What generally happens is that less virulent strains will circulate faster because there are more hypo-symptomatic (or possibly asymptomatic) spreaders, and so the less virulent strain tends to infect and inoculate more people while the more virulent strain fails to thrive. However, this assumes that both strains have a comparable immunoglobulin response; with the particular H1N1 variant responsible for the “Spanish Flu”, it is unclear whether the previous exposure immunized against the mutant strain, and because many deaths were (apparently) due to cytokine release syndrome, it may be that past exposure actually amplified the immune response that ultimately killed many healthy patients. It should also be noted that there was actually a third wave of the same virus in 1919 (starting in Australia and working its way back around the world) with comparable mortality rates but because of reduced travel it had less overall deaths.
The SARS-CoV-2 coronavirus mutates (as do all viruses) but none of the variants observed so far have distinct pathogenesis, and the S-protein that creates the ‘spike’ which binds to receptors on the host cells does not appear to be changing to be more infectious. Because of some of the unique pathogenesis specifics of the virus it is hard to say how much prior exposure provides in immune resistance but evidence is growing that it does convey at least limited immunity. However, with only an estimated 5% of the US population exposed, we are a long way from getting to any significant threshold of ‘herd immunity’ (which really needs a better term to describe it because it has led to a lot of misnomers) even in such immune resistance is long-lived. So, it is a statistical near-certainty that there will be a second wave, and because of the way reopenings of individual states are being (mis-)managed we can expect the second wave to be significantly worse in terms of both the geographic spread and overall mortality as the contagion expands into rural areas that are often poorly served by regional medical systems in a non-pandemic condition.
That’s what I actually meant; I was just using a shorthand. A random mutation is probably equally likely to be either more lethal or less lethal, although most probably don’t change the lethality at all. The less lethal ones survive in the long run.
The nursing home where my wife’s grandmother had been for the past six years had 120 residents. 87 of them have tested positive for COVID-19, and ~20 staff members. 18 deaths so far.
Too late for anything to be done to save that nursing home, but still the opportunity to keep the residents safe at the nursing home your gf’s brother’s wife works at. Thanks for doing your bit.
What happened with the Spanish Flu was different, simply because we were at war.
The first “wave” as you put it was mild, usually what happens is the worst strains strike first and people who get sick stay home and recover and/or die. The people with the mild strains spread it. Note both strains offer immunity when well. So now the deadlier strains die out.
What happened in the Spanish Flu was different, the returning soldiers did a lot to spread the second wave. Those who were very sick were taken OFF the front line and brought back to towns or back to America. But those were very sick soldiers. Those soldiers with milder strains, stayed at the front. Thus you had the situation opposite of the above. Instead of the usual sickest people at home quarantined you had the sickest people traveling and the people with mild strains who were de facto quarantined
The virus never mutated, at least not significantly because people who got the Spanish Flu the first time around were immune the second time, thus showing if it did mutate, it wasn’t enough.
Viruses tend to get less deadly over time. Even HIV in the span of ten years the rate years lived more than doubled from 18 months to four years (without antiretroviral treatment) by the mid 90s.
Where I live you cannot get an Covid19 test without symptoms or bearing a $250 charge. So also remember the curves are distorted because if you are only testing people likely to be sick, then you’ll get a lot more of these.
The relevant metrics is how many people does the virus infect before killing its host or being cured by the host so it is no longer contagious (the famous R coefficient). A virus can be deadly but extremely contagious (think Ebola, with all the infectious blood pouring out - not bad for the virus) or not deadly and still extremely contagious (think common cold - not bad at all for the virus). The situation that a virus “wants”* to avoid is being deadly fast but not very contagious.
I know that evolution has no “will”, it is a manner of speaking.
In a really abstract way, you can think of it like a fire in a trash can; if you catch it early, and try to put it out by putting a lid on the can, but don’t entirely succeed in extinguishing it entirely, it can very easily flare back up, assuming there’s oxygen and fuel. That’s basically what happened here- we put the lid on, and put out a lot of the embers, but not all of them. Now we’re taking the lid off, and those embers are going to burst into flame and start spreading again.
I want to correct a major assumption you’ve made. A virus does not necessarily kill off its host. It may kill off a few cells, then lie dormant until conditions are right for it to proliferate.
A good example of this is one I’m afflicted by - herpes simplex, aka fever blisters. The body doesn’t kill it, and as far as I know, it’s never killed anyone. It basically lurks in the body until conditions are right for it, then erupts as sores on the lips.
It’s communicable from just before the blisters appear until some point after the eruption has finished. By not killing the host (i.e., myself), it has the opportunity to spread itself to many other hosts.
Fortunately, I have enough to knowledge to prevent it from spreading - which I’ve managed to do the past 30 or so years. (I did apparently spread it to my father when I was young, that’s the only person I know that I transmitted it to)
Tell me exactly what part of my statement that you disagree with?? You seem to follow me around saying how dumb my statements are but I haven’t seen you successfully refute any of them yet.
The thing about the Spanish 'flu is that it also hit - and hard - areas that were unaffected by the war. Many of the dead were actually young and healthy people, it appears that their immune systems overreacted (cytokine storm, maybe the buzzword of the year?) and this killed them. This also appears to be happening with the current COVID-19 coronavirus.
As has been pointed out, past pandemics also went in waves, and the virus generally mutated in the second wave because virus do. It was the second wave of the Spanish 'flu pandemic that was deadlier. We don’t know what will happen in the current situation.
With luck, there will either be an effective vaccine or some sort of countermeasure by next year.