflects the tenacity of the contact residue in the RBD. The binding affinity to human ACE2 is indeed increased because of mutation N501Y in the variant.
It has been suggested that transmissibility of VOC-202012/01 (the variant) has increased by around 70% as a result of this change, but we're keeping an open mind at the moment for some technical reasons.
A number of other mutations have occurred but the one that's being looked at particularly closely is an amino acid deletion called 69-70del. Changes have happened here before and it's possible that the deletion when combined with mutation N501Y is enhancing the transmissibility of the variant. We know that this can happen. Some but not all of the other mutations are also significant, including P681H.
Funnily enough Peter, one discussion I had in the high containment lab yesterday morning went very much along the lines of your "you see that mutation at ...." although the key words were slightly different. We've even invented our own acronyms!
Still, let me reassure you it's onwards and upwards. Progress is being made and we'll beat this *** in the end. Further, expansive information on this matter is readily available on the web for those who wish to expand on the information I've provided.
Finally, no it's not a smaller particle. You can regard it as a structural change.
The number of individual virions needed to allow a person to become infected is immaterial as the human host cells manufacture the virus following infection. In slightly more detail, the spike protein binds with an enzyme receptor on the cell. The spike protein then cleaves and allows the virion to enter the cell where it releases its DNA and is translated into new viral proteins. Cell proteins then package the lot into new virus particles and can release up to around a thousand per day.
There are no additional precautions to follow - government advice on these measures is first rate.
thanks prof
I stand corrected
the second mutation you mention is meant to interact ( or lack of interaction ) with the immunosuppressed - but that is deffo too much detail for a non tech thread.
longer action leads to higher k was from Receptor Occupancy theory and I am quite prepared to be told: oh that, we have moved on from that
you know D + R goes to DR and then back to D + R
is a perfectly good model of virus, spike interaction
and if the cirus and spike sticks together for longer then there is a higher chance of endocytosis.
I stand corrected
the second mutation you mention is meant to interact ( or lack of interaction ) with the immunosuppressed - but that is deffo too much detail for a non tech thread.
longer action leads to higher k was from Receptor Occupancy theory and I am quite prepared to be told: oh that, we have moved on from that
you know D + R goes to DR and then back to D + R
is a perfectly good model of virus, spike interaction
and if the cirus and spike sticks together for longer then there is a higher chance of endocytosis.
1 to 10 of 10
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