Japanese man tests positive for coronavirus again(www3.nhk.or.jp)
www3.nhk.or.jp
Japanese man tests positive for coronavirus again
https://www3.nhk.or.jp/nhkworld/en/news/20200315_13/
98 comments
A commenter on Reddit claimed that rebound effects are known among patients that have been treated with antiviral medications, and that that could also be a possible explanation: https://www.reddit.com/r/Coronavirus/comments/fjuj24/5075_of...
The entire theory of the solution to coronavirus hinges on an assumption that it will eventually pass once a critical mass of people have been infected and developed immunity. The handful of stories like this trickling out might imply that the immunity assumption could be incorrect.
What would be the ramifications of this? Could corona just bounce around the population for the rest of time, putting everyone at a high percentage chance of dying or requiring hospitalization multiple times a year? Could it be the kind of thing that comes back as a novel form every year like the flu? Could we be seeing covid-20, covid-21, etc ad infinitum, with high mortality/low life expectancy just being a new reality of life?
EDIT: If this were the case, and immunity is very shortlived after the virus is gone, maybe it could be contained through giving everyone an extremely frequent regimen of vaccines until this particular strain is out of circulation?
What would be the ramifications of this? Could corona just bounce around the population for the rest of time, putting everyone at a high percentage chance of dying or requiring hospitalization multiple times a year? Could it be the kind of thing that comes back as a novel form every year like the flu? Could we be seeing covid-20, covid-21, etc ad infinitum, with high mortality/low life expectancy just being a new reality of life?
EDIT: If this were the case, and immunity is very shortlived after the virus is gone, maybe it could be contained through giving everyone an extremely frequent regimen of vaccines until this particular strain is out of circulation?
I’m unaware of _any_ illness where some measure of immunity is not developed. I find it incredibly hard to believe that recovering from covid infection does not afford some level of immunity.
I do wonder if recovery due to anti-virals prevents or weakens immunity, however.
I do wonder if recovery due to anti-virals prevents or weakens immunity, however.
Right. If our immune system didn't get better at fighting something, you would remain infected forever or die from it. Reference HIV as an example of a virus our immune system could not fight.
If anyone is getting better (and 98%+ of people are) it's because the immune system can effectively fight it.
If anyone is getting better (and 98%+ of people are) it's because the immune system can effectively fight it.
Wow, I didn’t even think of it like that. That’s a great way to reason about it that makes it immediately clear. Thanks!
Or it could go dormant, like the herpes virus.
Maybe it's sort of survivor bias. Maybe antivirals don't weaken immunity but people who survived thanks to antivirals have innately such a weak immune response that they wouldn't have survived without them.
Huh? Antivirals just eliminate the virus before the immune system gets a chance to step in and build up immunity. How about that?
I don't think that's true. I don't think they give antivirals to people before they have fever.
And fever is one of the results of immune system working.
And fever is one of the results of immune system working.
Sure, but the body still isn't done building up immunity.
Miniscule amount of pathogen in the vaccine can give you full immunity. I think when you have fever your immune system was already exposed to enough of the virus to build full immunity for the future. Now it's just the case of whether you survive to enjoy your future immunity. And anti-virals just help you with that part.
Okay, I'm not a doctor, so maybe you're right. It just doesn't seem plausible. Though, that doesn't mean much.
Your prior should be that immunity works as it does with every other virus and you should require very strong evidence to the contrary (evidence, not anecdotes) to convince you otherwise. Throughout our evolutionary history we have come into contact with innumerable viruses and to a greater or lesser extent we have immunity to all of them post exposure. For many our immunity is long lived, on the order of years.
It's not a boolean whether people become immune or not--maybe some small portion of the population have issues developing immunity and the rest are fine?
My reasoning is the same, but rather than it being binary, it’s a gradient.
So after recovery I might be able to ward off 80% of exposure events that would infect a non-immune person. But given enough exposures or just really bad luck, I could still get infected again.
That being said generally in these cases the infection resolves way sooner due to the same mechanism that leads to immunity: immune “memory cells” which wait dormant, ready to start production of immune cels when exposed to the characteristic antigens
So after recovery I might be able to ward off 80% of exposure events that would infect a non-immune person. But given enough exposures or just really bad luck, I could still get infected again.
That being said generally in these cases the infection resolves way sooner due to the same mechanism that leads to immunity: immune “memory cells” which wait dormant, ready to start production of immune cels when exposed to the characteristic antigens
With any non-negligible immunity rate (for example, 70% would be typical for immunity gained through an influenza vaccine [0]), we will still see exponential decay once a critical mass (R0 < 1) is reached. I believe immunity rates are higher after recovering from real infections, but still not perfect.
Therefore a headline reading "Japanese man gets reinfected" is not of particular concern while "50% of survivors get reinfected" would be highly concerning.
[0] https://www.ecdc.europa.eu/en/seasonal-influenza/prevention-...
Therefore a headline reading "Japanese man gets reinfected" is not of particular concern while "50% of survivors get reinfected" would be highly concerning.
[0] https://www.ecdc.europa.eu/en/seasonal-influenza/prevention-...
Interesting, I wasn’t aware immunity works this way. Thanks
the models already account for this. eg in compartmental models both SIS or SIRS have this assumption.
Doesn’t swine flu recur every now and then? Every virus could potentially become endemic.
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Is it at all possible that we become progressively more immune with each incidence or that we can only be infected N times? If either of these things are true our strategy will still work.
Viruses do mutate. So for many people, the body may never develop complete immunity.
SARS (including this new Coronavirus) does not mutate nearly as fast as the flu and other viruses though. It has built in error correction, and this is good news for us:
> But SARS has a molecular proofreading system that reduces its mutation rate, and the new coronavirus’s similarity to SARS at the genomic level suggests it does, too. “That makes the mutation rate much, much lower than for flu or HIV,” Farzan said. That lowers the chance that the virus will evolve in some catastrophic way to, say, become significantly more lethal.
https://www.statnews.com/2020/02/04/two-scenarios-if-new-cor...
> But SARS has a molecular proofreading system that reduces its mutation rate, and the new coronavirus’s similarity to SARS at the genomic level suggests it does, too. “That makes the mutation rate much, much lower than for flu or HIV,” Farzan said. That lowers the chance that the virus will evolve in some catastrophic way to, say, become significantly more lethal.
https://www.statnews.com/2020/02/04/two-scenarios-if-new-cor...
It is unclear if he was symptomatic in the first positive test. I have read at least some of the tests are capable of giving false positives. Could this have been the case here?
It's more likely that the tests that cleared him were false negatives.
There's a 9% chance of two false negatives in a row, so that could be the case. But why would he develop a fever so late after being first tested positive? His fever would have been 20 days after first detection of his infection.
Also, the article doesn't say whether he had fever initially and it went away and then came back, which is important information.
Also, the article doesn't say whether he had fever initially and it went away and then came back, which is important information.
He's in his 70s, he could be immune compromised etc... Many reasons why his body might not have actually cleared the virus.
I understand that false negative PCR tests are almost impossible?
EDIT: for those down voting. What about this paper then?
https://pubmed.ncbi.nlm.nih.gov/32133832/
EDIT: for those down voting. What about this paper then?
https://pubmed.ncbi.nlm.nih.gov/32133832/
I think you have that backwards.
False negative seems extremely plausible. If you're sick, but your viral load is low, it should be possible to collect a sample without a virus particle. If the sample doesn't contain a viral particle, it will necessarily come back negative.
False positive seems unlikely, as you'd have to have something that survives several cloning cycles that ends up looking exactly like the markers you're matching against.
False negative seems extremely plausible. If you're sick, but your viral load is low, it should be possible to collect a sample without a virus particle. If the sample doesn't contain a viral particle, it will necessarily come back negative.
False positive seems unlikely, as you'd have to have something that survives several cloning cycles that ends up looking exactly like the markers you're matching against.
It's the opposite. The PCR tests are more specific (99%) than sensitive (perhaps 90%, we're not really sure).
It’s the opposite. False positives are highly improbable. False negatives happen more regularly.
If there are very little viruses, and the swab/sample didn’t contain any you would get a false negative test.
If there are very little viruses, and the swab/sample didn’t contain any you would get a false negative test.
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Possibly if he had related symptoms from another illness and then caught the disease due to exposure in the hopsital. I don't know if this is more likely than a false that sent him home from the hospital.
Reinfection could not occur in SARS-CoV-2 infected rhesus macaques
"In this study, our results indicated that the primary SARS-CoV-2 infection could protect from subsequent exposures, which have the reference of prognosis of the disease and vital implications for vaccine design.Importantly, the unsuccessful rechallenge in NHP models suggested that the re-positivity from discharged patients could not be due to reinfection. It needs to consider more complicated issues to find out the causes."
https://www.biorxiv.org/content/10.1101/2020.03.13.990226v1....
That's a pretty good sign for an equal response in humans.
"In this study, our results indicated that the primary SARS-CoV-2 infection could protect from subsequent exposures, which have the reference of prognosis of the disease and vital implications for vaccine design.Importantly, the unsuccessful rechallenge in NHP models suggested that the re-positivity from discharged patients could not be due to reinfection. It needs to consider more complicated issues to find out the causes."
https://www.biorxiv.org/content/10.1101/2020.03.13.990226v1....
That's a pretty good sign for an equal response in humans.
They found them clean 14 days after infection and tried to re-infect them 28 days after initial infection.
So immunity lasts at least 14 days after complete recovery. In rhesus macaques who recovered in 14 days.
So immunity lasts at least 14 days after complete recovery. In rhesus macaques who recovered in 14 days.
Looking briefly at the study (I only skimmed the beginning), it seems they attempted the reinfenction quite soon after the recovery from the initial infection.
This doesn't tell us anything about how long one may be immune for afterwards.
Does anyone have knowledge about the length of periods of immunity (or lack thereof) in various infectious diseases?
This doesn't tell us anything about how long one may be immune for afterwards.
Does anyone have knowledge about the length of periods of immunity (or lack thereof) in various infectious diseases?
IIRC immunity for coronaviruses typicaly is 6months-two years. And I am not sure , but if you get reinfected after that, once you clear the second infection your immunity will last longer yet.
That sounds pretty good! I hope it's true. I was worried it might be much shorter than that.
In the current social climate (i.e, false positives perhaps being somewhat less likely, especially in a contrived situation like a cruise ship full of at risk patients) if we assume that the subject truly was infected, cleared, then infected again in such a short time window, what would that mean for all current containment strategies?
Containment is moot in this case. Quarantine only works when immunity or absence of infection vectors (infected individuals, individuals still in a shedding state, surfaces or aerosols) is the outcome.
> Containment is moot in this case
Please be very careful when writing such things. Containment has already been proven to work even with almost 100k known infected, now down to basically zero new infections. The new cases in China seem to be imported from abroad now.
Please be very careful when writing such things. Containment has already been proven to work even with almost 100k known infected, now down to basically zero new infections. The new cases in China seem to be imported from abroad now.
Without knowing how common reinfection is, it means little. For all we know at this point, the vast majority of people might resist reinfection and this guy is a fluke.
That wouldn't be unheard of either. Chicken pox is almost always something people get only once. In rare cases, some people get it more than once.
That wouldn't be unheard of either. Chicken pox is almost always something people get only once. In rare cases, some people get it more than once.
It essentially means we need a vaccine to create immunity at scale, and will need to have fairly strict measures in place until that can happen.
Another alternative to immunity at scale would be to have sufficiently strict measures to reduce R0 to below 1, so the virus dies out. China appears to have managed this. If it could be done near globally, it's possible the remaining outbreaks could be contained.
If prior exposure to the virus itself won't give a person immunity, I would expect it would be much more difficult to create a vaccine to grant immunity. I wonder if the 18 month vaccine timeline I have heard mention would be affected.
We have never successfully created a vaccine against a coronavirus before, so this is new territory. On the other hand, we have new tools like the RNA vaccine being produced by Moderna which doesn't work like a traditional vaccine and so might be more effective. Ultimately we won't know until we try.
Nano machines! Buy a proprietary immune system and let a single corporation control your health for the rest of your life!
I don't understand how a vaccine would work if prior exposure to the virus doesn't prevent re-infection :/ Honest question, no snark intended.
Well I think it wouldn't be an 'inactivated' or 'attenuated' vaccine, but we have other vaccine types designed to trick the body into developing the readiness for an immune response. I don't know if they could work for this type of disease.
Edit: I glanced at vaccines on Wikipedia, read the following on conjugate vaccines. Maybe we will develop a new technology to do something similar with viruses, training the immune system to recognize the virus by linking it to a toxin?
>Conjugate—certain bacteria have polysaccharide outer coats that are poorly immunogenic. By linking these outer coats to proteins (e.g., toxins), the immune system can be led to recognize the polysaccharide as if it were a protein antigen. This approach is used in the Haemophilus influenzae type B vaccine.[41]
Edit: I glanced at vaccines on Wikipedia, read the following on conjugate vaccines. Maybe we will develop a new technology to do something similar with viruses, training the immune system to recognize the virus by linking it to a toxin?
>Conjugate—certain bacteria have polysaccharide outer coats that are poorly immunogenic. By linking these outer coats to proteins (e.g., toxins), the immune system can be led to recognize the polysaccharide as if it were a protein antigen. This approach is used in the Haemophilus influenzae type B vaccine.[41]
Interesting, and thanks for replying. I realize I know very little about vaccines beyond the elementary-school-level basics (even though my brother is an immunologist... maybe I should ask him).
This is a single case in an elderly person. He may have poor immune system function - that doesn't mean a vaccine wouldn't be effective in the rest of the population.
Yes, I understand this. I also understand this may be a mistake in testing for this specific individual. I was wondering about the effectiveness of vaccines in the hypothetical scenario posited by the OP, "what if you can be reinfected after cured?".
Naively, if immunity from prior exposure lasts for a few months, then we might reasonably hope for a vaccine whose effects last for a few months.
I suppose if that happened people would get revaccinated frequently.
I suppose if that happened people would get revaccinated frequently.
Ok, but according to the article the man tested positive on Feb 14, then got cleared on March 2 (in Tokyo), returned home and relapsed very few days later. If there are no mistakes in the resting (or reporting), that's not even a few months of immunity...
While reinfection is ominous and unwelcome, the fact that individual cases like this are newsworthy makes me hopeful that it is a rare phenomenon.
That's what I was thinking. Especially if there is a genetic factor involved, and we can determine that only a small percentage of the population have it, then we could still achieve a level of herd immunity.
False negatives are a huge issue here. The tests aren't that sensitive. If it was truly recurrent we'd see a lot more than one person since the disease is so contagious.
What has caused the slow rate of transmission in Japan?
It seems that the number of cases in Europe and the US keeps climbing (despite limited/late containment actions), but Japan seems to have it under control, comparatively speaking.
It seems that the number of cases in Europe and the US keeps climbing (despite limited/late containment actions), but Japan seems to have it under control, comparatively speaking.
Many companies implemented work-from-home policies very quickly, almost all public events (sports, standardized tests) were canceled, schools and sports gyms closed, and some companies that didn't go to remote work had employees stagger commute times so trains would be less crowded. This all started, iirc, while the number of cases was still in the tens (not counting the cruise ship).
It is also more accepted to wear face masks, as many people have pollen allergies so it's quite normal, and there is less direct physical contact between people overall.
I remember reading that the number of flu cases was about half that of a normal flu season because of the precautions everyone was taking, which points to a high percentage of people doing their part to help prevent the spread.
It is also more accepted to wear face masks, as many people have pollen allergies so it's quite normal, and there is less direct physical contact between people overall.
I remember reading that the number of flu cases was about half that of a normal flu season because of the precautions everyone was taking, which points to a high percentage of people doing their part to help prevent the spread.
This is the big difference: people doing their part to help instead of, say, panic-hoarding or obstreperously insisting on going on as if nothing were happening.
Culturally there is very little physical contact. Bowing instead of handshakes being the big one. No kisses on the cheek as greeting. In general, more refrain when it comes to touching. Also widespread mask use.
On the flip side though we have crowded public transport, and I've heard that people often brave it to work even if slightly sick.
On the flip side though we have crowded public transport, and I've heard that people often brave it to work even if slightly sick.
Why do CDC and WHO discourage widespread mask usage? They suggest it only in a hospital setting or if caring for someone who has the virus. Is it because they are ineffective, or because they do not want to cause shortages?
Containment actions began less than a week ago in many european countries. It's expected the known cases grows unaffected for 7-10 days after containment comes into place.
The reason is that real cases start long before they become known cases.
The reason is that real cases start long before they become known cases.
Could be little testing.
Right, but even without testing, if the progression had followed what we've seen in Iran or Italy, there would be hundreds dying from Covid-19. This is not happening in Japan, and the virus has been in Japan much longer than those countries.
Also most of Europe does very little testing, but assuming they have uniform criteria, the growth rate should still give some idea of the propagation.
For example in Switzerland, they barely test anyone, but it's pretty clear that with +30% d/d growth this is either already everywhere or going to be.
For example in Switzerland, they barely test anyone, but it's pretty clear that with +30% d/d growth this is either already everywhere or going to be.
The virus has been in Japan a lot longer than Italy.
Over 2,000 have died in Italy, fewer than 50 in Japan.
I have yet to see anything close to a satisfactory explanation.
Over 2,000 have died in Italy, fewer than 50 in Japan.
I have yet to see anything close to a satisfactory explanation.
First detected case in Italy was January 31st, in Japan it was January 16th and/or 10th (quick Japanese and English Wikipedia check, correct me if you have a better source).
This may have something to do with it, 83% of the cruise ship did NOT get infected even though population was mostly elderly people: https://twitter.com/ecosensenow/status/1239952942234402816?s...
Here's what Ralph Baric, an epidemiologist from the University of North Carolina Chapel Hill, had this to say on episode 591 of This Week in Virology[1] a few days ago:
Ralph Baric: I saw some very interesting data from Stan Perlman the other day, who has been looking at serum neutralization titers of MERS patients from the Middle East kingdom of Saudi Arabia area and it's quite intersting that people peak fairly quickly with high neutralization titers but then they wane over the next year to almost background levels or just slightly above background levels by the second year, and with MERS there have been several reports of people who have seroconverted. They were RT-PCR positive and their serum neutralizing titers and even ELISA titers went to almost zero within a few months.
Baric: And it has not been studied and it should be studied, and this is the contemporary human Coronaviruses -- nobody knows how they maintain themselves in human populations. They don't undergo rapid antigenic variation like influenza. There's not 115 common cold or corona virus type genotypes or whatever they're called, serotypes. Sorry Vincent, I just butchered the coronaviruses.
Vincent Racaniello: That's ok. <laughter>
Baric: So one hypothesis is that they cause a transient protective immune response that wanes quickly and then they can reinfect and cause mild upper-respiratory tract infections and that's how they maintain themselves. So it is quite possible.. there's been a number now of reported cases in China of SARS2 infections where people were documented to be infected and recovered. They were RT-PCR negative. They went home and they became reinfected a month later or so.
Baric: In this case the United States has sufficient cases that we can actually track the serologic responses of the individuals and their general immune.. both B- and T-cell responses after infection and we can get a handle on the long term immunity that may be elicited after infection.
On the other hand, from a letter read on an earlier TWiV[2]:
I'm an infectious disease doctor and would like to point out an important factor in diagnosing this infection (and all respiratory pathogens that use nucleic acid probes for specimen collection). This is of particular concern now that China has transitioned to a much more problematic clinical diagnosis based more on clinical symptoms than PCR testing.
While it may seem trivial how a health care worker jams a swab in to someone's throat or nose, technique is important. If anterior naries (front of nose) swabs or side of mouth swabs are done, rather than the true posterior nasopharynx or oropharangeal swabs, the sensitivity drops dramatically.
We have shown this to be true repeatedly with diagnosis of influenza and respiratory pathogens, and I am disappointed that it has not been mentioned more in discussions about the PCR tests, missing the diagnosis in people who are positive and negative then positive again.
We often see people admitted from the ER with the perhaps carelessly collected flu test who miraculously are flu positive by the time they are admitted. Like so many cultures and diagnostics in infectious diseases, specimen collection and handling is critical.
I warn my patients about the unpleasantness of a nasopharangeal swab and jokingly tell them that if it doesn't cause a wincy-face reaction we haven't collected specimens from where the viruses reside.
[1] - http://www.microbe.tv/twiv/twiv-591/ about 15 minutes and 50 seconds in to the program
[2] - http://www.microbe.tv/twiv/twiv-588/ at about 1 hour and 38 minutes in
Ralph Baric: I saw some very interesting data from Stan Perlman the other day, who has been looking at serum neutralization titers of MERS patients from the Middle East kingdom of Saudi Arabia area and it's quite intersting that people peak fairly quickly with high neutralization titers but then they wane over the next year to almost background levels or just slightly above background levels by the second year, and with MERS there have been several reports of people who have seroconverted. They were RT-PCR positive and their serum neutralizing titers and even ELISA titers went to almost zero within a few months.
Baric: And it has not been studied and it should be studied, and this is the contemporary human Coronaviruses -- nobody knows how they maintain themselves in human populations. They don't undergo rapid antigenic variation like influenza. There's not 115 common cold or corona virus type genotypes or whatever they're called, serotypes. Sorry Vincent, I just butchered the coronaviruses.
Vincent Racaniello: That's ok. <laughter>
Baric: So one hypothesis is that they cause a transient protective immune response that wanes quickly and then they can reinfect and cause mild upper-respiratory tract infections and that's how they maintain themselves. So it is quite possible.. there's been a number now of reported cases in China of SARS2 infections where people were documented to be infected and recovered. They were RT-PCR negative. They went home and they became reinfected a month later or so.
Baric: In this case the United States has sufficient cases that we can actually track the serologic responses of the individuals and their general immune.. both B- and T-cell responses after infection and we can get a handle on the long term immunity that may be elicited after infection.
On the other hand, from a letter read on an earlier TWiV[2]:
I'm an infectious disease doctor and would like to point out an important factor in diagnosing this infection (and all respiratory pathogens that use nucleic acid probes for specimen collection). This is of particular concern now that China has transitioned to a much more problematic clinical diagnosis based more on clinical symptoms than PCR testing.
While it may seem trivial how a health care worker jams a swab in to someone's throat or nose, technique is important. If anterior naries (front of nose) swabs or side of mouth swabs are done, rather than the true posterior nasopharynx or oropharangeal swabs, the sensitivity drops dramatically.
We have shown this to be true repeatedly with diagnosis of influenza and respiratory pathogens, and I am disappointed that it has not been mentioned more in discussions about the PCR tests, missing the diagnosis in people who are positive and negative then positive again.
We often see people admitted from the ER with the perhaps carelessly collected flu test who miraculously are flu positive by the time they are admitted. Like so many cultures and diagnostics in infectious diseases, specimen collection and handling is critical.
I warn my patients about the unpleasantness of a nasopharangeal swab and jokingly tell them that if it doesn't cause a wincy-face reaction we haven't collected specimens from where the viruses reside.
[1] - http://www.microbe.tv/twiv/twiv-591/ about 15 minutes and 50 seconds in to the program
[2] - http://www.microbe.tv/twiv/twiv-588/ at about 1 hour and 38 minutes in
Edit: Is this lousy testing? Or mutation? It'll be interesting to see how this develops.
I chose to assume it was not a re-infection and it just came back in a rare case, which is very possible.
If not, we are dead and it's pointless planing around collapse of society.
It makes much more sense to assume we have a solid ( IE at least a year in most cases) herd immunity.
Planning around no herd immunity is like planning in depth around bankruptcy at round one funding.
If not, we are dead and it's pointless planing around collapse of society.
It makes much more sense to assume we have a solid ( IE at least a year in most cases) herd immunity.
Planning around no herd immunity is like planning in depth around bankruptcy at round one funding.
I was under the impression that one typically becomes immune to diseases like this, but apparently that's not the case? Does anyone have any reliable information here? Is this particular instance what we would typically expect, or can it be explained by test inaccuracy, something unusual about this person, etc.?
The Chinese say their are two distinct strains in circulation.
Tests are not perfect.
Plenty of explanations. Most of them quite uncomfortable.
Tests are not perfect.
Plenty of explanations. Most of them quite uncomfortable.
Do you have a source for that? Because the does not really match my reading of the data on https://nextstrain.org/ncov.
https://www.hopkinsguides.com/hopkins/view/Johns_Hopkins_ABX...
> Preliminary evidence suggests two strains of SARS-2-CoV circulating: one associated with milder illness (~30%), the other with severe illness (70%).
> Preliminary evidence suggests two strains of SARS-2-CoV circulating: one associated with milder illness (~30%), the other with severe illness (70%).
"The Chinese say their are two distinct strains in circulation."
This has been debunked on This Week in Virology[1]:
Vincent Racaniello: There are a series of articles here, where there have been some claims about different circulating lineages and what that means. Are you on this, Cathy?
Cathy Spindler: Right. So, there was an article that I first saw in the LA Times "Chinese Scientists Say Second Coronavirus Strain Is More Dangerous"[2]. But in that there's a link to virological.org, which we talked about another article posted there a couple of weeks ago[3], and they really debunk this and think even that this Chinese article about a second Coronavirus should be retracted. Two of the key claims that are reached by misunderstanding and overinterpreation of data and an additional analysis suffers from methodological limitations. So this long thing on virological.org goes in to the reasons why there's no real evidence for two different strains, a more severe strain and a less severe strain.
Rich Condit: It also provides a nice summary of this sort of variation in sequence that's being observed in the virus over time, which is good.
Vincent: Yeah, it's a good aritcle. We'll put a link. It's worth reading, but as everyone should know, when these [indistinct] viruses, every replication cycle they sustain mutations in their genomes and the lethal ones are gone, the viruses don't reproduce, but some of them stay and if they're neutral they remain. So they can be characteristic. So the virus introduced in to the Washington area is a single introduction and then it's spread and you can tell that because it has a unique set of mutations compared to say, the Chinese isolate, but it doesn't mean anything biologically. It's just markers.
Rich: And the markers are really interesting because they give you insight in to, I mean the insight that I got from observing what came out of the Washington cases is that from looking at the sequence of the virus they concluded that in fact it had been circulating for some time, and they could even get a very very rough estimate of how many cases might be out there based on the variation in sequence and the time at which the disease first showed up in a person.
Vincent: I think there are some emails later about this. People are concerned that, and people suggest in these papers, at least the one here, that we're being critical of that it could be evolved to be more virulent or more transmissible. There's no evidence for that whatsoever.
Rich: This is the kind of thing that... it just won't go away!
Vincent: Oh, it doesn't go away... new outbreak and it comes back.
Rich: Yeah, and there's no evidence. People have looked at this. We've gone over this for several.. Zika, Ebola, where's there's been variation and people point to a particular variation and they say, "This is going to make it more virulent" or something, and then the experiments ultimately get done and no. It hasn't made a difference.
Vincent: And also the issue of increased transmissibility, I think this virus is already very transmissible as it is, and I think the mutations that made it effectively transmissible among humans, which happened very early on, I don't know, either in animals or in humans early on, before we knew about it, they're done, and it's going to be hard to know what they were. MERS coronavirus has never acquired those high transmissibility changes and it keeps fizzling out and then you have another reintroduction from camels but this particular SARS-Cov-2 sustained them probably early on and it's a very good transmitter. It doesn't need to get better, at least from my anthropocentric view. We never really know what viruses are selected by, but I don't think there's eny evidence, and it's very hard to get that evidence. That paper tells you what you need to prove that mutations are doing something phenotypically. It's very hard to get that.
Rich: It has occurred to me that people who don't think about this stuff every day might be a little confused by this discussion relative to the discussion that goes on all the time about variation in influenza virus strains, and new strains coming up and having to change the vaccine and stuff. But that's different. That's variation in the influenza virus that makes it evade the existing immunity, and those sorts of variations arise so you get circulation of viruses that you don't have as good an immune response to, but that's different than a virus making mutations that make it more virulent. It's a different story.
[1] - at about 13 minutes in to episode 590 - http://www.microbe.tv/twiv/twiv-590/
[2] - https://www.latimes.com/science/story/2020-03-05/chinese-sci...
[3] - http://virological.org/t/response-to-on-the-origin-and-conti...
This has been debunked on This Week in Virology[1]:
Vincent Racaniello: There are a series of articles here, where there have been some claims about different circulating lineages and what that means. Are you on this, Cathy?
Cathy Spindler: Right. So, there was an article that I first saw in the LA Times "Chinese Scientists Say Second Coronavirus Strain Is More Dangerous"[2]. But in that there's a link to virological.org, which we talked about another article posted there a couple of weeks ago[3], and they really debunk this and think even that this Chinese article about a second Coronavirus should be retracted. Two of the key claims that are reached by misunderstanding and overinterpreation of data and an additional analysis suffers from methodological limitations. So this long thing on virological.org goes in to the reasons why there's no real evidence for two different strains, a more severe strain and a less severe strain.
Rich Condit: It also provides a nice summary of this sort of variation in sequence that's being observed in the virus over time, which is good.
Vincent: Yeah, it's a good aritcle. We'll put a link. It's worth reading, but as everyone should know, when these [indistinct] viruses, every replication cycle they sustain mutations in their genomes and the lethal ones are gone, the viruses don't reproduce, but some of them stay and if they're neutral they remain. So they can be characteristic. So the virus introduced in to the Washington area is a single introduction and then it's spread and you can tell that because it has a unique set of mutations compared to say, the Chinese isolate, but it doesn't mean anything biologically. It's just markers.
Rich: And the markers are really interesting because they give you insight in to, I mean the insight that I got from observing what came out of the Washington cases is that from looking at the sequence of the virus they concluded that in fact it had been circulating for some time, and they could even get a very very rough estimate of how many cases might be out there based on the variation in sequence and the time at which the disease first showed up in a person.
Vincent: I think there are some emails later about this. People are concerned that, and people suggest in these papers, at least the one here, that we're being critical of that it could be evolved to be more virulent or more transmissible. There's no evidence for that whatsoever.
Rich: This is the kind of thing that... it just won't go away!
Vincent: Oh, it doesn't go away... new outbreak and it comes back.
Rich: Yeah, and there's no evidence. People have looked at this. We've gone over this for several.. Zika, Ebola, where's there's been variation and people point to a particular variation and they say, "This is going to make it more virulent" or something, and then the experiments ultimately get done and no. It hasn't made a difference.
Vincent: And also the issue of increased transmissibility, I think this virus is already very transmissible as it is, and I think the mutations that made it effectively transmissible among humans, which happened very early on, I don't know, either in animals or in humans early on, before we knew about it, they're done, and it's going to be hard to know what they were. MERS coronavirus has never acquired those high transmissibility changes and it keeps fizzling out and then you have another reintroduction from camels but this particular SARS-Cov-2 sustained them probably early on and it's a very good transmitter. It doesn't need to get better, at least from my anthropocentric view. We never really know what viruses are selected by, but I don't think there's eny evidence, and it's very hard to get that evidence. That paper tells you what you need to prove that mutations are doing something phenotypically. It's very hard to get that.
Rich: It has occurred to me that people who don't think about this stuff every day might be a little confused by this discussion relative to the discussion that goes on all the time about variation in influenza virus strains, and new strains coming up and having to change the vaccine and stuff. But that's different. That's variation in the influenza virus that makes it evade the existing immunity, and those sorts of variations arise so you get circulation of viruses that you don't have as good an immune response to, but that's different than a virus making mutations that make it more virulent. It's a different story.
[1] - at about 13 minutes in to episode 590 - http://www.microbe.tv/twiv/twiv-590/
[2] - https://www.latimes.com/science/story/2020-03-05/chinese-sci...
[3] - http://virological.org/t/response-to-on-the-origin-and-conti...
If you read the virological.org link, the first comment is from a Japanese team that independently reached the same conclusion as Tang et al.
I've seen a bunch of scientists who will nitpick any Chinese paper to bits. Mostly older scientists. In the case of this virus, the need to publish before the usual review means there are guaranteed to be flaws. The Glasgow call to retract was a pretty aggressive way to go after the people who know the most about the virus but couldn't prove everything they had learned.
I've seen a bunch of scientists who will nitpick any Chinese paper to bits. Mostly older scientists. In the case of this virus, the need to publish before the usual review means there are guaranteed to be flaws. The Glasgow call to retract was a pretty aggressive way to go after the people who know the most about the virus but couldn't prove everything they had learned.
Apparently in the case of viral infections it is normal to still be tested positive for some time after recovery, up to a few weeks. Unless there is really a confirmation of symptoms reappearing etc. I think this is the most plausible explanation.
Immunity seems to last only for a short period (few months) but there is not enough evidence to conclude anything yet really.
This man might just not have recovered entirely at all though.
This man might just not have recovered entirely at all though.
Different corona viruses show different immunity periods after infection. The common cold is one that gives immunity of about a year after infection. We don't know how long immunity will last with covid-19.
I know it's possible to have an issue with your immune system not storing the antibodies after fighting off a virus, so you can catch it again. But it's pretty rare?
This is just one example, what conclusions can we draw from just that one?
[deleted]
What is the rate of false positives given a positive test result for these tests?
Isn't it possible his negative was a false negative? Or even his initial positive was false while having other flu-like symptoms? Then his negative was accurate. And finally he became infected properly.
I've also read reports of similar cases that turned out to be just administrative errors. Mixed up identities or just misspellings.
I have read many reports of people improving during the middle of the disease when it suddenly takes a bad turn (respiratory failure/cardiac arrest). I wonder if that is at all related to this.
> I have read many reports of people improving during the middle of the disease when it suddenly takes a bad turn (respiratory failure/cardiac arrest)
Medecine is not an exact science. There is a lots of things that can suddenly go wrong in the background.
There is the possibility of secondary infection in hospital with opportunistic resistant microbes.
And there is also the possibility of foul game, that can't be discarded and would be difficult to prove. Is a low probability but real risk. Unfortunately angels of mercy appear sometimes, often enough to have their own category.
https://en.wikipedia.org/wiki/Angel_of_mercy_(criminology)
Medecine is not an exact science. There is a lots of things that can suddenly go wrong in the background.
There is the possibility of secondary infection in hospital with opportunistic resistant microbes.
And there is also the possibility of foul game, that can't be discarded and would be difficult to prove. Is a low probability but real risk. Unfortunately angels of mercy appear sometimes, often enough to have their own category.
https://en.wikipedia.org/wiki/Angel_of_mercy_(criminology)
dr. Campbell[1] (the guy on YT explaining the situation every day) said that this seems to be because some people do not clear the virus effectively the first time ... and are picked up again on a later test, but that no proof has been shown that people can get reinfected and will probably be immune for at least a year.
[1] https://www.youtube.com/user/Campbellteaching
[1] https://www.youtube.com/user/Campbellteaching
He started getting symptoms again, which is the most worrisome part. It is not just simple virus is still lingering around, but it caused an infection again 35+ days after he had it once.
I hope this is just a fluke
I hope this is just a fluke
Is it feasible to create a vaccine against a virus if even infection with a live virus and catching the disease does not give you immunity?