What other coronaviruses tell us about SARS-CoV-2

https://www.quantamagazine.org/what-can-other-coronaviruses-tell-us-about-sars-cov-2-20200429/

by theafh • 6 years ago

205 186 6 years ago

dmix• 6 years ago

In cats, for example, infection with feline enteric coronavirus may last for months or longer. When this happens, the virus mutates so much that its very nature seems to change. What starts out as a relatively mild gastrointestinal infection eventually causes serious peritonitis (inflammation of the membrane lining the abdominal wall) in some animals. Examining the virus at this point in the infection, researchers found that the mutations had resulted in the emergence of a related virus, feline infectious peritonitis virus — and this one has a higher fatality rate.

Can someone explain this to me, are they saying that the virus mutated into another virus? What conditions would it need to be a new virus rather than a variation of the original one?

celticninja2• 6 years ago

this also sounds a bit like the new childhood illness that health services are being warned about.

sjg0074• 6 years ago

Could be. Also a good reason to keep the schools closed.

maxerickson2• 6 years ago

Seems to be arbitrary:

https://www.vet.cornell.edu/departments-centers-and-institut...

sndean• 6 years ago

What conditions would it need to be a new virus rather than a variation of the original one

The Carl Woese (Woesian?) [0] definition that's been taught for a while is that when a certain sequence within two organisms exhibits a similarity score of < 97%, then it's new species. The certain sequences is generally 16S rRNA. That definition has its problems, but it's even more complicated for viruses: I think it differs for each virus family (e.g., Filovirus [2]). I just messaged a virologist and they said it's too complicated to explain over G-chat.

[0] https://en.wikipedia.org/wiki/Carl_Woese

[1] https://en.wikipedia.org/wiki/16S_ribosomal_RNA

[2] https://www.ncbi.nlm.nih.gov/pubmed/21046175/

oehtXRwMkIs• 6 years ago

That's recently been narrowed down to 98.7% and really only applies to microorganisms, definitely not the definition used for species with sex. Furthermore, the DNA-DNA hybridization technique is considered outdated at this point so one has to take it with a grain of salt. Also, viruses aren't even organisms so I'm not really sure you can even talk about species with them. I have heard the term quasispecies used for them however.

entee• 6 years ago

As others note it's super complicated with viruses. If you want to track the mutations in real time, check out the Nextstrain project (https://nextstrain.org/). The main person behind it, Trevor Bedford, is also a good person to follow on twitter for these topics and had a brief thread on mutation rate and immunity. (https://twitter.com/trvrb/status/1244750382338719745?s=20) TLDR: Though there's some uncertainty, given what we know today, it doesn't appear to be mutating in a way that will substantially affect immunity or morbidity.

danieltillett3• 6 years ago

Virologists often take a functional definition of how much mutation is required to make a new virus. If two different strains have changed so much that immunity to one strain doesn’t provide protection from the other strain then they are considered different viruses.

twic3• 6 years ago

These are two forms of virus. My guess would be that they were isolated and named separately, and retained their original names even after it was discovered they were the "same" virus.

The mechanism sounds similar to what happens with HIV. Simplifying wildly, there are M-tropic strains that infect macrophages, and T-tropic strains that infect T lymphocytes. People tend to get infected with M-tropic strains, because it's macrophages that come into contact with invading viruses. However, over time, the virus can mutate to become T-tropic. It's the T-tropic strains that cause immunodeficiency, and hence AIDS.

sjg0074• 6 years ago

The two viruses are related. One is thought to have evolved from the other.

pfdietz4• 6 years ago

On the plus side, a compound closely related to remdesivir (the drug to which remdesivir is the prodrug) showed great promise in curing this disorder (also known as FIP, Feline Infectious Peritonitis). Gilead stopped the trial because it might have interfered with marketing for human diseases, but if remdesivir goes into large scale production, as now seems likely, cats and their owners will benefit.

sterlind• 6 years ago

iirc there's a sort of black market for concerned cat owners getting an experimental (but apparently quite effective) drug for feline leukemia. there's Facebook groups you can join where they'll check you're not a fed and they'll direct you to a supplier.

mirimir• 6 years ago

Basically, taxonomy isn't all that meaningful for viruses.

If a given cell is infected with multiple ~related viruses, various chimeric viruses will be produced. Then there'll be selection on the basis of infecting other cells. And then the process repeats, until the host recovers or dies.

csours• 6 years ago

"Could SARS-CoV-2 become endemic among humans and just never go away? What then?"

I really don't see how we can avoid this. I think it will take too long to create a vaccine, and there will be mutations and recombinations that reduce vaccine effectiveness. I'd love to be wrong though.

standardUser• 6 years ago

"I really don't see how we can avoid this."

Some viruses just peter out, but I don't assume this one will just because it's possible. Some virus become endemic, but why would we assume that about this virus either?

SpicyLemonZest• 6 years ago

There are a handful of endemic coronaviruses, and historical respiratory disease pandemics have consistently become endemic, so it seems like a reasonable assumption.

SketchySeaBeast• 6 years ago

Just like the normal flu and H1N1 I imagine it may just become part of the yearly flu-shot - I imagine giving a large proportion of the population resistance changes the math considerably on how much it affects us.

kzrdude3• 6 years ago

Who gets a yearly flu shot? Genuinely curious.

CydeWeys2• 6 years ago

We can avoid it by developing a vaccine and vaccinating everyone. It would no longer be endemic in the population by the next generation. If there are no susceptible hosts because everyone is immune either from having it or from being vaccinated against it, it will die out like smallpox.

This really hinges on whether the vaccine confers long-term immunity. If it works like the flu vaccine, then being endemic is inevitable.

maxerickson2• 6 years ago

It's the rapid mutation of the flu virus that undermines the flu vaccine.

People often have differing immunity to a flu based on their past exposures. People that had been exposed to the 1950s strain were not hit as hard by the H1N1 that emerged in 1977: https://mbio.asm.org/content/6/4/e01013-15

twic3• 6 years ago

It's worth noting that while we have eradicated smallpox, we have only eradicated smallpox. We have not managed to eradicate any other infectious disease of humans.

danieltillett3• 6 years ago

Even if we create a vaccine how are we going to vaccinate people in conflict zones? If we can’t immunise everyone with the oral polio vaccine, then we have no chance of immunising everyone against SARS-Cov-2.

There is a possible ecological solution - we drive the dangerous strains to extinction by deliberately spreading a harmless strain. Unfortunately few people seem interested in investigating this idea.

jamiek88• 6 years ago

That's like vaccinating the virus itself.

Interesting idea - what's to stop the harmless one from mutating back though?

Presumably it'd be engineered to be both a) harmless to humans and b) spread better than existing SARS/COV strains.

If that super spreader then mutated to become harmful to humans we could end up in a worse spot, no?

Symmetry5• 6 years ago

We're not seeing much in the way of mutation in the SARS-CoV-2 structural proteins. And for other coroanviruses where we've developed vaccines, for dogs and pigs, we haven't had the same sort of problems with having to produce new vaccines that we do with the fast mutating flue.

Now, resistance does fade and to keep your dog protected you need to give it a booster shot every year or two and it might very well be the same with humans and SARS-2. But at least we wouldn't have to play the game of guessing which strain would be dominant in an upcoming season.

jjuel• 6 years ago

This is what worries me the most. More research needs to be done, but if you can get reinfected it seems like herd immunity is a pipe dream. If immunity doesn't last long then does a vaccine even work? Now I am very clueless on all this so I could be way off. In fact if someone does know more about virology and could explain to me where I am wrong that would be great!

f38zf5vdt• 6 years ago

Immunity will presumably last at least a few months, and the problem always reaches its greatest severity in the winter months because people are indoors more. We will just default to the influenza model, where there are circulating betacoronaviruses every season and we try to predict and vaccinate against them. The Middle East deals on and off with MERS.

matwood• 6 years ago

Presumably immunity goes away once the antibodies are gone, but does the body remember the virus for next time? Assuming the virus does not mutate too much from year to year, at what point will it not be novel anymore to the human body? Will subsequent infections be easier for the body to fight?

kbenson• 6 years ago

If you get reinfected, can you expect the same level of severity? That's what I'm wondering. Does having antibodies for a a virus that's very close, but not quite exact result in less severe symptoms and/or a quicker time to showing symptoms? If so, that doesn't necessarily help the spread greatly right now, but it does point towards a time in the future where this virus actually is more like the regular colds and flus we are used to.

CydeWeys2• 6 years ago

It maybe more that immunity within the body fades quickly, not so much that the virus mutates to the point it's different enough. The linked article talks about a sharp drop-off of coronavirus antibodies over time, which doesn't happen with antibodies for some other viruses (e.g. varicella antibodies are lifelong). And it doesn't sound like we really know why this might be.

vikramkr5• 6 years ago

Depends on the virus. For diseases like dengue you get antibody mediated enhancement of the infection, making it far worse, so the first time you're nearly asymptomatic and the second time you're on deaths door. For other diseases, even partial binding helps make the disease more mild. Biology is super variable.

Symmetry5• 6 years ago

For coronaviruses subsequent infections seem to be less severe. Some scientists speculate this coronavirus might not be intrinsically any more virulent than the 4 common cold coronaviruses, it's just that with this one we weren't able to train our immune system to handle it in childhood.

christkv2• 6 years ago

Well it makes it the same as the flu. We get a new vaccine every year that is slightly changed to match the dominant strain of the coronavirus.

Assumer• 6 years ago

Well the article oversimplifies the linked source quite a bit in my opinion:

The article says

Volunteers experimentally inoculated with HCoV-229E showed a steep decline in antibody response over time, and the majority could be successfully reinfected a year later.

while the linked source for that 1990 study says that while the 10 study participants were reinfected, none of them developed colds a second time, and the virus shedding period was much shorter.

heavyset_go• 6 years ago

If immunity doesn't last long then does a vaccine even work?

A flu shot-like regime would address this problem. If a vaccine is found, it won't be a vaccine you get once, but each year.

dathinab• 6 years ago

Can you really infer much from other corona viri?

I mean "corona virus" is a extreme corse category of viri which contains all viri of which the outer shell has a certain kind of structure which looks like a corona (crown).

While this puts some constraints on how the virtual can survive outside if the body and similar thinks it still does say hardly anything about e.g. what cells the virus hijacts, what syntoms it causes, etc.

Edit: maybe from other SARS corona viri

jnbiche3• 6 years ago

The plural is virus is viruses, or "virus" if you insist on its Latin form. It's a Latin word, but it only occurs in Latin as a singular collective noun:

https://jdebp.eu/FGA/plural-of-virus.html

anticsapp• 6 years ago

True, but everyone used "virii" on downloadable sections of hacker BBSes from the 80s/90s. It's a hard habit to break.

gus_massa2• 6 years ago

The classification of virus is difficult, but it is not based only in the shape. The shape may give some hints, and help to get a friendly name, but it is not the only property. Moreover, in the last (10?) years it is easier and easier to sequence the genome of them, and understand the relations.

For an more familiar example, think about the distinction of rabbits and hares. I can't for the life of me distinguish them, but they are not very related and biologist can classify them and get the more related species of them (specially if the rabbit/hare is dead and they can open it and look at the inner parts and bones, or even better, make a genetic analysis).

Another example is sharks vs dolphins. Both live in water and they look somewhat similar. (I think I can distinguish them.) Why are sharks a type of fish, but dolphins are not?

vikramkr5• 6 years ago

Coronavirus is the name given to a family of related RNA viruses. The family is named for the spikes. The family is not defined by the spikes. The family is defined by genetics and evolutionary relationships. So yes, we can infer plenty. The covid virus is actually so closely related to another one of the coronavirus (the sars virus) that it's considered just another strain of the sars virus (hence the name Sars-cov-2)

numpad0• 6 years ago

Idk but my impression is SARS-CoV-2 was named that way because it causes a SARS, Severe Acute Respiratory Syndrome, though it’s not the SARS. “SARS” include SARS-CoV SARS and other “SARSs” like COVID-19.

Probably the SARS was too generic of a name... in complete hindsight, SARS should have been named as “SARS COVID-02” and MERS as “SARS COVID-12” or something like that.

bigdict• 6 years ago

people from Phoenix are called Phoenicians

29athrowaway5• 6 years ago

There are many more coronaviruses in the wild and we will continue to see pandemics until unsanitary practices like wet markets with exotic animal products are outlawed.

Simian Inmunodeficiency Virus (SIV) could jump to humans, becoming HIV, through the manipulation of raw meat from infected apes.

We have immunity or at least some control over diseases coming from more common species of cattle.

the_af5• 6 years ago

we will continue to see pandemics until unsanitary practices like wet markets with exotic animal products are outlawed

I'm really no expert and don't know what to think, but Wikipedia asserts that as of April 2020 investigations are still trying to determine whether the Huanan market was really the source of COVID19. Even if it was, can we even conclude getting rid of these markets would solve pandemics as a general problem?

So at this point we can't really say the "fix" is to remove these markets, can we?

29athrowaway5• 6 years ago

It is known it comes from certain animals, like bats.

So, how can the virus jump from a bat to a human, either directly or indirectly?

Sure, you can randomly run into a bat anywhere in the world. I know a person that found a bat in her balcony some weeks ago.

But the probability that the virus jumps across species is low. You have to increase the odds, and a good way of doing that is creating a wet market full of them.

And it has been known for a long time that those markets were a disaster waiting to happen.

jmull• 6 years ago

Epidemics are a statistical game, not a black-and-white one.

We aren't realistically out to completely eliminate high-mortality pandemics, but reduce the changes. E.g., perhaps we can make the hundred year event a thousand year event, and the population mortality 1-2% rather than 10-20%.

The question is not whether the Wuhan wet market was definitively the origin of SARS-Cov-2/Covid-19 in humans, but whether it, and similar markets significantly increase the chances of a similar event in the future.

So at this point we can't really say the "fix" is to remove these markets, can we?

Yes, I think we can. Given what we know of how viruses evolve, mutate and the mechanisms by which they move from various animals to humans, we want to minimize the points where people come into contact with large amounts and variety of raw animal matter in highly unsanitary conditions. Wet markets are probably the lowest hanging fruit in that category.

jlg232• 6 years ago

There are many more coronaviruses in the wild and we will continue to see pandemics until unsanitary practices like wet markets with exotic animal products are outlawed.

Before trying to find a global definition for "exotic" we could start with washing hands or not sneezing or coughing at people nearby.

rrdharan• 6 years ago

Sneezing and coughing, sure, but lots of folks don't have easy access to clean water, a problem that is likely to exacerbate over the next few decades. Excessive hand washing among the people who do isn't gonna help a lot particularly in drought-prone areas.

I don't think it is a bad idea to keep looking for ways to prevent these outbreaks as close to whatever their origin is as possible.

Note that in some very poor countries (India comes to mind) it's not at all clear that more total lives are saved via lockdowns since they will result in famine and all sorts of other terrible consequences.

In Africa folks are worried about a huge spike in malaria that could dwarf the projected CoVid impact in certain populations.

Every country for themselves and the current lockdown strategies are what we are gonna get, and I'm not angry about it since the action-reaction-logic of all of this is pretty straightforward, but it's not at all quite clear to me that it leads to the fewest number of human casualties vs just some local minima.

droopyEyelids2• 6 years ago

I don't believe a 'wet market' is any worse than a confined animal feeding operation in terms of breeding pestilence.

CAFOs have continued to exist through indiscriminate use of antibiotics, but the potential future impact of their practices seems like it's even bigger than the impact of bush meat in a wet market

(Also, the wet markets are not the definitive source of sars-2. I thought the pangolin-as-pets trade seemed to be the more likely source?)

29athrowaway5• 6 years ago

Pangolins as pets? No. Pangolins as traditional medicine.

https://en.wikipedia.org/wiki/Pangolin_trade#Asia

Symmetry5• 6 years ago

There are many potential sources for serious zoonotic diseases. As long as we keep large number of pigs and chickens in farms there'll be the possibility of a flu pandemic caused by viruses going from humans to animals and back.

clarkevans• 6 years ago

Does the amount of virus exposure affect disease severity? It looks that way.

Besides reducing the transmission rate, social distancing measures could also be reducing the initial viral load of each exposure, leading to milder disease profiles, lowering population hospitalization and fatality rates.

eveningcoffee3• 6 years ago

Some people have tried to infer SARS-CoV-2 severity based on common corona viruses https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7102597 (currently hospitalized 89998, CFR so far in hospitals 17%).

But, it does not mean that the question is wrong of course and it is an interesting piece.

Also Sweden is not having some clever strategy. Anders Tegnell messed up so bad that they had to claim it to be a strategy https://www.project-syndicate.org/commentary/swedish-coronav...

toolz• 6 years ago

Why does it seem like both sides seem to be so sensationalist about Sweden. They have middle of the road all-cause mortality and most recently their sero studies suggest an extremely low IFR but that got pulled due to bad randomization of test subjects so that might go up to middle of the road for Europe for Sweden too. They haven't performed great and not poorly either. It's strange to see people so polarized over them.

tigershark2• 6 years ago

Because they should be compared with the neighbouring Nordic countries.

  Norway 38 deaths/M
  Finland 37 deaths/M
  Denmark 76 deaths/M
  Sweden 244 deaths/M

It’s an order of magnitude more deaths per million than Norway or Finland.

joe_the_user2• 6 years ago

Whether Sweden is doing well or badly is a big question for the overall debate about how to handle the virus. While I aim my discussion to always be calm, cool and collected as a general rule, who ever claims approach X for dealing with a deadly pandemic is good has to claim some other approach is bad and I don't see how that can avoid being a strong statement if not "sensationalist". Inded, if Sweden had just an average death rate without a lockdown, their approach would be a win, would be preferable. But they don't have an average death rate, they have a much higher rate than comparable countries and their deaths basically continue exponential growth whereas things in Norway seem relatively under control.

https://ourworldindata.org/grapher/total-covid-deaths-per-mi...

-- Fair warning, Italy's death are higher still, of course but Italy isn't really comparable. Even more, Sweden's in the exponential phase and so we don't know how they will go - they providing a laboratory for the world but I don't think human beings should be volunteered for such experiments.

alvah• 6 years ago

Many (if not most) people have "picked a team" so to speak, and they want to be correct. If Sweden's way proves to be better in the long run, many of those people will have been wrong. Nobody wants to be proven wrong, hence the passion.

freetime2• 6 years ago

Unfortunately I think that in the US at least the decision to lock down or reopen has become very highly politicized and we are starting to see virtue signalling enter the equation. People now have a vested personal interest in seeing Sweden's approach fail or succeed, in order to reinforce their own political opinions and/or sense of morality.

I find it very frustrating to see the way it's being spun. Firstly, social distancing is not a binary thing that you either do or don't do. Sweden has certainly implemented some social distancing measures and will continue to make adjustments to their strategy as new data comes out. And second, what works for Sweden may or may not be applicable in other countries. The virus spreads differently in different places, and different cultures may have differing attitudes about what constitutes an acceptable risk. I suspect that if Stockholm saw the same sort of explosive growth that was seen in New York, they would have reacted with stronger social distancing policies.

It's certainly good to look at what other countries are doing in their response to covid-19 and ask if there are things that are worth adopting. But I think it's much more important for countries (and states and cities) to be paying attention to their own data... and that is what should be primarily driving their response.

senderista4• 6 years ago

Re: Sweden, it couldn’t have been a thought-out “herd immunity” strategy because otherwise they would have locked down nursing homes and they admit they didn’t until very recently. Tegnell simply didn’t take it seriously until it was impossible to do otherwise. Not so different from Trump, even if his motivations were very different.

eveningcoffee3• 6 years ago

It is interesting to see how "saving the face" is so important in Sweden when other countries around have been much more flexible to adapt to the evolving situation.

nfc2• 6 years ago

"This deletion likely hindered its ability to bind effectively, making it harder to produce severe infections. Such evolution by deletion is actually a common feature of these viruses."

Is this really the case?, how would that be a common feature?, how are the strains where this deletion takes place more successful than those where it doesn't happen?, is it because it favors faster spread and somehow the organisms infected by these strains with deletion become inmune also to strains without deletion?, or there are other mechanisms that come into play?

vikramkr5• 6 years ago

Deletion is an easy mutation to occur in the process of replicating a genome. The reason these strains would be successful is because they dont kill or hurt their hosts that badly. If the infected person is bedridden, they're not going to be out and about spreading the virus, while a less severe infection would make it easier for them to mingle amd infect others to pass on the gene pool.

nfc2• 6 years ago

So from what you are saying the explanation for the paragraph from the article would be that a more severe infection would be more likely to have R0 < 1, so on aggregate viruses would "commonly" evolve this way. I understand this, but thank you for the reminder of the mechanism :)

However if the the R_0 of COVID-19 is between 1.4 and 5 (https://en.wikipedia.org/wiki/Basic_reproduction_number), how likely would it be that another mutation more lethal would appear and still be successful?, that is with R_0 > 1. I think that's a more relevant question than whether most successful mutations will be less lethal. Specially knowing that one of the characteristics of the virus is asymptomatic spread which could invalidate the point of a more lethal strain having much lower R_0.

Symmetry5• 6 years ago

Scientists speculate that while this change slows down reproduction and decreases virulence it also makes it harder for the immune system to track down virus infected cells, so it basically slows down the infection. In the long run zoonotic viruses tend to become less deadly. But I wouldn't expect this sort of mutation to be selected for when the number of cases is increasing exponentially.

hristov• 6 years ago

I think everybody should carefully read the short section that says "Does the amount of exposure affect the severity?".

Some people are looking at antibody studies that show that large parts of the population are somehow affected and then doing back of the napkin math and deciding that this is really not worse than the flu in terms of death rate. They are further encouraged by the fact that people that die tend to be older and with pre-existing conditions. Then they say we should open everything up and get everything "back to normal", and sometimes they add that this is just a way to winnow out the old and the weak.

As problematic as the latter statement is, the above thinking is actually dangerously optimistic. Experience shows us that in specific situations with prolonged/repeated exposure, the death rates are much higher. Also young and healthy people may get seriously sick and die due to high level of exposure.

This has already been happening in hospitals that did not have sufficient protective equipment/procedures.

If we open everything up and get into a situation where the virus is all over the place we can get into a horrible spiral of increased exposure and increased death rates etc.

Bnshsysjab• 6 years ago

As someone who hasn’t followed, and I understand I’m asking a random internet user this and not a scientist, but what is the definition of ‘prolonged exposure?’ Are people who contract the disease less likely to die that someone who is in close contact for a prolonged period of time? How long is that period? 15 minutes? Two hours?

bdamm• 6 years ago

To wit; if my wife gets sick and I care for her, does that mean I am experiencing "prolonged exposure"?

sjg0074• 6 years ago

It’s dose. So you get a higher dose the longer you are exposed. A smaller dose infected less cells are initially infected and maybe you get less sick. Higher dose may mean you get more sick.

nisa4• 6 years ago

Not a scientist, I can only attempt to retell what virologist Prof. Christian Drosten from Charité Berlin told in in his podcast[1]:

It's not really clear at the moment but it could be due amount of dose (more virus particles, faster replication) and where the virus makes contact with the body (if you are unlucky you are breathing a high dose directly into your lungs i.e. coughing patients in a hospital) - your immune system does not know the virus and it takes a while until it's able to fight it off and if the virus is directly in the lungs or you've got a high dose it has less time to do so. If you have it only in the throat it takes a lot of time, like multiple days until it goes into the lungs (if at all, this is also not clear when and when not this happens) and he suspected that in this time period you already have a better immune response.

Besides that (not from the podcast) I've read that the virus can induce inflammation that can can cause blood clots and other nasty things - so you may die from stroke or heart problems and not pneunomia.

There was also a paper that hypothesized that the virus can either replicate in the throat and go the lungs but it's probably also possible for the virus to use the nervous system to reach the brain via the olfactory bulb.

China did isolate ill patients from their families and it was hypothesized that sharing a bed/room with a sick person is a bad idea because the virus is in high doses in the air. So you can read that you should keep fresh air flowing in and possible avoid too much direct contact.

1: https://www.ndr.de/nachrichten/info/podcast4684.html (only in german)

kpennell• 6 years ago

60+ NYC MTA employees have died from Covid. Are we thinking that this happened because they had high viral loads?

slimed• 6 years ago

Something like 0.2% of NYC residents have passed away from the virus. As of 2018 the MTA had 50k employees. 60 out of 50,000 is 0.12%.

nyc_pizzadev• 6 years ago

The NYC subway system has me concerned. Not only is it filthy, but there is zero air circulation. This means that anything airborne will stay put, possibly in high concentration for a long time. Given the amount of people going thru these spaces, there is a high chance your going to be exposed to something. My concern is that I haven't heard anything on making the stations and cars cleaner or safer.

mfer• 6 years ago

Strokes, kidney disease, and other problems are happening to people who get this. Looking at death rate alone doesn’t tell of all the consequences

nradov2• 6 years ago

And how many strokes, kidney disease, and other problems were caused by other respiratory system viruses before COVID-19? We don't know because we've never really looked.

nyhc992• 6 years ago

I read that there was visible lung tissue damage forming the characteristic broken glass pattern on CT scans of 58% of the infected but asymptomatic carriers on the Diamond Princess cruise. That to me adds a sobering footnote to the process of developing herd immunity. Most of us won't die, but do we walk away with long-term impairment of our lungs and possibly other organs?

cvwright• 6 years ago

True, but is this information actionable?

The point of flattening the curve is to keep the healthcare system from being overwhelmed, in order to avoid a catastrophic death rate.

With a vaccine still 18-24 months away, we're all going to get infected sooner or later no matter what we do.

paypalcust833• 6 years ago

Yep. Heart and lung damage, obviously, also. COVID isn't a mild or trivial infection.

thdrdt• 6 years ago

My thoracic diaphragm sits too high on one side due to a issue with the phrenic nerve probably caused by some virus I had some time ago.

So yeah a virus can do more harm than you can see from the outside. It is not just a cough. You don't know what else is going on.

nerdponx• 6 years ago

I've also been wondering if this is a factor in the high death rates of people who've already been hospitalized, or in their rapid/unexpected deterioration. In a quarantine unit there must be a large amount of the virus all over everything.

pfdietz4• 6 years ago

It is my understanding with some viruses that one doesn't become infected with a single virus particle, but rather with a population. That's because the viruses mutate enough that no single virus has all the machinery necessary for replication. Only when a cell gets hit a few times to get all the parts does replication kick in.

I don't think the mutation rate of this particular virus is very high, though, so this situation doesn't seem as likely here.

akiselev• 6 years ago

Do you have a source for that first paragraph?

My understanding is that viruses don't have replication machinery at all - it's one of the defining features of viruses. Their host cells are essentially tricked into producing copies of the virus.

scentoni• 6 years ago

That is incorrect. The virus particles are mostly identical. The reason the dose matters is because each individual particle doesn't have a 100% chance of infecting an individual. That is partly due to the https://en.wikipedia.org/wiki/Innate_immune_system

snissn• 6 years ago

Some people are looking at antibody studies that show that large parts of the population are somehow affected and then doing back of the napkin math and deciding that this is really not worse than the flu in terms of death rate.

i feel like a lot of people are ignoring that a ton of people have relocated outside of NYC. i don't think the 25% antibody positive study in nyc is accounting for that

epistasis• 6 years ago

Already 0.2% of NYC has died of COVID19. That's completely consistent with the very initial, very dire infection fatality rates of 0.6%-1.0%. (Which is different than the case fatality rate.)

When you combine this 10x increase of the IFR along with the 5x-8x increase in suspected attack rate of flu, one would have to quite ignorant of reality, and perhaps an unknowing tool of others, to somehow look at the NYC study and think that it supports the silly "flu" conflation.

(And for that matter, flu kills a ton of people every year, are we going to add another flu to the world without fighting back at all? What sort of wimpy, defeatist person looks at the world that way?)

flatline• 6 years ago

Assuming it’s about as bad as the flu, fine, but we have herd immunity to the flu via vaccines and antibodies, plus people with the flu are symptomatic relatively quickly. Infect the entire US population with covid-19 and you lose ca. 0.5% of the population in one swoop, or about 1.5 million people. Just like the flu, but not, and the full consequences of the infection won’t really start showing up for a couple weeks.

jliptzin• 6 years ago

It would be way more than that as most would not be able to seek medical attention

AuryGlenz2• 6 years ago

In a good year the flu vaccine is 50% effective, and that’s pretty rare (though getting better). That’s not enough for herd immunity, and flu viruses mutate enough where we also don’t get it from naturally formed antibodies.

jnbiche3• 6 years ago

I can't agree with this enough. People are failing to account for viral load. I think that's part of what may be happening in areas like N. Italy and NY where the health system gets overloaded and the death tolls are high. People are getting such high initial inocula that they get really, really sick.

pnako• 6 years ago

Like most people I'm 1) not a specialist at all and 2) still have an opinion.

One thing I'm looking at is the excess mortality in a country like Sweden, which had an outbreak (in the top 25 countries by cases) but has not done any lockdown.

https://www.euromomo.eu/graphs-and-maps/

It's flat.

djsumdog3• 6 years ago

I've heard that, but then this article says:

In practice, however, this strategy, which was rejected in the United Kingdom, is leading to a much higher death rate in Sweden than in other Nordic countries.

and they cite a CNN source. But then I look at this data plotted on a log chart and it appears they're leveling out:

https://covidly.com/graph?country=Sweden#growth

I think it's way too early to make any inferences about which method is working better. There is a lot of noise in all the data.

gnopgnip• 6 years ago

Flat depends on your perspective. The death rate per capita is higher than anywhere in Asia, despite many of those countries being denser

aaron6952• 6 years ago

Sorry but this sounds like junk science.

Nurses and doctors work in close proximity to people who are sick. So 50 cm compared to 2 meters.

This is why their viral load would be more.

Given a default R of 2 to 2.5 what model are you implying makes this worse in terms of viral load given a reduced R? How would this work?

This bit need explaining because it sounds like you are implying with a R of 2 to 2.5 then the average person might get a higher viral load than if R was .9 lets say.

gvjddbnvdrbv• 6 years ago

Lets say you have 20 people im a room and one of them has a mild. Now you have up to 20 mild cases.

If 20 people spend a day in a room and 10 of them have mild cases maybe you now have 10 mild and up to 10 severe cases.

In order to be in a situation with many mild or pre-symptomatic cases in the same room the disease must spread fast through society.

softwarejosh2• 6 years ago

maybe all the permenant lung damage will pave way for stem cell researchers and well finally get something done

mattkrause• 6 years ago

If you’re not a biologist, it may have flown under the radar that there’s quite a bit of stem cell work going on already.

The development of induced pluripotent stem cells (iPSCs), which can be made from adult tissue rather than embryos, sorta sidestepped much of the ethical debate. They’re not exactly equivalent, but iPSCs have opened the door to a lot of exciting research because you can culture tissue that’s very similar to a patient’s. A few clinical trials were starting to get underway too....

dr_• 6 years ago

It should be noted, with respect to acquiring immunity, that with SARS-CoV(1), the amount of time after which immunity theoretically could be lost would be => 3 years. If SARS-COV-2 offers a similar level of immunity, that may not be a ton of time, but its not insignificant either, especially if a vaccine could be developed within that time frame.

known• 6 years ago

   Q: How close we are to achieving herd immunity?

   A: To achieve herd immunity we need 60-70% of the population to carry antibodies to the virus. The results of antibody tests suggest that in Europe and the US, in general, we are in the low single digits

https://archive.vn/UEgL5

agildehaus• 6 years ago

Herd immunity threshold is (R0−1)/R0. CDC pegs R0 at 5.7 with a CI of 95%.

(5.7-1)/5.7 = 82%

https://wwwnc.cdc.gov/eid/article/26/7/20-0282_article?deliv...

saalweachter3• 6 years ago

Oof, that's an increase over previous estimates of R0.

Navedkhann• 6 years ago

The theory of using Famotidine for COVID-19 has been thoroughly explained in the following articles: https://preprints.jmir.org/preprint/19199 https://preprints.jmir.org/preprint/19583?

What other coronaviruses tell us about SARS-CoV-2

Related Stories