There has been a lot of talk that the COVID19 is likely to peak again in the autumn and winter and much like the Spanish flu of 1918, this is likely to be much worse, I have read stuff like that a similar result to the NYC and Lombardy experience in this first wave would be seen a having dodged a bullet in the second wave.:eek:
It appears that second waves are almost always worse than first ones (besides the Spanish flu, the 1957 Asian flu, and the 2009 Swine flu pandemic’s second waves were also worse, with the 1968 Hong Kong flu being an exception).
Why is this case? Surely by the time a second wave hits, the population is no longer virgin as it was in the first wave, there should be some resistance.
You’ll always have pockets of people who miss exposure the first time around.
The whole “flattening the curve” tactic proposed by Dr Fauci and the experts was to move the bulk of the population away from exposure. So the US has a huge number of people who are vulnerable to COVID-19.
With the stay-at-home restrictions lifted, you’ve got all these unexposed people out and about, mingling. And in many places, the infection is still spreading. Much much more slowly, but it is still in existence.
And remember that there are asymptomatic carriers.
The second wave can easily surpass the numbers created by the first wave. The fatalities aren’t always in the portion of the population “just waiting to die.” The greatest number of fatalities came from the 18-44 age group.
And now there is a rare form of COVID-19 infecting children. It attacks their hearts.
This second wave is due to hit around the start of the regular flu season. Some people might end up infected with both simultaneously.
~VOW
As I understand it the reason to explain such in past influenza pandemics is seasonal forcing: transmissibility of influenza (and the common cold coronaviruses) are decreased during summer months. The first wave in those influenza pandemic cases began later in the season and were able to spread it around but then seasonality of spread suppressed it to lower levels. Increased transmissibility with season change to Fall/Winter then picked up with scattered seeds early in the next season favoring its faster spread.
In this particular (COVID-19) case it is not known if there is decreased transmissibility during summer but it is suspected that there may be to some degree. The concerns for a much worse Fall peak then include suppression of the first peak by season and mitigation, with both brakes potentially being released to some degrees in the Fall, still with the vast overwhelming majority of the population susceptible, and overlapping with influenza demands upon the system.
Here’show it’s explained as one possible potential pattern in a recent model published in Science.
Even the the 1968 pandemic followed that pattern everywhere else but in North America.
Accuracy is important in these discussion. Experts are not yet sure that COVID-19 is causing that syndrome (it is rare enough that they cannot be so sure) but the consensus opinion of the experts is that if it is caused by COVID-19 it is not the virus attacking the hearts, but an over response by the immune system that is doing it.
There is no indication that there is a separate strain of SARS-CoV-2 (the virus that causes the COVID-19 disease); it appears that a small proportion of children who have been infected and show antibodies may also have some kind of susceptibility to post-infection immune response that produces a Kawasaki disease-like sequela which causes inflammation and necrosis of endothelial tissue (not just the heart).
While this may happen and is a real concern, the reason that second waves of infection are sometimes larger than the first is primarily that the disease has had time to spread geographically. This is especially true if there are a significant number of asymptomatic carriers or a suppression due to seasonal effects. When the virus reemerges it has a wide spread of infection clusters that are very difficult to control. The particular 1918 H1N1 strain that caused the Spanish Flu is unknown but was uniquely virulent and infectious compared to other Type A H1N1 influenza viruses, causing cytokine response syndrome (a “cytokine storm” that results in the immune system attacking healthy cells of the body) that has not been seen since.
The number of people infected in a “first wave” of any novel virus strain is generally not that high because people who are infectious also tend to not circulate because they feel unwell, and thus, an outbreak is self-limiting. However, as the virus establishes itself in a population and/or finds an reservoir like domestic animals, it tends to winnow out non-viable mutations and becomes better adapted to its host, such that when it reenters a population or gets transferred to a previously unaffected population it can spread rapidly, hence why smallpox ravaged Eurasian populations over and over again for hundreds of years, and then when introduced to the Americas was catastrophic in its mortality.
In the case of SARS-CoV-2, we’ve collectively been very effective in squashing its spread even in countries that took less-than-comprehensive steps or were dilatory in their response, but even with that most populations likely have less than double digit percentage of exposure, and with what is an often poorly measured lifting of isolation measures and hygiene practices we can expect the second wave—which is going to come well before influenza season starts in October—will almost certainly grow to have a greater daily mortality rate than the first wave of the pandemic.
And we’re going to see successive waves of greater or lesser mortality and morbidity until there is enough exposure in the population to achieve a herd immunity threshold, which we currently don’t have enough information to evaluate and it is possible will not even exist of the virus can remain persistent in its spread or find a reservoir in domestic animals. We never achieved a herd immunity with respect to chicken pox until a vaccine was available despite the fact that nearly every person on the planet was exposed to it in childhood and developed significant lifelong immunity from the main presentation.
Stranger, thanks for the excellent and well-informed reply. Why don’t we achieve herd immunity with certain viruses without a vaccine? Are they less contagious? My mom had me play with every pox-y kid on the block and finally concluded I was immune. I got chicken pox as an adult and was very ill.
I’ve read speculation we may not get a COVID vaccine, but I hadn’t considered that without a vaccine, we’d never achieve herd immunity.
My totally non-scientific, non-expert, proposal: We just have to race that Covid-19 vaccine out much faster than usual. Yes, there will be dangers of a vaccine that hasn’t gone through the normal, slow, drawn-out-over-years regulatory process that vaccines normally go through. But if this fall/winter second wave is going to claim 500,000 lives and cause organ damage to 4 million other people, it’s worth the risky gamble.
It might come back in Autumn in a big way. It is one possible outcome. Not the only one. One to want to avoid to be sure.
Unknown how many got exposed so far and definitely regional variation. More in NYC say than in Minnesota. Data still incomplete at best.
Uncontrolled would clearly have overwhelmed many systems. Flattening the curve was required. The debate now is between those who think of flattening the curve as keeping within system capacity while capacity is built up, while more become resolved, yes slowly approaching herd immunity, and those who believe the curve can be flattened to near zero and maintained there ad infinitum and are wanting to do that at any cost or risk. And in both camps how to structure easing off the brakes.
Strong seasonal suppression facilitates a bigger Fall spike but allows quicker release of the brake now. The risk of that though is the need to reapply the brakes hard in the Fall … which as a practical matter would be hard to accomplish once eased off.
It is cray cray to explicitly go for herd immunity in a short period of time as the goal when there is not enough known to model with any confidence. Step one has had to be to first get it cooled down, under control, and to not let it get back out of control. Still not enough to have more solid inputs into the models? Then proceed slowly and cautiously. It is harder in many ways to successfully reapply brakes than to release them with caution. How much caution, what to measure? Discussions ongoing!
It is not cray cray to have an understanding that depending on a vaccine as the only way out is reckless planning, and to have a slow path that keeps the disease within some controlled level while opening up, and understanding that if a vaccine never arrives that path will, at some unknown right now point, lead to herd immunity and some level of the disease that is lived with as normal moving forward.
Racing a vaccine out would be reckless as well, and unsuccessful. Too few would agree to take it to reach herd immunity and they would be right to refuse.
To be clear, I’m just stating that this is a potentiality, not a likelihood. The vast majority of viruses either achieve a level of infection that results in a degree of herd immunity and the virus becomes endemic in the population, or they disappear entirely or become much less virulent such that they are no longer a serious threat. Chickenpox in particular became a seasonal epidemic because of a combination of its extreme infectiousness, low morbidity and almost no mortality in children, and because exposed humans are actually a reservoir for the varicella zoster virus which resides in the dorsal ganglion of sensory nerves.
There has been a lot of handwringing about the notion that SARS-CoV-2 could mutate like seasonal influenza and negate any attempt at a vaccine. Now, it is true the virus, like all RNA viruses, will mutate frequently. However, the reason influenza strains mutate so aggressively into more virulent strains is because of recombination where two viruses will infect a host and swap genomic material. We’ve seen no evidence of this so far, and the amount of variation seen in viable SARS-CoV-2 subgroups has been very small with no variation seen in the aggregate in regard to the pathogenesis, morbidity, and mortality. There may be some evidence that some subgroups are more or less infectious due to changes in the receptor binding domain of the spike protein but the test data is so scattered I doubt any real epidemiological conclusions can be gathered at this point. The big concern is whether the genes that produces the spike protein mutates and an antibody will no longer recognize the virus, which is what happens with the unrelated coronaviruses. However, even alterations to the spike protein will probably not completely negate antibody response from a prior exposure.
We don’t know that it will peak again in fall; in fact, in the United States at least I expect it start swinging up again by June, and depending on how states react or fail, we could see a peaking in July or August. The point of the ‘lockdown’, e.g. distancing and self-isolation measures was never to stop the virus; it was to get enough time to assess what data we had, develop better testing, allow health systems to better prepare, and figure out how to enable crucial systems like education, medicine, courts, and essential businesses to function while preventing the spread from achieving epidemic levels.
The notion of herd immunity needs to be addressed in a definitional fashion; that is, achieving herd immunity isn’t a strategy; it is (hopefully) the end result regardless of what approach we take. That is, the virus will no longer be able to outbreak at epidemic levels once a threshold percentage of the population is exposed. Vulnerable people will still be vulnerable (and that isn’t just the elderly and immunocompromised, which should be readily apparent now) and the virus will almost certainly not go away, but if it can only infect every second or third person that cuts its effective basic infection number to half or a third, and if that brings it down close to unity, we can track and trace individual infections versus just having to look at community spread in the aggregate. Just shooting for maximum infection rate to achieve herd immunity as quickly as possible is like trying to surf into a wave; it doesn’t work, you look stupid trying, and there is a good chance you’re going to break something.
Barring a vaccine that, frankly, is not going to be available by the end of the year (and I would not bet the mortgage on the end of 2021 either) a large portion of the population is going to be exposed, which is how we managed infectious pathogens prior to vaccines. As long as we can care for those people who experience serious presentation but can be saved by medical treatments (and hopefully find interventions that prevent people from being put on intrusive ventilation) we can minimize mortality to the degree possible but people are going to die regardless of when and how we chose to reopen. However, if we just open everything at once and encourage people to mingle without regard for distancing guidelines we will maximize the mortality by overwhelming the health system. And this doesn’t just affect the people who die; it affects their families, the businesses they work for or patronize, the institutions they support, and perhaps most poignantly, the medical personnel and first responders trying in vain to save them and becoming infected in the process. And if for no other reason, we need to minimize mortality to protect our health care workers and health systems for everyones’ benefit.
As for “we have managed to wreck hue economy”: this virus is a love tap compared to what a truly virulent influenza pandemic could be like; instead of a case fatality rate of ~1%, we could be looking at a pandemic of 20% or greater, and nobody would argue that we should just operate like normal if one in five people were dying. And we’d better figure that out, because that pandemic is out there somewhere in the future. The history of civilization–ever since we’ve lived in large concentrated populations–has been one of repeated epidemic disease which devastated entire empires and laid waste to civilizations. Unlike those pre-industrial civilizations with no good notion of the infectious model of disease or the ability to stockpile perishable goods and manage supply chains, we can actually take effective measures to prevent disease spread and protect critical food production and distribution systems. But doing so clearly requires a more measured and thoughtful approach than simply assuming that an invisible hand will take care of it via market forces. The damage this has wrought on our economy is a wakeup call that we need more robust systems for the future.
One of those “dangers of a vaccine that hasn’t gone through the normal, slow, drawn-out-over-years regulatory process that vaccines normally go through” is antibody-dependent enhancement (ADE):
*Abstract
In general, virus-specific antibodies are considered antiviral and play an important role in the control of virus infections in a number of ways. However, in some instances, the presence of specific antibodies can be beneficial to the virus. This activity is known as antibody-dependent enhancement (ADE) of virus infection. The ADE of virus infection is a phenomenon in which virus-specific antibodies enhance the entry of virus, and in some cases the replication of virus, into monocytes/macrophages and granulocytic cells through interaction with Fc and/or complement receptors. This phenomenon has been reported in vitro and in vivo for viruses representing numerous families and genera of public health and veterinary importance. These viruses share some common features such as preferential replication in macrophages, ability to establish persistence, and antigenic diversity. For some viruses, ADE of infection has become a great concern to disease control by vaccination. Consequently, numerous approaches have been made to the development of vaccines with minimum or no risk for ADE. Identification of viral epitopes associated with ADE or neutralization is important for this purpose. In addition, clear understanding of the cellular events after virus entry through ADE has become crucial for developing efficient intervention. However, the mechanisms of ADE still remain to be better understood.*
So, a bad vaccine could have the effect of making a virus more infectious, more virulent, and capable of reproducing and mutating faster.
That is exactly what is happening. The big catch is that there are tests and other steps which can’t be skipped, and those take time. A vaccine that doesn’t work, or is even harmful, doesn’t do anybody any good.
I won’t speak to the medical side of things, but in this respect, the first part of your statement is rather hollow. There never was a real choice between public health or economic health. The economy was always going get wrecked, it’s just a matter of degree. Consider the best and worst cases.
In places where the virus spread out of control such as New York or Italy, economic activity pretty much just ground to a halt. Society simply couldn’t handle normal activity with a severe disease spreading and a. Governments hands wree forced, they locked down and b. People stopped going out of their own accord.
However, in countries where effective lockdowns take place, economic activity reduces hugely too as many workers can’t do their jobs and many businesses go under or lay off workers. In my country of New Zealand, we appear to have stopped community transmission (touch wood!) but no one currently knows what the future will hold as the massive tourism sector is dead as well as half a dozen specialized export sectors. Unemployment has skyrocketed.
So essentially there was never a case that any economy in an interconnected world would escape unscathed from the moment things got out of control in Wuhan.
I just want to thank Stranger for such a thoughtful, evidence-based analysis.
Do you have any thoughts on the likelihood of a 20% morality rate influenza pandemic? I do just wonder if there is some phenomenon where increased mortality correlates with decreased transmission rate, such as with SARS and MERS. Or did we just get lucky with those? My understanding is that viruses with fast-onset of symptoms tend to “burn out” more quickly, and of course one of the tricky elements of COVID-19 is the long latency period. But I don’t see a reason why a virus couldn’t have a long latency period and a high morality rate.
So, I picked 20% mortality as an extreme worst case for a virulent influenza (smallpox ran upwards of 30%, and some strains of Ebola virus are around 90% mortality) but even 5% would be horrific if combined with an R[SUB]0[/SUB]>4. In such a case, with, say, a week-long infection cycle at 5% mortality you’d be looking at over 800K deaths in three months and as many as 200M deaths a month after that; essentially, it would just run until it burnt itself out unless we were able to respond affirmatively and effectively to completely lockdown the population and drive down the effective replication number. Most viruses that are really infectious tend to be fairly mild (even influenza generally has an R[SUB]0[/SUB]<2) and most really virulent pathogens like those that cause viral hemorrhagic fevers tend to be not much greater than 1 because of how quickly the virus disables the host.
But a just-so pathogen could have the right combination of infectiousness and virulence, and if it had a long enough latency period or caused hosts to start shedding very quickly after infection we might not be able to track it quickly enough to forestall outbreaks. That was the case with the 1918 H1N1 strain, which if it reappeared today would likely have similar mortality (which is why epidemiologists were so paranoid about the predicted 2009 A(H1N1)pdm09 pandemic even though it ended up having a CFR that was no worse than typical seasonal influenza strains. With SARS we were lucky that patients didn’t really start to be infectious until they were already presenting signs & symptoms, and with MERS it just really wasn’t all that infectious for person-to-person contact; most infections were due to either direct interactions with the zoologic host (dromedary camels) or intimate contact (direct contact with bodily fluids) between people. SARS-CoV-2 has all the criteria to be that kind of just-so pathogen except it seems very limited about the people it can severely affect although it presents mild symptoms in a large proportion of people. Some alteration in the viral genome that would make it more virulent would turn this from a ‘love tap’ to a serious threat to modern civilization, and I don’t mean crashing the stock market or putting people out of work. And the virus that can do that is hypothetically out there in the virosphere of countless billions of different strains of viruses, and even if it doesn’t exist now, viruses mutate and recombine so easily that it will come eventually just as plagues have ravaged and destroyed civilizations that have come before us despite not being as dependent on a fragile network of global manufacturing and distribution.
We really need to put some serious work into preparing for this, because no amount of blue-shirted security guards or advanced fighter aircraft is going to stop a viral pandemic.
I had another question–when you suggest a late summer peak, are you thinking that’s when we will achieve herd immunity, and therefore do not anticipate another upswing in the fall/winter (assuming low mutagenicity and persistent immunity)? Do you think the warm weather and increased sunlight will not have a noticeable attenuating effect on the virus?
The economy was probably unsavable by the time most of the planet began to enter lockdown, mid March 2020.
And entering lockdown was the right call, no question about it. The bloody thing was spreading like wildfire and as DSeid has said, the brakes needed to be applied and fast.
The point I was making was that if a second wave is likely a lockdown might have made it guaranteed to be worse and continuing with one right now might be a bad idea.
