We've found pre-existing T-cell immunity in many individuals (cross-protection from other coronaviruses?) so even if we don't have long-term perfectly sterilizing immunity, the odds are stacked in favour of this becoming just another winter respiratory disease once some level of herd immunity kicks in.
There is a lot of confusion around herd immunity. Think of it more like an equilibrium state than an elimination state. It is where this virus will end up whether we have a perfectly sterilizing vaccine or not.
> the odds are stacked in favour of this becoming just another winter respiratory disease once some level of herd immunity kicks in.
The thing is, looking at the seasonality of the other strains of coronaviruses, you can see how it kind of looks to what we had this year (only worse as no one was ever infected with this). See Fig. 1 here : https://smw.ch/article/doi/smw.2020.20224
But people do sure like to blame and shame everyone in Europe and the US as if 1 billion people in the Northern hemisphere are somehow all to blame they weren't compliant enough. Viruses will doo what they always did.
Viruses can be stopped. See South Korea, China, and Taiwan for a few examples. Sure, the Chinese approach would not be possible in a democracy. But Taiwan? My friends there continue to live a very free life, yet COVID-19 is nowhere to be seen... Arguably, they are much freer than we are in North America and Europe right now.
"Viruses can be stopped. See South Korea, China, and Taiwan for a few examples."
China just had an outbreak of hundreds cases in the Uighur region.
What seems more likely: that China has truly "stopped" the virus, and it just re-appeared, miraculously, in one of the most heavily travel restricted places on earth...or that it's actually spreading in China, and testing isn't catching it?
Taiwan's success at managing the virus has come ~entirely from strict border controls. Being a tiny island nation certainly helps with this. They still have cases, but so far, they're all amongst travelers:
The overall picture here is that some nations have done better than others at controlling the virus (at considerable expense) but almost nobody can claim to have "stopped" it.
The country has 23M inhabitants, most of them are clustered in a few densely populated metro areas (Taipei, Kaohsiung, Taichung–Changhua, Taoyuan–Zhongli, Tainan and Hsinchu). Taiwan had many daily flights to/from China, including daily directs from Wuhan (stopped 31 December 2019). Taiwan is one of the world's older countries (median age ~43). Taiwan permitted the docking of the Diamond Princess [2] and allowed passengers to disembark in Keelung (near Taipei), on 31 January, before the ship left for Japan. The ship was subsequently found to have numerous confirmed infections onboard. In reaction, Taiwan's government published the 50 locations where the cruise ship travelers may have visited and asked around 600k citizens who may have been in contact with the tour group to conduct symptom monitoring and self-quarantine if necessary. None were confirmed to have COVID-19 after 14 days had passed. (The only advantage Taiwan had was that facemasks were widely used and even expected on public transport for years.) For all those reasons, Taiwan was at unusually high risk from Covid.
Yet, no lockdown.
No country managed the disease better than Taiwan. We should learn from Taiwan. See [1] for an analysis of Taiwan's response from early March 2020.
It is interesting to reflect upon why most countries ignored Taiwan. The World Health Organization's locking out Taiwan on China's request is probably one reason. Is it the only one?
[1] C. Y. Wang, C. Y. Ng, R. H. Brook, Response to COVID-19 in Taiwan: Big Data Analytics, New Technology, and Proactive Testing. https://pubmed.ncbi.nlm.nih.gov/32125371/
Regardless of what you think of the response, facts from now trump facts from five months ago. The point of citing the Time article was to show that they continue to have imported cases on a regular basis (fact), and that they prevent these from spreading by strict border controls (fact), not to provide commentary on the quality of their overall response.
Taiwan is a tiny island, with relatively little international travel (compared to the US, China, etc). If they have no cases internally, and they seal the borders before those cases are introduced, then almost nothing else matters. Small, isolated, island countries can do this -- but even then (i.e. New Zealand) one mistake will mean rapid endemic spread. So sure, as long as Taiwan continues to effectively isolate itself from the outside world, they can probably carry on. But they're not going to: they're already talking about re-establishing travel with the rest of Asia.
It's virtually impossible for a country like the US to do the same thing Taiwan did. Even if we could seal the borders like Taiwan, our population is about 13 times larger, we have large land borders with other countries, and a proportionally large number of expatriate residents with right-of-return. Even with our bans on international travelers, the US has had 6.6 million foreign arrivals in 2020 [1]. Effectively 25% of the entire population of Taiwan has arrived in the US in 2020. And that's just non-citizens.
Both New Zealand and Australia performed strict lockdowns. The US/Europe is unlikely to be able to achieve the same level of compliance needed to make those successful.
Depends on time scale, suppose for argument no vaccine works, then these countries just have to have massive border control and limit travel massively as they are now.
There is no ‘they are much freer’ argument in the diverse states, because people are dealing with this thing in a huge diversity of ways. Some people have exactly the same life, but they wear a mask, no big deal...
Except there are populous, prosperous countries (e.g. Taiwan) which have kept the virus 100% in check and eliminated it from community spread. I do blame other countries for not doing enough.
Yeah, the mathematics around herd immunity are often misused.
People seem to always assume independent identical random variables. Corona Virus are seasonal - infections highly locally clustered.
The spreading might refuse to follow slow brownian motion of the herd. If e.g. an aircondition blasts an entire room of people with bad air, how much do herd effects really help?
Does the term "herd immunity" make sense for a seasonal virus at all?
Does the term "herd immunity" make sense for a seasonal virus at all?
Yes. For instance, one of the benefits of widespread flu vaccination is that it slows the rate that the virus spreads at. Herd immunity is just the threshold where enough people have immunity that the spread diminishes. That we don't necessarily reach the threshold doesn't make the lesser effect useless.
> Herd immunity is just the threshold where enough people have immunity that the spread diminishes.
So herd immunity is not about immunity. Quite a misnomer then! Always thought herd immunity protected those still vulnerable, but according to you it merely means the vulnerable may merely be having a few more healthy hours falling sick non the less.
It is about immunity, just not about the individual. It means that if the virus spreads to a non-immune individual from the outside the spread inside the herd will eventually stop (but we don't know when). It can still reach an arbitrary number of non-immune individuals, but given infinite time and an infinite herd, it will eventually stop.
Low level zero friction school physics analogy: think of a ball rolling onto an inclined plane. If the plane is angled upwards the ball will slow down and eventually stop rolling further upwards, if the plane is angled downwards it will just continue accelerating forever. But in the upwards case no place on the plane is truly safe from getting reached by the ball, because speed and angle is not specified. Herd immunity means that the slope is upwards, but the velocity would still be an open-ended random distribution.
A more accurate model for virus spread would replace momentum with dice rolls and slope with success thresholds, but that's just more difficult to imagine (unless your biography contains a phase of obsessing over p&p rpg rules).
With more individuals having immunity, it's likely the disease won't reach as many individuals who are vulnerable because they lack immunity and have underlying medical conditions. It's the level when outbreaks can stay localized instead of spreading to everyone.
A good friend of mine has done a lot of research on infectious diseases.
An individual has immunity when the immune response is triggered. By definition. It was very confusing to me at first before I caught on to the meaning of the term.
It makes sense when you think about it. Can you "get" the virus a second time? Of course of can. That doesn't contradict the fact that you have some level of "immunity".
After all, the immune response is a big part of what most of us feel when getting sick.
Yes, herd immunity does not prevent a given individual from becoming infected, it's a group measurement. Of course, as the rate of spread diminishes, the likelihood of a given individual becoming infected does go down.
You probably shouldn't rely on some random HN poster for your definition of what herd immunity means. It's a well defined term in the epidemiological field, and definitions are readily available via sites such as Wikipedia and search engines.
Yeah, but this one can cause lasting cardiovascular and nervous system damage in a significant number of people, in addition to permanent lung damage. It's not just another respiratory disease.
post-viral fatigue syndrome, myocarditis, and other complications are actually very common complications for viruses. Pneumonia is miserable and can take a long time to recover from.
>In the UK, where it is (often incorrectly) known as ME (myalgic encephalomyelitis), 150 000 people are said to be affected. Other terms used for the condition are postviral fatigue syndrome (PVFS) and chronic fatigue and immune dysfunction syndrome (CFIDS). Symptoms may begin suddenly, sometimes after an acute viral infection, and commonly include incapacitating and persistent fatigue, muscle aches, joint pains, weakness after exercise, headaches, swollen glands, digestive disorders, inability to concentrate, memory loss, recurring minor infections or low-grade fevers, depression, an increasing sense of being unable to function, sleep disturbance, light sensitivity, food intolerance and environmental allergies.
> Viruses. Many viruses are commonly associated with myocarditis, including the viruses that cause the common cold (adenovirus); COVID-19; hepatitis B and C; parvovirus, which causes a mild rash, usually in children (fifth disease); and herpes simplex virus.
The WHO is suggesting that in the UK we have as many people with long covid as have died from it, so talking about 60k - far far higher than we for new ME cases each year.
Also the 'new' symptoms the long covid sufferers face are often very different to the initial illness - my wifes heart function was impacted hugely, only just starting to recover 7 months later.
What is good is that unlike ME, it appears many of the long covid sufferers are recovering, it just takes a long time, similar to SARs - where as for many ME is a life long condition. So I wouldn't draw to many parallels just yet until we know more.
Do you (or anyone else) have scientific numbers, sources and/or comparisons for:
a) quantification and definition of lasting cardiovascular/ nervous system damage
b) quantification of a significant number of people
c) comparisons to rates comparable to other respiratory diseases (like influenza strains or the bird flu strains etc. )
Understand I ask this not as a coronavirus skeptic, but as a science-literacy proponent who hasn't yet read any reliable source or study for the claim you're making.
I'm putting the kids to bed so don't have time to dig out any figures of interest, but my wife caught covid back in March, was OK but pretty ill, but then moved into the long covid phase and was wiped out. Heart rate all over the place and terrible numbness and loads of other rubbish. A full body scan showed issues with her heart function back in August, which is only just starting to recover now, a 'low ejection fraction' and other bits I forget. Latest scans show improved function but nothing like she should see at her age or fitness. This time last year she was lifting 47kg in the gym and working out 4 days a week.
The long term studies showing what you are asking are only just starting to show results - but everything we see so far shows that this is causing more issues, in more people than flu.
Also of note, a partner of my wife's friend got covid (positive test) back in April with only light symptoms. Just got it again (tested again) and is very ill this time - had to go to hospital but wasn't kept in. So immunity might not be what we think.
I realise covid is highly politicised right now, but give me the benefit of the doubt. I said I'm not a covid skeptic and I meant it. In its current form it's more virulent than the flu (albeit with a different distribution of mortality outcomes). And of course we have to deal with the general additional affect of immunity (or lack thereof) in the general populace.
But it's possible to seek out new information on covid, and also to seek to stop spreading disinformation on it, while still accepting its serious nature.
I've not yet seen a lot of good research released due to it being so new.
It felt like we spent 3 months trying to convince doctors here that long covid was even a thing, then another couple helping them understand how they can help people like my wife and it is only that last couple of months that there has been a mobilisation of research and interest in this area, so good quality information is currently hard to find.
CoverScan.com moved quite early - https://coverscan.com/news-%26-updates - have done some great work and are starting to release info - my wife was part of the trial. I'm sure there are others, but these things take time.
I'm sure that we will have loads of useful data points next year, but right now even the collection of the data has been poor to understand anything other than just 'deaths' and in some countries 'recoveries' (which was generally just a measure of those that were ill enough to be hospitalised)
No, indeed, neither have I. And it may or may not be coming or true, i don't know :) That's why I keep asking to see the evidence when I keep seeing someone making the claim: I actually want to see it if it exists or if they're just repeating the news stories.
To me, it's not the position that Covid has long term effects that's incredulous, because we know that a proportion of a lot of viral infections can develop into longer term complications and effects. But it's the idea/observation that the longer term effects are both comparatively worse than other viruses, and splitting the quantumn of those effects into a "general covid effect" (that is to say, the probability of the effect for a given case of covid), and those of a "general pandemic effect" (that is to say, the population-size effect of having all these infections happening at once due to a relatively vulnerable population with little immunity, in contrast to some of the older/other viruses).
But I admit myself a little more than disturbed how every time I ask to see comparable figures/studies to see how we have knowledge of long-term effects of a virus that's only been around for the short-term, and claims that are usually made without any reference to the viruses to which covid needs to be compared, that I generally get hit by a quick wave of downvotes.
Fair enough, give it time. On the inverse - SARs which this seems to be similar in some ways to (though more transmissible and less deadly) is well known to have a wide range of long term effects on a proportion of those that get ill with it.
Come join some of the long covid reddit, Facebook, slack or other groups if you want to research first hand - there are plenty out there!
I think the burden of proof is on you since you are the one contradicting the prevailing thought. You must “reject the bull hypothesis” as it were. Personally I have seen one case of a 17 y/o with lingering nerve damage covered on national news.
It is logically impossible to prove a negative. The burden of proof can only possibly be on the people claiming there is an effect.
To put it technically, it is "inappropriate to draw substantive conclusions on the basis of a lack of statistically significant effects." You are not proving the null-hypothesis, you are failing to demonstrate the alternative hypothesis.
Or to put it another way, lack of evidence is not evidence that a thing doesn't exist.
My good man, i propose that outside of news stories focusing on relatively small samples and individual case studies, which generally make no comparison to other virus' comparative effects or mention of the biases inherent in their sample, it is no longer being reported because it has not yet been established.
And the reason for this is nothing conspiratorial or denialist, but just due to the fundamentals of good science: that is to say, it's REALLY REALLY hard to accurately establish the long-term effects of a novel virus that has only been around in the human population for the short-term.
Nicely put. I appreciate you taking the time to be civil. Such a rareity these days. A nice change from being insulted for daring to think different. For what it's worth I have evaluated some of my premises based on our exchange here. Thank you.
I fundamentally disagree that I'm conflicting with prevailing thought (at least of medical experts), both because I don't accept that it's prevailing thought, but also because I'm just being proactively and constructively sceptical.
If someone proclaims to know the long term effects of a recent novel virus, that's an interesting claim. then they compare the outcomes to other viruses (or declare its fundamentally different), that's also interesting.
I've seen news articles about specific cases, and alarmist tabloid-esque case studies, but as someone who actually reads medical studies, I don't let media or hand-picked cases set my opinion, because in a pandemic with countless millions infected, and with a disease that disproportionately affects co morbid patients, of course one will find individual reports of bad cases and complications. But the information I asked for is presumably the minimum required for your claim to be justified. And if it is so "prevailing", it would be widespread and easily findable, whereas I have yet to see a single source that has them.
An effective vaccine in the near future is a much better option than natural herd immunity due to the lives lost.
Longer term it gets interesting because young people are at a dramatically lower risk of death and older people will have been exposed several times. So, if things go endemic it’s likely for long term annual deaths to be dramatically lower.
PS: The error bars in what you linked are very wide repressing significant uncertainty around those tests.
As you noted, a vaccine allows us to target immunity, typically by risk profile, as we currently do with common cold viruses.
Herd immunity does not.
So while less virus circulating due to greater population immunity (and therefore lower individual risk of infection) is good, it doesn't help when SARS-CoV-2 does chance into a nursing home.
People still have a strong immune response in 2020 for the original 2003 SARS virus. This is consistently the case every time they do a study of 2003 SARS immunity, including the new study a few months ago. Many people with 2003 SARS immunity also show significant immune cross-reactivity with 2019 SARS.
All of the evidence suggests that immunity against coronaviruses is quite durable.
There is absolutely no way one can claim "strong immune response in 2020 for the original 2003 SARS virus" unless it was actually verified by reinfection. I am aware of the article claiming that there is some kind cellular reaction to SARS, but first of all, it might be not enough at all to protect from reinfection, and secondly, it might be case of well documented cross-immunity from some common cold viruses.
Then why the reinfections? People still too weak after the initial infection? Different strains? I just want to understand but it's probably still puzzling doctors and virologists.
AFAIK there have been very few reinfections. Humans have very diverse genes and over 47 million people have been infected. It's entirely normal that there will be outliers whose immune system doesn't produce a response that lasts as long. The rest is the media engaging in fearmongering.
Unless it isn't. I thought that ~15% of common cold infections come from Coronavirii - wouldn't that imply that these 15% should cease to exist at a point in time?
It wouldn't imply anything of the sort. It's rare for a single viral infection to cause life long sterilizing immunity. Reinfections are possible with most viruses, including other coronaviruses. As long as your immune system is otherwise healthy the memory T cells will kick in and symptoms will usually be less severe.
The only reason that other coronaviruses like OC43 don't kill a lot of people is that almost everyone catches it first as a youth, and builds up a level of immunity. But it can be quite deadly to someone who first catches it later in life, or to immunocompromised patients.
> The only reason that other coronaviruses like OC43 don't kill a lot of people is that almost everyone catches it first as a youth, and builds up a level of immunity. But it can be quite deadly to someone who first catches it later in life, or to immunocompromised patients.
As an aside, OC43 is strongly suspected to be the cause of the 1889-1890 pandemic which killed around 1 million.
The response to covid19 (e.g. lockdowns and mask mandates) have been very politicised. Other political topics on HN seem to follow similar vote patterns.
Probably just people getting radicalised with all sorts of ideas, maybe due to imperfect information, lots of misinformation, the topic being politicised, people being stressed because of the pandemic and its consequences. It's not only this topic, I've noticed it in any other less polarising ones as well.
The title seems misleading to me. Does the fact that "...blood samples from a cohort of more than 2,000 clinical and non-clinical healthcare workers..." might seem to indicate a near-constant exposure to SARS-cov-2? That might increase the chance that the individual is re-exposed and thus his or her immune system has continual "boosts". It seems noteworthy and something worth investigating. Would this apply to the population at large who do not risk continuous exposure?
More likely it's because 6 months have elapsed. Cellular immunity to SARS-COV-1 (2003 outbreak) is still robust 17 years later - the two coronaviruses are fairly similar.
People keep parroting that article. "Cellular immunity" mentioned in it may be not enough at all to prevent reinfection. Unless there is a direct rechallenge with the SARS-1 virus someone who already had it in 2003, there is no way to make such a strong statement. Good luck finding volunteers.
It's amusing how you put "cellular immunity" in scare quotes. It's not a new or novel concept, but an extremely well understood mechanism that has been taught to immunology first years for decades. That a coronavirus should exhibit a cellular immune response should be the baseline assumption, rather than the inverse.
From the article, it seems like the latter. They tested at 6 months. If they test those same people again later, then we will possibly have a new high-water mark for the duration of immunity. For now, we can only say “at least 6 months”
This is good news because it suggests that immunity for SARS-CoV2 isn't worse than that for other coronaviruses (e.g. those causing the common cold), even for those individuals who didn't become so sick they had to be hospitalised.
In a nutshell, you can't catch it again right away after having recovered.
Extrapolating from other coronaviruses, it's probably that you CAN catch it again but it's "very unlikely" to produce serious consequences after the first time.
So basically only first time you will experience more serious symptoms like a fever, the subsequent infections would be trivial common cold.
I think we should consider it to be as yet unproven - a person I know through my wife caught it in April (and tested positive them) and wasn't that ill.
They just got very ill again in the last week and tested positive again. Might be totally a-typical or it could just be that we've not seen that many people actually have the chance to catch it twice yet.
I'm an absolute layman, but "no worse than the common cold" doesn't sound too great to me since I've always been told you can keep getting the cold over and over again. What am I missing?
If you look at the Wikipedia article, you will find more detailed information, but the common cold is caused primarily by rhinoviruses. However, some are also coronaviruses and even influenza viruses. There are hundreds of viruses that cause "the cold."
Here's my understanding (also a layman but trying to read as much as possible):
A new coronavirus jumps from an animal to humans. No human body has seen this type of virus before, so when it infects the immune system has to work a lot to learn how to fight it. This causes symptoms like a fever which is a sign of the ongoing struggle. For frail people it means the immune system is not strong enough to counteract the infection and it spreads and potentially kills them.
However, if the immune system learns quickly enough how to fight it, antibodies are killing the virus faster than it can multiply and you get better. The antibodies then disappear in a few months but the long term memory cells remain.
Later, the virus infects you again. You develop the symptoms of a light respiratory infection but the immune system quickly references the memory cells and is able to produce suitable antibodies really fast. The fight is short and easy, the antibodies defeat the virus before it has time to spread. There is no sign of the struggle like first time (no fever) but only the light symptoms we don't even think of (common cold).
Now, how about children? Well as we see already they're unlikely to be seriously affected (low mortality). And children get lots of fevers (parents can confirm). So probably sometimes in the early years we get infected by some coronaviruses our bodies have never seen, the immune system puts up an intense fight and builds the long-term immunity that will be with us as adults.
There are several coronaviruses that cause what's commonly known as "the cold". If you catch one and recover you're likely to be immune against infections from the same viral strain for some time.
For SARS-CoV2 and the COVID-19 disease it causes this means that even without the - quite likely - availability of a vaccine over time natural immunity will build up within individuals and the population as a whole, which has the potential of both making the resulting disease less severe and future waves spreading less.
If most individuals who contract the virus during the next few months can't get sick anymore and can't spread the virus anymore for the about 6 months those individuals are taken out of the equation, which leaves less individuals for the virus to spread to in the next wave.
> In a nutshell, you can't catch it again right away after having recovered.
If that's the case, out of curiousity why there has been numerous reported cases of people that catched covid again after already recovering from it?
Edit:
So... after reading the article I'm not sure this is the case for all people as this research has been done only on a group of asymptomatic & low/mild response people. IMHO for a sentence like that to be valid, it should be demonstrated on the other part of the population, those that have a high immune response against the virus and end up in a critical state from it.
"If that's the case, out of curiousity why there has been numerous reported cases of people that catched covid again after already recovering from it?"
There have been many, many news articles that speculate about this, but to date, I'm aware of two papers that document re-infections. Both papers isolated and sequenced the viruses involved, and both papers documented re-infection with significantly mutated variants of the same virus.
No honest scientist would say what you wrote as your “nutshell.” Specifically, T cell response is not equivalent at all to “you can’t catch it.” Still all scenarios are possible: 1) you can still catch it, and still get more sick 2) you can catch it, and be less sick 3) you can be “sterilizingly immune” meaning that you won’t get sick and won’t be able to transmit to somebody else.
But which of those will be by majority the study just didn’t investigate.
In immunology no answer is “yes” or “no” but the range. The range is different between different people, and we can conclude what the typical ranges are, if there’s enough data collected. But the ranges are still unknown at the moment.
The same reason (a need to find the ranges) is why you can’t make a vaccine candidate and be sure how it will work, unless you run big and long enough trials. And that’s why that takes time.
Here’s what this study figured out, quoting from the article: “The size of T cell response differed between individuals, being considerably (50%) higher in people who had experienced symptomatic disease at the time of infection six months previously. Further research will be needed to determine the significance of this finding.”
As you see, again some range, but also not concluding what you claim.
I'm not sure we can rule out the idea that reinfection after 6 months is common but almost always asymptomatic in people with healthy immune systems. There was that British common cold coronavirus challenge trial where most subjects could be reinfected after 1 year, confirmed by PCR, but none of them developed symptoms.
Yeah, exactly what I was talking about. There is no way to say this just by looking at the genome, all you can do is to say that is not very probable, and that would still be a dubious claim. There is a plenty of gnome manipulations that leave no trace. Having said that, lab origin does not neccesarily mean genetic manipulation. Serial passage through animals (say, minks) will leave no trace of genetic engineering, but may make the virus contagius to humans (minks and humans have similar ACE2 receptor). Or just poorly handled sample from the would do.
That are all bogus claims. Biology doesn’t work how somebody not in the field in his simplistic theory think it does. The claims as written show a complete distance from the field and the necessary understanding needed to be able to even understand how wrong the claims are. Theoretically anything can be synthesized, practically, nobody would ever be even near to synthesize what we actually observe. Human controlled “passage through animals” would need many decades to produce the patterns. Totally wrong claims based on bad understanding of how that all works.
Can we really? Infection itself is still somewhat uncommon, thanks to the global reaction to the pandemic.
I don't doubt that reinfection will be rare, at least over the span of a few months, but to my mind that would seem unproven given how hard we're (generally) working to keep people from being infected in the first place.
Unfortunately, your hope is unfounded. My spouse is a physician and when coughing (acute bronchitis) could not get a test without job consequences (being forced to take 10 days off and reschedule all patients regardless of the outcome of the test). There has been an exposure in a neighboring ward through a fellow healthcare worker and tests are not being made available broadly. Remember, in the US healthcare workers generally have to go through insurance to get approved for tests, etc., even though they work in healthcare -- they're not at this time provided anything more than the general public in terms of diagnostics. (At least spouse gets free masks at work, haha...)
Do you know how academic, narrow and unpractically stiff are criteria for a proof of reinfection? You need to have the viral genome sequenced TWO times, and both times it must be a slightly DIFFERENT virus. In that context "very rare" is not a useful term.
There is a temporal component here. As an ancestor commenter said, "you can't catch it again right away" (emphasis added). We do not know (because we cannot know) if reinfection is possible after two years, for instance, because we have not had the virus for two years yet.
Don’t forget there are lifestyle factors that can effect your immune response. You’ll typically fight off a cold except for that one time when it catches you tired, or stressed ...
> From that, we can already tell that reinfection, although possible, is very rare.
No. From the current papers, we just know that the reinfection where people have had their virus sequenced in both first and second infection is very rare.
The problem is technological. Up to now there are around 50 million confirmed cases in the world but probably less than 100 thousand sequencings performed, and only a few sequencings by those who had strong enough symptoms twice and had the chance to have sequencing twice.
Without sequencing one just can’t prove that some case is an actual reinfection. All other cases are just “possible” (i.e. unprovable) reinfections and nobody can claim anything worthy of a scientific paper about them.
Sounds like good news, its observed that 6 months after recovering from SARS-CoV2 viral infection, the immune system in most of recovered people was able to identify and work fight off SARS-CoV2 virus. So if these people get in contact with the virus again, there will be less chance of them getting sick and transmitting it to other people.
I'm not sure if it even counts as "news", but it means that an infected-then-recovered person would be "resistant" for at least six months, which is exactly what the SIR model of infections would suggest.
There were some suggestions that Covid-19 would be an exception to this somehow, and having recovered, you would still be just as susceptible to getting it again. Which, if it had been true, would have been really bad news, although I suppose it would also have meant there was no reason to wait for a vaccine, because if even the actual virus itself doesn't teach your immune system to look out for it, then there's no way a vaccine could.
But, it's good scientific/medical work to verify that it works like most other viruses, and people who have recovered, are at least almost always going to be resistant thereafter (for at least six months, because that's all the time that has passed yet, although evidence from SARS suggests 10 years or more).
> because if even the actual virus itself doesn't teach your immune system to look out for it, then there's no way a vaccine could
I wouldn't say that completely follows. It would certainly indicate that developing a vaccine would be harder, but not impossible.
Modern vaccine development is essentially fly fishing at this point: the amount of control and options we have with the immune response-generating stimuli exceeds naturally-ocurring scenarios.
As an example, most of the spike-protein-expressing vaccines generate / deliver modified spike proteins, distinct from those found on actual SARS-CoV-2 coronavirus.
Indeed. There are even some vaccines for diseases that our bodies do not defeat. I'm perhaps misremembering, but I seem to recall that the HPV vaccine is one of those.
I haven't even looked at much of anything vaccine related much less have any expertise, but the explanation I remember hearing at some point is that by priming the immune system our bodies can prevent the virus from getting established. Polio and smallpox are also hard for the body to fight off but were some of the earliest vaccines (smallpox being the first according to Wikipedia). I don't think it implies that it is possible to create vaccines in cases where our body can fight the disease but then does not retain that resistance over time, although I would guess there is at lest some chance that is possible.
A better way to look at it, for me, is to start with what a vaccine is doing: it's not giving you resistance to a pathogen.
It's triggering your immune system to produce and/or store things, the presence of which then confers resistance when subsequently exposed to the actual pathogen.
So from that perspective, the next question is, "Do naturally occurring pathogens, presented in a natural manner, produce an optimal triggering themselves?" To which the answer, as you might guess from the messiness of real-world biology, is "No."
It turns out that while amazing our immune systems are also general purpose and adaptable, and such systems can get confused, or go off on a tangent, or focus on the wrong thing, etc etc.
Vaccines interact with this system by balancing two things: (1) how do I trigger the strongest, purest immune response that's effective on the thing I want to immunize against & (2) how do I avoid triggering such a strong immune response that I convince the body to attack itself?
It turns out, with modern biology, we actually can do better than nature on (1). Even if (2) still requires some guesswork (and a lot of testing).
I wouldn't assume that the reason resistance doesn't last in some case is just due to suboptimal triggering, although as I said I don't know much of anything about vaccine development. I do often encounter people with inflated opinions of modern medical understanding that does not match reality, so I am suspicious that your claims are not necessarily grounded in reality. I'm also not interested enough in the topic to look into it in any detail. I do agree that it isn't necessarily impossible for a vaccine to cause lasting resistance even if direct exposure does not.
IANAD, immunity is complicated, and long term immunity after having recovered from CoVID-19 infection is not likely.
This is bad news because it means that herd-immunity is not naturally achivable. It means you most get a vaccine at regular intervals to be protected against this strain of the virus.
It also means that lockdown is best strategy to reduce strain on health services until vaccine is ready and freely distributed to all.
>IANAD, immunity is complicated, and long term immunity after having recovered from CoVID-19 infection is not likely
Replicated studies have already found that prior exposure to other coronavirus infections (common cold, animal viruses) leaves behind t-cells that are activates for covid-19, as long as 17 years. And that a large percentage of the population has these t-cells. [0]
Thanks for sharing! All science affects my opinion. For me, not knowing, makes me have a pessimistic attitude. Lesson learnt is to keep this to myself.
The article certainly doesn’t say anything about “people” at all. It demonstrates immune response in the serum, but not at all the effect of the said response, especially not if any person is actually “immune.”
Reinfected! and the reinfection becoming a bad case! No immunity... Article hints that you can expect to be relatively protected for up to 6mo after infection.. But there are no guarantees.
From the article: "There is still a lot for us learn before we have a full understanding of how immunity to COVID-19 works. (..) we all should still follow Government guidelines on social distancing to ensure we play our part in minimising the spread of COVID-19 within our communities." -Professor Paul Moss
This is great and all, but I'd be interested what proportion of the entire cohort demonstrated a T-cell immune response, not just the 100 who tested sero-positive for SARS-COV-2. There is growing speculation that a significant minority of people may mount a T-cell immune response without ever contracting SARS-COV-2 itself, based on exposure to other coronaviruses. This would be great news since it further reduces the effective threshold for endemic equilibrium.
With millions of cases worldwide there will always be some statistical outliers. Those are individually tragic, but not very relevant to most of us. The best estimate for infection fatality rate in the 20 - 49 age group is only 0.02%.
They are still scary due to the way they are portrayed to people. You could probably inject a million people with medical grade saline and still see some crazy reactions.
Many of the long term issues described for COVID already messed up my life as a result of Epstein-Barr 14 years ago (brain fog, fatigue). Post-viral syndrome is real and now it's getting some public attention for the first time.
Unless you're the person who has a second infection or the doctor who has to deal with this life and death situation, then yeah, fear mongering...
But the other side to this is that if the reinfection is due to the virus mutating into a more virulent state, then it's MORE likely to propagate as that virulent state, meaning more and more COVID19 infected people's will be open to reinfection over time.
I've noticed with Covid is that there is a lot of attention to edge cases with folks implying that the scenario is common. That's a very alarmist approach.
Hundreds (thousands?) of healthy people gets the flu in the US every year and die from it. Not because they have a comorbidity, they just have a really bad reaction to the flu.
But we don't assume that those edge cases are the most typical course of disease. Yes, you may be one of those really unlucky ones that die from a normally non-fatal disease, but the risk of that is pretty low.
This is how social media works; keep people engaged and cause them to experience large swings in emotion.
So as with almost everything nowadays (e.g. look up police brutality statistics and compare to common perception re: pervasiveness), the formula is simple: paint an exciting/horrifying view of reality by sensationalizing rare events.
> Hundreds (thousands?) of healthy people gets the flu in the US every year and die from it.
Way off! Tens of millions catch and tens of thousands die from the flu every single year in the US. And that's with a vaccine! You probably didn't know that though because news stations don't have rolling infection and death counters going 24/7 during flu season.
Why doesn't anyone question the ECMO machines? I'm definitely no doctor, but as a software engineer if my system failed 30-40% of the time I'd stop using it.
Last I read they have 30-40% instance of internal bleeding with many other TERRIBLE things as a side effect of all the blood thinners and other pharmaceuticals needed to use the machine.
I really find it hard to believe that COVID caused the PE, hemorrhage, etc. that ultimately put an end to that young man's life.
"Why doesn't anyone question the ECMO machines? I'm definitely no doctor, but as a software engineer if my system failed 30-40% of the time I'd stop using it."
ECMO is a hail-mary treatment for people who would almost certainly die otherwise. A 40% chance of death is better than a 99% chance of death.
What you're saying here actually happened with ventilators (though ventilators are nowhere nearly as invasive or complex as ECMO).
Tens of millions of cases, there are going to be a few outliers. Unless it starts happening at a statistically meaningful rate, these are just unfortunate one-offs.
