Japanese man tests positive for coronavirus again
www3.nhk.or.jp
www3.nhk.or.jp
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?
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
I do wonder if recovery due to anti-virals prevents or weakens immunity, however.
If anyone is getting better (and 98%+ of people are) it's because the immune system can effectively fight it.
And fever is one of the results of immune system working.
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-...
> 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...
EDIT: for those down voting. What about this paper then?
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.
If there are very little viruses, and the swab/sample didn’t contain any you would get a false negative test.
Also, the article doesn't say whether he had fever initially and it went away and then came back, which is important information.
"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.
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?
So immunity lasts at least 14 days after complete recovery. In rhesus macaques who recovered in 14 days.
I suppose if that happened people would get revaccinated frequently.
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]
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.
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 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.
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.
Over 2,000 have died in Italy, fewer than 50 in Japan.
I have yet to see anything close to a satisfactory explanation.
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.
The reason is that real cases start long before they become known cases.
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.
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
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.
This man might just not have recovered entirely at all though.
Tests are not perfect.
Plenty of explanations. Most of them quite uncomfortable.
> Preliminary evidence suggests two strains of SARS-2-CoV circulating: one associated with milder illness (~30%), the other with severe illness (70%).
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...
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.
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.
I hope this is just a fluke