To the people who support a lockdown and who are still receiving an income(either because you are a "essential worker ", able to work from home, or business is not affected by the lockdown):
Would you support the government taking away 50% of your income and distributing it to people with no income because of the lockdown?
If you don't, why not? I mean about the concept in general- if you support a lockdown and still have an income, in addition to the taxes you already pay, are you willing to give up more of your money?
I am flexible about the 50% or about who should receive the aid (obviously dont mean a millionaire ).
BTW, just to be clear, as I didn't mention it in my previous post regarding the shutdowns, I was merely presenting more info about the effects of the shutdowns specifically in regards to the spread of the disease.
Again, I'm not arguing in favor of the shutdowns, I'm just pointing out that it broke the exponential growth rate.
I'd much rather the majority exercised personal responsibility to mitigate the risk of catching the disease themselves AND importantly, infecting others and perpetuating the spread.
Another thing I didn't address in my recent posts (I may have mentioned it in a post weeks ago), is the misunderstanding about viral mutation.
I've seen and heard idea repeatedly, that viruses always mutate to a weaker version. This is an oversimplification the illustrates a lack of understanding of the subject.
Any pathogen has traits that can be categorized as such:
- Infectivity: how easily it infects a person who's been exposed
- Pathogenicity: how readily it causes disease in an infected person (there are pathogens that cause infections, but not disease, i.e. SARS-CoV-2 is the pathogen, Covid-19 is the disease. If everyone infected was completely asymptomatic, the pathogenicity would be low).
- Virulence: the severity of the disease resulting from infection
- Fatality: how likely the disease is to result in death
There are already a few thousand mutations recorded in the SARS-CoV-2 virus from samples from across the world (this is how they confirmed the reinfection cases, by comparing the virus samples from a patient's 1st and 2nd infections to see if it might just be a case of persistent infection, or reinfection from a variant showing enough mutational variance that it's unlikely to have developed within the host/patient).
The vast majority of these small mutations don't have an effect one way or the other, but one mutation that HAS demonstrated an effect is the D614G mutation I mentioned a while back.
The D614G mutation altered the spike protein that the virus uses to attach to the ACE2 receptors that the virus targets and uses for replication. This mutation that increased the binding ability of the spike protein gas resulted in an increase in the infectivity, as well as the pathogenicity and virulence.
This mutations infectivity has increased enough that it is now the dominant circulating strain worldwide (~70% of worldwide submissions to GenBank show this mutation).
Because the mutation affects the ability of the virus to bind to the ACE2 receptors, it affects how easily a dose of the virus causes infection, AND how easily the virus replicates within the body (hence increasing the pathogenicity and virulence).
For the virus to 'weaken' worldwide, would require a mutation that both increases the infectivity, while simultaneously decreasing the pathogenicity and virulence, but as mentioned, the spike protein is tied to both how infectious the virus is, and how easily it reproduces within the host which affects the pathogenicity and virulence.
A mutation that results in a lower binding affinity would be less infective and thus, selection pressure would mean the more infective version would continue to be the dominant circulating version.
We'd need to see a mutation that somehow both increases the infectivity, yet somehow decreases the virulence and pathogenicity, all within the same sample.
The hypothesis that a virus mutates to be weaker because it's more easily spread, lacks an understanding of virology AND this particular pathogen.
Yes, if we're talking about a pathogen with a short incubation and even higher fatality, a variant that has longer incubation and lower fatality/virulence will allow an infected individual to continue spreading it longer and to more people, as they continue exposing contact because they're "just a little under the weather" vs bedridden or dead.
The thing about the SARS-CoV-2 virus is that it already demonstrates a medium long incubation, coupled with presymptomatic and asymptomatic transmission, meaning there's already ample opportunity for people to continue spreading it when they're infected.
One other concern is that the greater the spread of the virus, the greater the chance of a more dangerous mutation occurring, whether from natural mutation within a host, or recombinant variants appearing due to
confection coinfection (saw my typo quoted in Lorien's reply. Concurrent infection with 2 or more pathogens, not something related to pastries), or another species jump (as evidenced by the fact that this virus has proven to be able to infect cats, dogs, ferrets and other animal species).