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<p>Barry -</p>
<p>Really great writeup from your daughter in Wellington. It
reinforces and adds well to what I've been hearing from my own
daughter (Molecular Biologist in FlaviVirus lab at OHSU in Oregon)
who have actually run PCR based tests using the WHO information on
themselves (a dozen or so scientists/techs) as preparation for
possibly participating in the testing with their own gear. <br>
</p>
<p>Joanna's clarification on the likely problem with the "failed"
test kits was useful in particular.</p>
<p>The talk about asymptomatic transmission is central to my own
personal thinking and the models we are assuming in the SimTable
work in-progress that Stephen described yesterday. It doesn't do
as much good to only build contact graphs with people who are
already diagnosed (or self-diagnosed via symptoms) as it does to
have location/contact information for the pre-symptomatic as well
as (fully?) a-symptomatic. <br>
</p>
<p>I am also wondering what others are hearing about (or better have
references to) the possibility of COVID19 survivors antibodies
being a resource for transmitted (via transfusion?) immunity.
Something to recruit all those "irresponsible youth" for... as I
said on the call yesterday "pay them to stay on the beach in
drunken revelry another month until they all pass it around and
recover" and THEN impress (persuasively not conscriptively) them
into providing serum to their grandparents instead of having them
return from Spring break to closed schools and moving in with
their grandparents, accidentally killing them in the process
<satire>.</p>
<p>How, by the way, is NZ doing with this themselves? I always
think of them as a sort of safe-haven being as relatively isolated
as they are yet with an anglophone first-world embedding.</p>
<p>- Steve<br>
</p>
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<p dir="auto">In the distributed FRIAM meeting yesterday I
mentioned these results, but I thought you might also want
to see the commentary with them. This is an email from last
week from one of my daughters (Joanna) who is a
microbiologist at Victoria University in Wellington, NZ.</p>
<p dir="auto">—Barry</p>
<p dir="auto">————————————</p>
<p dir="auto">First, the tests. I don't know what happened in
the US with testing, maybe some of that has come out or
maybe will come out. What I do know is that testing for RNA
viruses is pretty straightforward - you extract RNA from the
sample and try to quantify it using a PCR-based method. This
is done around the world for routine surveillance of various
RNA viruses (norovirus, influenza). There may be a few
viruses that use antibody-based testing, but that wouldn't
be used for the coronavirus. The RNA genome sequence of this
virus was published early on by Chinese scientists, which
countries were meant to use to design tests. The WHO
normally only provides tests to low income countries,
relying on high income countries (like the US or NZ) to
develop their own tests. The primers and other reagents that
work, all that information is out there. There was no need
to reinvent the wheel with the tests, but from what I
understand, the problem with some of the kits sent out by
the CDC early on had a problem with one of the reagents (not
the science behind the test). Validation is of course
important, but again, tests have been clearly validated
overseas. The usual regulatory safeguards will have to be
relaxed around the world to keep up with the need for mass
testing. The WHO says, test, test, test! That is going to be
the key to beating this thing. I should add that I have full
confidence that, despite initial missteps, the US is going
to eventually get the testing right. It's absolutely
essential if you (1) don't want to be under nationwide
lockdown for 18 months, or (2) don't want 2 million
Americans to die.</p>
<p dir="auto">The craziest thing about this virus is the
degree to which transmission is being driven by asymptomatic
people. A Science paper just came out claiming about 85% of
cases were transmitted by an asymptomatic person.
Asymptomatic people may be less contagious, but they likely
make up for it by going to family dinners, work, getting on
airplanes, shaking hands, giving hugs, etc. Here's the
Science paper:</p>
<p dir="auto"><a
href="https://science.sciencemag.org/content/early/2020/03/13/science.abb3221"
style="color:#3983C4" moz-do-not-send="true">https://science.sciencemag.org/content/early/2020/03/13/science.abb3221</a></p>
<p dir="auto">When I first heard about asymptomatic
transmission of the virus being key, I was very skeptical.
Asymptomatic people don't cough or sneeze - so how do they
transmit the virus? It turns out that they shed large
amounts of virus anyway - such that breathing or talking is
enough to infect someone nearby. I became less skeptical
when I saw how insanely rapid the spread of this thing has
been around the world. When asymptomatic people are your
vectors, tests are absolutely critical. It's the only way of
knowing if someone could be transmitting the disease. And if
you don't have testing, you have to assume everyone is
infected, which is why lockdown is the only alternative
response.</p>
<p dir="auto">The other reason I was skeptical about
asymptomatic transmission, or the presence of a lot of
asymptomatic people, is that this virus kills. How can it
kill 15-20% of people over 80 but cause an asymptomatic
infection in so many other people? I don't have an answer
for that, but it's the essential reason that this virus has
shut down the globe like it has. All our usual tricks don't
work particularly well. I will say that microbes with these
two extreme outcomes (no apparent illness, vs deadly
infection) are relatively unusual, and that's why we are in
this unprecedented situation. On the other hand, that
particular combination is probably what largely drove the
AIDS epidemic, so some of this is not new. But for a
respiratory infection, it is unusual, and unlike AIDS, it is
spreading much more rapidly.</p>
<p dir="auto">And there is still much we don't know about
asymptomatic people. Are many people never showing symptoms?
Or do most of those asymptomatic people eventually go on to
develop illness? This information is coming - for that you
need serology - a retrospective look into a population to
see who was actually exposed to the virus. The great news is
that a paper that was posted in the past couple of days
describes the first ELISA test for the virus. That is, they
synthesised the (presumed) main viral antigen, the spike
protein, in the lab, coated plates with it, and are now able
to tell whether people have antibodies to that spike
protein. Although this paper hasn't been peer-reviewed yet,
it is out of a credible lab.</p>
<p dir="auto">If you want to read the paper yourself:<br>
<a
href="https://www.medrxiv.org/content/10.1101/2020.03.17.20037713v1"
style="color:#3983C4" moz-do-not-send="true">https://www.medrxiv.org/content/10.1101/2020.03.17.20037713v1</a></p>
<p dir="auto">The implications of this paper are important:<br>
They only tested a small sample, but people who'd recovered
from the virus clearly had antibodies to the spike protein.
Non-infected people, and one person who had recently
recovered from a confirmed infection with a common, milder
coronavirus (which has a similar spike protein, attaches to
the same human cell receptor) had ZERO antibodies. To make a
huge extrapolation, there is likely little or no existing
immunity to this thing (possible exception of SARS
survivors), which is another explanation for why it has
spread so rapidly.<br>
Scaling up will enable screening of people to see whether
they have protective immunity to the virus (due to natural
infection). This would enable you to deploy healthcare
workers with immunity to the frontlines - i.e., hospitals,
caretakers in nursing homes.</p>
<p dir="auto">This will also enable people to go back and
study the wider population of places like Wuhan or Seattle.
The current data suggest that about 20% of Wuhan residents
got the illness. But it's possible that many more people
were infected entirely asymptomatically (i.e., never became
ill but carry antibodies to the virus). If only 20% of your
population infected crashes the healthcare system, there is
no clear strategy for relying on herd immunity. If it turns
out it was actually closer to 60 or 80% who were infected
(enough for herd immunity) that changes things.
Specifically, it would suggest that Wuhan is less likely to
get a resurgence of disease if restrictions are eased. At
this point we have no idea.<br>
Adoptive antibody transfer - giving antibodies from someone
who has recovered to someone fighting off the illness - can
be explored.</p>
<p dir="auto">To extrapolate even further, it may turn out
that the differences in mortality or degree of sickness are
not due to preexisting immunity; more likely the answer will
be in variations in our underlying physiology (for example,
maybe the virus mainly infects a cell type that hasn't
matured in most children, rather than that children are
largely immune).<br>
In the meantime, we all want to avoid crashing the
healthcare system, as has now happened in Wuhan, Italy, and
Iran. And avoid getting ill, especially if in a more
vulnerable category. I don't think there's any reason to
assume that you will necessarily eventually get it. Even in
the worst case scenarios being played out, it is not 100% of
the population that is infected. Being very careful, until
there is a vaccine, can ensure you can be in that part of
the population that can avoid it altogether. Life is long,
and we'll get through this challenge together!</p>
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