
What other coronaviruses tell us about SARS-CoV-2 - theafh
https://www.quantamagazine.org/what-can-other-coronaviruses-tell-us-about-sars-cov-2-20200429/
======
hristov
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.

~~~
mfer
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

~~~
cvwright
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.

~~~
nyhc99
A vaccine isn't the be-all-end-all. We can still potentially hold out until
there's an effective treatment. Famotidine? Remdesivir? Anything that would
reduce the severity of the infection would lead to a better outcome than
you're facing currently.

~~~
senderista
Universal mask wearing could keep us out of lockdown for a long time before a
vaccine.

------
dmix
> 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?

~~~
sndean
> 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](https://en.wikipedia.org/wiki/Carl_Woese)

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

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

~~~
oehtXRwMkIs
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.

------
clarkevans
> 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.

------
dathinab
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

~~~
jnbiche
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](https://jdebp.eu/FGA/plural-of-
virus.html)

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

~~~
droopyEyelids
And if you don't break it, then eventually Websters will add it to the
dictionary and you'll have been right the whole time.

------
nfc
"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?

~~~
vikramkr
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.

~~~
nfc
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](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.

~~~
vikramkr
I've linked at the bottom a great video from minute earth with some food for
thought on this that I recommend watching, I found it really
helpful/interesting.

R0 is not necessarily inherent to the virus (although I think australia might
use a more restrictive definition that makes it more inherint to the virus),
it's based on our behavior to a large extent. MinuteEarth has a great video
(i'll link it below) that discusses how Cholera, for example, stayed very
severe and yet had a high R0 because it spread through sewage and the
sanitation system was not so great, so it didn't matter whether people stayed
home since their fecal matter ended up in drinking water anyway. But after
sanitation systems improved, cholera's R0 dropped and the less severe mutation
meaning higher r0 thing kicked in since you needed more human interaction to
get it to spread again.

So with coronavirus, if it mutates to become more severe, maybe it'll mutate
back to a SARS like form where it's super lethal which also means it doesn't
spread really far. Both SARS and ebola are on that end of the spectrum. But
let's say people get overconfident and think they've beat it and don't stay
home in the earlier days of the infection when they're not bedridden yet, you
could still get a lot of spread. Or, let's say it becomes more severe, but
also gains the ability to survive on surfaces for weeks and become airborne
when dislodged. Now, your santation procedure for your instacart delivery is
no longer enough and the virus could keep spreading through a lockdown. And
then there are diseases like HIV, which are ultimately incredibly severe, but
have a latency period that allows for infection to keep occuring even with a
mechanism of transmission that is a lot more effortful than accidentally
coughing near someone. As you mentioned, the asymptomatic spread aspect has
echos of htis, where even though the mutation could be severe, it might not
have the chilling effect on transmission you'd expect because of asymptomatic
and presymptomatic spreaders.

So long story short, I don't know how likely it is that a more lethal mutation
appears, but I do think you're right in intuiting that it is possible. Perhaps
there are ways to estimate a probability by running simulations on the genome
of the most common types of mutations to see what sort of effects we can
anticipate. SARS-COV-2 is very closely related to SARS-COV after all, it's
just a slightly different straing, even though the SARS outbreak and the COVID
outbreaks look so different. I don't think it's impossible that COVID could
mutate to have SARS' severity while maintaining COVID's presymptomatic
shedding and asymptomatic spread. Maybe as we learn more about it we'll
discover that both come from the same mutation and it's a fundamental
tradeoff, but I think it's possible that that's not the case.

A disease's guide to world domination from minuteearth:
[https://www.youtube.com/watch?v=Ch4d9qEKmHE](https://www.youtube.com/watch?v=Ch4d9qEKmHE)

------
Navedkhann
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/19199)
[https://preprints.jmir.org/preprint/19583](https://preprints.jmir.org/preprint/19583)?

------
known

       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](https://archive.vn/UEgL5)

~~~
agildehaus
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...](https://wwwnc.cdc.gov/eid/article/26/7/20-0282_article?deliveryName=USCDC_333-DM25287)

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

------
eveningcoffee
Some people have tried to infer SARS-CoV-2 severity based on common corona
viruses
[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7102597](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...](https://www.project-
syndicate.org/commentary/swedish-coronavirus-no-lockdown-model-proves-lethal-
by-hans-bergstrom-2020-04)

~~~
toolz
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.

~~~
joe_the_user
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...](https://ourworldindata.org/grapher/total-covid-deaths-per-
million?tab=chart&year=2020-04-29&country=DNK+FIN+NOR+SWE+USA)

\-- 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.

~~~
kzrdude
Is Netherlands comparable with Sweden and Denmark? If not, why not?

~~~
joe_the_user
Netherlands has a much higher density than Sweden (densest country in Europe
and one of the densest countries in the world, dense places don't do well once
the virus is released, sadly), so it's clearly not as comparable as the
countries in the chart (originally put together by Vox). Nonetheless, if you
add Netherlands, you'll notice while it has a higher per-capita death rate,
Sweden has been approaching it over time.

[1]
[https://www.holland.com/global/tourism/information/general/f...](https://www.holland.com/global/tourism/information/general/facts-
figures.htm)

~~~
kzrdude
What kind of density are you looking at? The majority of cases in Sweden are
in the capital, so the whole area of the country doesn't matter for anything.

------
csours
> "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.

~~~
CydeWeys
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.

~~~
twic
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.

------
29athrowaway
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_af
> _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?

~~~
jmull
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.

~~~
robocat
> but whether it, and similar markets significantly increase the chances of a
> similar event in the future.

I’m not defending wet markets but on that theory we should also ban all pets.
And ban all livestock. And ban all hunting and eating of hunted meat.

------
dr_
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.

------
jjuel
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!

~~~
kbenson
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.

~~~
vikramkr
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.

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

~~~
mattkrause
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....

