At the moment I’ll be pretty happy if we can even deal well with the first one!
As viruses spread over time they become less virulent. Even with HIV a decade later it was still deadly but the time it took from infection to death was increasing.
Viruses cannot reproduce without a host, so if they kill off their hosts, they too die or rather their young do. (if you can call it that).
We’ve had much worse plagues in the past and they burn themselves out or they decrease where people can live with them. For example Lassa Fever is very dangerous but in West Africa where it is endemic, people test positive for it without ever having symptoms.
Look at Ebola’s near twin Marburgvirus. It caused a bunch of deaths then disappeared basically for a decade. Then it came back with a few cases here and there for the next two decades. Then in the late 90s outbreaks took the form of Ebola, which first came on the scene nearly a decade after Marburg.
So yes, it will likely be around but the deadliest types will kill their hosts and thus kill themselves off. Leaving the less deadly ones that will not kill their host but enable the virus to reproduce.
And that’s when we’re really gonna need all that toilet paper people have been hoarding.
This is the “long term effects” thread. You can’t infection half the population every year.
SARS was caused by a coronavirus, SARS-COV. It is, technically, always with us, but you haven’t heard about it in awhile. It’s just how these things work.
Who knows? It’s highly unpredictable.
In some cases infants have greater exposure however it is commonly accepted a primary reason that infants have so many infections is because of their immature, developing immune system cite cite cite
Which all seems contrary to the hypothesis that the difference in infection incidence between adults and infants is solely down to behavioral differences, right?
I didn’t say anything was weaker or more powerful as such; I said infants rely more on their innate immune system because, for example, they lack T and B cell memory triggered by previous infections.
Hopefully, we are manufacturing ventilators as we speak.
Vaccine.
Now that’s something I haven’t even heard discussed. Do we know where ventilators are normally manufactured? Is it … China? How long does it take to manufacture a ventilator anyway?
I’m really not getting what part you are missing here.
The issue is not the mystery of why infants are not getting as sick or serving as the drivers of contagion with COVID-19 while they do with influenza. The curious case of the dog that did not bark is the lack of those 19 years old and under as getting sick enough to diagnose and being the drivers of the infection through the community, as they do for influenza and many other communicable diseases.
Children, outside of infancy, have quite strong adaptive immune systems. It is why they have a strong response to vaccines like the influenza vaccine (in comparison to the weaker response seen in higher risk older adult populations) and have a low mortality rate from influenza. But they frequently get symptomatically ill with influenza and spew the virus around them in large numbers; they are the drivers of influenza contagion in communities. All the current evidence is that such, especially the latter, is NOT the case for COVID-19. SARS was also notably much less severe in children than in adults. There were however never enough cases to be able to determine if they had less infectivity.
So what are the differences between adults and kids (all ages of them) specific to the families coronaviridae and influenza?
One difference is that the typical child has had much greater fairly recent repetitive exposure to other human coronaviruses than adults have. Adults, especially older adults who are not around kids much, don’t get exposed to those viruses nearly as often, nor as recently. That kid with the near perpetually runny nose has an HCoV a good fraction of the time. The one who just gets the several colds a year probably has an HCoV at least annually.
Which does not rule out the possibility of innate system dysfunction with aging contributing to larger morbidity and mortality with differences in how the innate system works in the contexts of COVID-19 and influenza infections. In both the innate system working correctly and in concert with the adaptive response protects from infection in the first place and its out of control response causes the Acute Respiratory Distress Syndrome (ARDS) with multi-organ failure that is the most common cause of death. Yes, even without differential exposures to similar viruses different patterns of function in different age groups may react differently to different viruses, causes greater protection at one age and greater vulnerability at another. But for this to be the explanation it has to be true for all of the variation in function as both systems variably develop from infancy to early adulthood, which seems improbable to me.
(By the way, do you realize that your very first cite is explicitly discussing how the innate takes years to fully mature to adult function?)
the function of containment is to slow it down to reduce casualties until a vaccine is available.
The good news here is a worldwide attempt to deal with it. China turned over their genetic mapping of the virus to all countries. The US is using a supercomputer to calculate the best avenues of tests to expedite a vaccine. Common sense techniques are being used for testing such as drive-through tests. This keeps people away from hospitals and infecting people who are already vulnerable. Hospitals should only be used for people who have the virus ANDneed medical care.
My mom and dad cancelled thier florida trip and disneyworld is closing also ONLY UNTIL THE END OF MARCH!!
Why are all these places closing ONLY UNTIL END OF MARCH?? – Is it gonna dissapear somehow??
I dunno…
They don’t know how long things are going to be like this, so they’re taking steps to minimize the damage. They are starting with a smaller window, and can extend it later. If they close for 1-2 months, and conditions allow them to open earlier then they’ve lost business to all those folks who had to cancel their arrangements.
Granted, people are going to cancel anyway. And extending the closing repeatedly is just going piss people off. They want certainty, not to be put on hold for a long time. In reality there’s no perfect answer.
Ahhhhhhh ok that makes sense,thank you 
I’m also staggered by your responses. Nothing I’ve said is controversial in any way.
The immune system develops (and later seneces) throughout life. And by “develop” we don’t just mean grow and then die, we mean the whole catalog of complex changes occurring as described in my previous cites.
The effect this normally has with regards to contagion is that they have a U-shaped incidence curve. Because in the very young the immune system is still immature and developing, and in the very old the immune response becomes smaller in numbers and less efficient.
When the incidence graph differs from this e.g. children largely unaffected by a virus, or e.g. most fatalities happening to people in their 20s, we can look at the more specific developmental changes to the immune system to why that is the case.
Very low numbers, yes. But what is your hypothesis at this point: that 19-year olds are putting their friends’ legos in their mouth?
Not as strong as an adult’s. Do you dispute that?
Well, as often, because adults were children once.
They might plausibly not had as much *recent *exposure but I fail to see the relevance of that.
Sure, but it’s still a good cite to use because for example, it begins with “It is well established that adaptive immune responses are deficient in early life, contributing to increased mortality and morbidity”. In other words, it begins from the position that I am describing, but is trying to say that as well as that there is a less established, less obvious developmental path for the innate immune system too.
I have not, and would not claim that a child’s innate immune system is already optimal. I have simply said that they rely on it more than the adaptive immune system.
Let’s stick to these two items to start -
The 19 year olds (call it late teens), relatively yes. They are much higher “contact”, in many ways than most older adults, even just a decade older, including putting their friends’ … uh … “legos” in their mouth. Just more touch of all sorts and close contact with a greater number of each other in general. And much closer to the age of extremely frequent common colds than they are decades later.
In terms of your belief that children’s adaptive responses are not as strong as an adults, yes, I 100% dispute that. The opposite is true. I’ll illustrate such in one very simple way, the HPV vaccine. We start to give this around age ten and as long as we start the series before kids turn 15 we can go with a two dose schedule. Start at 15 or older and we need to use a three dose schedule. Because even that young the adaptive response is LESS strong as you get older, studies have shown the two doses at 9 to 14 give as strong or stronger protection than three doses later on. It’s true with other vaccines as well - nonresponse rates to Hepatitis B vaccination increases as one ages; infants have great response with lasting protection; primary nonresponse rates start to climb even by age 30.
In short, kids have more powerful and consistent adaptive immune responses than do most adults, even by age 30.
I’m guessing that you’ve then not been good about keeping up with your adult tetanus vaccine every ten years, or bother with getting your flu shot annually even if the components have not changed … because time elapsed since last having the response boosted is of no relevance that you see.
The “well established that adaptive immune responses are deficient in early life” is before 24 months of age and specifically to glycoproteins and polysaccharides not protein antigens. By two they’s good.
But really this is getting down a rabbit hole tangent off the OP. The issue of potential relevance to speculating what happens is the why kids seem so much less significant COVID-19 and spread it so much less relative to influenza viruses and even many other common viruses. Whatever is the cause for COVID-19 being specifically different in kids than influenza and many other viruses may inform what happens over the next season or so.
I remember playing spin-the-bottle in high school. But not since.
My grandkids put their leggos in MY mouth!
He may be loathe to bring it up but you should probably know, Mijin, you’re arguing childhood immunity development with a pediatrician.
Exactly right and is why for influenza, and many other communicable diseases, kids are the drivers of contagion, getting influenza very often themselves and spreading it widely.
The apparent fact that this is not the case for COVID-19 is a huge significance, minimally for epidemiological modeling and rational public health decision making.
IF kids function epidemiologically more as non-susceptibles do (not spreading it much when exposed) rather than the huge amplifiers for spread, like they do for influenza, then what happens in regions of different demographics is very different than with influenza. Influenza spreads most where the population of children is fairly high; this (if such is actually true) would spread slowest in those populations, and most in populations with an older average age (and of course cause the most harm per case there as well). The plus side is that implementing meaningful social distancing measures (and what is meaningful remains to be determined but might not require draconian measures) is much more achievable in an adult population.