COVID-19 News, Info, Discussion /// Tracking the Spread of the Virus and its Effects /// October Lockdown for UK (pg. 774)

Only just cottoned onto the situation in Paraguay looking at the other thread. Societal breakdown on the cards.

https://twitter.com/_/status/1366310993014497283

I’m confused about Malta. Didn’t someone from there post recently saying that the whole population had been vaccinated?

Here is your weekend-doom:
There is something inside the big picture, i would like to clearify.

Any new virus seeks to infect as many new hosts as possible. This infection number is dominated by two main factors:
The rate of infection during the illness and the selective pressure by the response from human society. Let's examine the various scenarios.

Scenario A: The rate of infection is more or less steady during the illness.
Then
the longer the infected person lives, the more new potential hosts are reached,
the spread of a dangerous virus will be hampered by the social response.

This results into a selective pressure which favours new virus mutations which are less dangerous/lethal. This is what is mostly observed in new viruses: The mutation into harmlessness.

Scenaio Br: The rate of infection strongly varies during the infection

B1: Stronger infection during the end of the illness and high lethality. A good example is Ebola, which is very lethal and spreads mostly near the death of the victims. It kills the host too fast and evocs a strong social response (quarantine) . Therefore Ebola will never be a global threat.

B2: A strong infectivity at the very beginning of the sickness. The current example is Covid. The first few days are most infectious, before the virus moves into the body. For the spread of the virus it does not matter whether the host will die shortly after these highly infectious days or lives to old age. There is a natural selective pressure for increased viral multiplication during these first few days, which will favour mutations with a higher reproduction rate. Therefore more mutations will spring up and spread, which may have multiple pathways for cell-entry. In future the ACE2-pathway might not be as much in the focus as it is for now.

This natural selective pressure will produce new immuno-evasive mutants with a much higher viral load and therefore will have a resulting higher lethality.
A good example is the P1-mutation: The average CT-threshold in PCR-tests is 1.91 times lower for the P1. This translates into a ~4 times higher viral load. Not to talk about the upcoming California-strain....

This virus will mutate further into a monster.

So, you better buckle up, it is going to be messy.

Here is your weekend-doom:
There is something inside the big picture, i would like to clearify.

Any new virus seeks to infect as many new hosts as possible. This infection number is dominated by two main factors:
The rate of infection during the illness and the selective pressure by the response from human society. Let's examine the various scenarios.

Scenario A: The rate of infection is more or less steady during the illness.
Then
the longer the infected person lives, the more new potential hosts are reached,
the spread of a dangerous virus will be hampered by the social response.

This results into a selective pressure which favours new virus mutations which are less dangerous/lethal. This is what is mostly observed in new viruses: The mutation into harmlessness.

Scenaio Br: The rate of infection strongly varies during the infection

B1: Stronger infection during the end of the illness and high lethality. A good example is Ebola, which is very lethal and spreads mostly near the death of the victims. It kills the host too fast and evocs a strong social response (quarantine) . Therefore Ebola will never be a global threat.

B2: A strong infectivity at the very beginning of the sickness. The current example is Covid. The first few days are most infectious, before the virus moves into the body. For the spread of the virus it does not matter whether the host will die shortly after these highly infectious days or lives to old age. There is a natural selective pressure for increased viral multiplication during these first few days, which will favour mutations with a higher reproduction rate. Therefore more mutations will spring up and spread, which may have multiple pathways for cell-entry. In future the ACE2-pathway might not be as much in the focus as it is for now.

This natural selective pressure will produce new immuno-evasive mutants with a much higher viral load and therefore will have a resulting higher lethality.
A good example is the P1-mutation: The average CT-threshold in PCR-tests is 1.91 times lower for the P1. This translates into a ~4 times higher viral load. Not to talk about the upcoming California-strain....

This virus will mutate further into a monster.

So, you better buckle up, it is going to be messy.

Portugal concerned about P1...

https://twitter.com/_/status/1368256317547249664

Here is your weekend-doom:
There is something inside the big picture, i would like to clearify.

Any new virus seeks to infect as many new hosts as possible. This infection number is dominated by two main factors:
The rate of infection during the illness and the selective pressure by the response from human society. Let's examine the various scenarios.

Scenario A: The rate of infection is more or less steady during the illness.
Then
the longer the infected person lives, the more new potential hosts are reached,
the spread of a dangerous virus will be hampered by the social response.

This results into a selective pressure which favours new virus mutations which are less dangerous/lethal. This is what is mostly observed in new viruses: The mutation into harmlessness.

Scenaio Br: The rate of infection strongly varies during the infection

B1: Stronger infection during the end of the illness and high lethality. A good example is Ebola, which is very lethal and spreads mostly near the death of the victims. It kills the host too fast and evocs a strong social response (quarantine) . Therefore Ebola will never be a global threat.

B2: A strong infectivity at the very beginning of the sickness. The current example is Covid. The first few days are most infectious, before the virus moves into the body. For the spread of the virus it does not matter whether the host will die shortly after these highly infectious days or lives to old age. There is a natural selective pressure for increased viral multiplication during these first few days, which will favour mutations with a higher reproduction rate. Therefore more mutations will spring up and spread, which may have multiple pathways for cell-entry. In future the ACE2-pathway might not be as much in the focus as it is for now.

This natural selective pressure will produce new immuno-evasive mutants with a much higher viral load and therefore will have a resulting higher lethality.
A good example is the P1-mutation: The average CT-threshold in PCR-tests is 1.91 times lower for the P1. This translates into a ~4 times higher viral load. Not to talk about the upcoming California-strain....

This virus will mutate further into a monster.

So, you better buckle up, it is going to be messy.

Has it ever been discussed, when all viruses mutate millions or Billions of times (influenza & all viral pneumonia’s). These viruses will have errors within the genome. Preventing them becoming more deadly or specifically an ELE.

Never in history has a virus mutated to become more deadly to an extent that caused an ELE. We are still here. Overall picture , the fact appears human Immunity adapted and overcame/ with combination of to many errors after mutations.