B
bluemax_1
- what's your read on the "g" strain/mutation of the Covid virus. I'm sorry to say I really don't know the lingo, but I understand there is some evidence that there is a mutation of the Covid virus which has a G in one of the amino acids that used to have a D protein. This is somehow far more infectious/contagious (although not all that more lethal?).
I am wondering if that is part of why the curve has taken on the shape of a hockey stick... (which cannot be helped by the reopening around Memorial Day and protests nationwide).
The weeks after memorial day have been remarkable. Then next 3-4 are going to be even more so. The brakes failed on the freight train, it seems....
Thanks again for the rational posts you make.
Short answer: The D614G mutation is bad news. It's a mutation that altered the spike proteins you may recall them talking about on the news. It increases the stability and binding ability of the spike proteins, which increases SARS-CoV-2's infectivity and virulence. Due to this higher infectivity, the D614G mutation has rapidly become the predominant spreading variant, accounting for 70% of the new samples isolated by the gene bank studies not just in the US, but from worldwide sampling.
The spike proteins in the surface of SARS-CoV-2 are what allow it to attach to cells and infect them, which is why this mutation increased not only the infectivity, but also the virulence.
The first cases of community spread occurred on the West coast, hitting WA and CA with the older D614 variant.
NY and the East coast got hit with the D614G mutation which likely arrived from Italy. Notice not only how fast it spread in the East coast states once community spread levels were reached, but also how the CFR is higher.
Viruses mutate regularly. Most of the mutations are benign. Sometimes the mutations increase the virus's ability to infect, sometimes they decrease it. Sometimes the mutations increase the virulence, and sometimes they decrease it.
I've heard more than one person who's read some article or other, say, "I heard/read that viruses all eventually mutate to a milder version. Their goal is to spread, so killing the hosts isn't beneficial. Mutating to a milder form allows them to continue spreading more effectively. Look at the 1918 Spanish Flu, the regular coronaviruses. And SARS 1 and MERS died out".
The above is an example of folks who don't understand pathogenesis and epidemiology.
Infectivity = how easily an organism can infect you.
Pathogenicity = the ability of the organism to cause disease. (eg. In some cases/organisms, you can be infected, but not develop disease from it. Eg. SARS-CoV-2 is the pathogen, Covid-19 is the disease. HIV is the pathogen, AIDS is the disease. Helicobacter Pyloridis is the pathogen, gastroenteritis is the disease).
Virulence = the severity of the disease resulting from infection.
Viruses don't think or adapt intentionally. They're simply unstable enough to mutate often.
Selective pressure (in pathogens) = natural selection from factors that affect an increase or decrease of the pathogens ability to infect and spread.
If a mutation (such as D614G) increases the pathogens ability to infect and spread, then the higher infectivity means it spreads faster and preferentially. In this case, the mutation also means that it binds to cells more easily, also increasing its virulence.
SARS 1 and MERS were never even close to SARS-CoV-2's infectivity. With a far smaller spread, a mutation that either decreased the infectivity or pathogenicity, potentially means the pathogen naturally disappears.
The problem with something that's spread as wide as SARS-CoV-2, is that IF a mutation develops that has lower infectivity, it won't result in the pandemic dying out, because a variant with higher infectivity that's already widespread spreads further and faster.
We'd need a variant that develops BOTH a mutation that enhances its infectivity (so it spreads much more easily and rapidly) AND a mutation that decreases the pathogenicity and virulence (so it reduces the chance of severe disease from infection), while simultaneously conferring lasting immunity not just to the milder variant, but to the more virulent strains.
With the infectivity and virulence both tied to the spike protein's ability to bind to cells, the likelihood of that occurring isn't something I'd wager on.
The 1918 H1N1 strain circled the globe in 3 waves. The 1st wave predominantly killed victims with weaker immune systems, much like the regular flu. The 2nd wave was the anomalous mutation that exhibited far higher fatalities amongst younger, healthier victims. There was a 3rd wave in the Spring of 1919, that didn't result in quite as many deaths as the 2nd wave.
The 1918 Spanish flu didn't 'die out' though. It continued circling the globe for decades. It's just that after 1919, so many people had been exposed and infected across the planet, we'd developed partial herd immunity.
With the reliable testing showing that even countries like Sweden (who tried to let it 'burn through' quickly) are at less than 10% of the population infected, we would see a LOT more deaths trying to reach herd immunity naturally.
The US is realistically at maybe 6% infection. To attain some kind of herd immunity, we'd need 60-80%, and the thing is, we still don't know enough about this bug.
More recent studies indicate that SARS-CoV-2 positive victims who've had milder cases, may not have developed sufficient antibody titers to ensure immunity. The highest antibody titers were from patients who survived more severe cases.
Stay safe, and take precautions. I know I'm personally trying to avoid catching this as much as possible.
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