If you haven’t seen it already, you might find this video interesting. I posted it earlier in the thread, but will spam it again as it’s topical:
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Ya I mean the majority of us have been shitting on that model for at least a week now.
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When we have a vaccine
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Talks about a study recently published in Nature.
.
Working in two separate laboratories, the scientists carefully studied the spread of SARS-CoV-2 in the bodies of nine patients, taking daily measurements in order to understand each phase of the infection.
SARS-CoV-2 starts replicating in the throat, not the lungs. For that reason, a simple throat swab is enough to test for the virus. There’s probably no need for an intrusive, unpleasant nasal swab.
The antibodies our bodies produce in response to COVID-19 infection don’t actually destroy this virus. In that way, it is a lot like HIV.
“When aligned to viral load courses, it seems there is no abrupt virus elimination at the time of seroconversion,” the scientists wrote. “Rather, seroconversion early in week two coincides with a slow but steady decline of sputum viral load.”
“This means that the antibodies are not effective at clearing the virus,” Ostrov told The Daily Beast. “This is relevant when thinking about viruses and vaccines. HIV also stimulates production of antibodies that fail to clear the virus, as do many other viruses, such as hepatitis virus C.”
“People have tried and failed to generate vaccines against such viruses, so we should not be overconfident that a vaccine strategy will work,” Ostrov added.
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rutrow
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what does “anti-pollution” mean when describing gloves?
I hope that study is wrong
If our antibodies don’t kill it, what does?
Could you work in a call centre?
edit. Just saw I missed a whole discussion.
If you have sales experience, I would look at that. Not all sales centres are the same. Look for larger, brand names, and or highly regulated industries. Telco, utilities, etc.
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It’s not very clear, but I think maybe it means they do kill it, just not very efficiently and so it takes time?
“When aligned to viral load courses, it seems there is no abrupt virus elimination at the time of seroconversion,” the scientists wrote. “Rather, seroconversion early in week two coincides with a slow but steady decline of sputum viral load.”
I think sputum viral load = how they measure virus elimination, so they’re the same thing. So it’s saying “It seems there is no abrupt virus elimination… rather… a slow but steady [virus elimination]”.
Best I can make of it, but somewhat knocked for a loop by the final para:
Instead of leaning on vaccines to inoculate us, doctors could treat SARS-CoV-2 infections like they do HIV. With a cocktail of drugs that manages, but does not eliminate, the infection.
My diagnosis: Bad science journalism.
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Well we know antibody-filled plasma definitely helps.
My science pedant instincts bristle at the idea that antibodies are ever killing viruses. That’s what T-cells are for.
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it the latest lol-IHME model update, US projected deaths up to 68k, UK projected deaths down to 24k
they also have this in the update notes, which i think is based on historical data rather than projections
my county has the weirdest test results:
2800 tests and 200 are inconclusive.
next county over. 11,000 tests, 40 inconclusive.
wtf?
Definitely this. This bit seems like utter bullshit:
I have no idea the context in which Ostrov said these things or whether he was misquoted or what, but HIV is a fucking retrovirus that writes itself into cell DNA and hepatitis C is a rapidly-mutating virus that comes in a bunch of strains, all presenting different antigens. There is no sense in which SARS-CoV-2 is “like” either of these viruses.
The paper (here) does note the increased difficulty of a vaccine:
When aligned to viral load courses, it seems there is no abrupt virus
elimination at the time of seroconversion. Rather, seroconversion early
in week 2 coincides with a slow but steady decline of sputum viral load.
Whether certain properties such as glycosylation pattern at critical
sites of the glycoprotein play a role in the attenuation of neutralizing
antibody response needs further clarification. In any case, vaccine
approaches targeting mainly the induction of antibody responses
should aim to induce particularly strong antibody responses in order
to be effective.
This might make it more difficult to produce a vaccine, but it seems hard to say. There are various ways in which you can go about it.
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The Tasmanian police will investigate the claim that an outbreak of coronavirus cases among healthcare workers in two Tasmanian hospitals is linked to an illegal dinner party.
Australia’s chief medical officer Dr Brendan Murphy said today the staff from The North West Regional Hospital and North West Private Hospital in Burnie had attended a dinner party, according to reports.
The gathering has now been linked to more than 60 cases of coronavirus in the state including 45 health workers and nine hospital patients.
Nothing like a healthcare-worker dinner party to pass the time during lockdown.
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Dammit now you ponied me by one post. Here’s the entire conclusion of the paper for anyone who’s interested.
https://www.nature.com/articles/s41586-020-2196-x_reference.pdf
Conclusions
The clinical courses in subjects under study were mild, all being youngto middle-aged professionals without significant underlying disease.
Apart from one patient, all cases were first tested when symptoms were
still mild or in the prodromal stage, a period in which most patients
would present once there is general awareness of a circulating pandemic disease5. Diagnostic testing suggests that simple throat swabs
will provide sufficient sensitivity at this stage of infection. This is in
stark contrast to SARS. For instance, only 38 of 98 nasal or nasopharyngeal swab samples tested positive by RT-PCR in SARS patients in HongKong15. Also, viral load differed considerably. In SARS, it took 7 to 10
days after onset until peak RNA concentrations (of up to 5x105
copies
per swab) were reached13,14. In the present study, peak concentrations
were reached before day 5, and were more than 1000 times higher.
Successful live virus isolation from throat swabs is another striking
difference from SARS, for which such isolation was rarely successful16–18.Altogether, this suggests active virus replication in upper respiratory
tract tissues, where SARS-CoV is not thought to replicate in spite of
detectable ACE-2 expression19,20 . At the same time, the concurrent use
of ACE-2 as a receptor by SARS-CoV and SARS-CoV-2 corresponds to
a highly similar excretion kinetic in sputum, with active replication in
the lung. SARS-CoV was found in sputum at mean concentrations of 1.2-
2.8x106
copies per mL, which corresponds to observations made here13.
Whereas proof of replication by histopathology is awaited, extended
tissue tropism of SARS-CoV-2 with replication in the throat is strongly
supported by our studies of sgRNA-transcribing cells in throat swab
samples, particularly during the first 5 days of symptoms. Striking
additional evidence for independent replication in the throat is provided by sequence findings in one patient who consistently showed
a distinct virus in her throat as opposed to the lung. In addition, the
disturbance of gustatory and olfactory sense points at upper respiratory tract tissue infection.Critically, the majority of patients in the present study seemed to be
already beyond their shedding peak in upper respiratory tract samples
when first tested, while shedding of infectious virus in sputum continued through the first week of symptoms. Together, these findings
suggest a more efficient transmission of SARS-CoV-2 than SARS-CoV
through active pharyngeal viral shedding at a time when symptoms
are still mild and typical of upper respiratory tract infection. Later in
the disease, COVID-19 then resembles SARS in terms of replication
in the lower respiratory tract. Of note, the two patients who showed
some symptoms of lung affection showed a prolonged viral load in
sputum. Our study is limited in that no severe cases were observed.
Future studies including severe cases should look at the prognostic
value of an increase of viral load beyond the end of week 1, potentially
indicating aggravation of symptoms.One of the most interesting hypotheses to explain a potential extension of tropism to the throat is the presence of a polybasic furin-type
cleavage site at the S1-S2 junction in the SARS-CoV-2 spike protein that
is not present in SARS-CoV17. Insertion of a polybasic cleavage site in
the S1-S2 region in SARS-CoV was shown to lead to a moderate but
discernible gain of fusion activity that might result in increased viral
entry in tissues with low density of ACE2 expression21.
The combination of very high virus RNA concentrations and occasional detection of sgRNA-containing cells in stool indicate active replication in the gastrointestinal tract. Active replication is also suggested
by a much higher detection rate as compared to MERS-coronavirus,
for which we found stool-associated RNA in only 14.6% samples in 37
patients hospitalized in Riyadh, Saudi Arabia22,23. If virus was only passively present in stool, such as after swallowing respiratory secretions,
similar detection rates as for MERS-CoV would be expected. Replication
in the gastrointestinal tract is also supported by analogy with SARSCoV, which was regularly excreted in stool, from which it could be isolated in cell culture24. Our failure to isolate live SARS-CoV-2 from stool
may be due to the mild courses of cases, with only one case showing
intermittent diarrhea. In China, diarrhea has been seen in only 2 of 99
cases25. Further studies should therefore address whether SARS-CoV-2
shed in stool is rendered non-infectious though contact with the gut
environment. Our initial results suggest that measures to contain viral
spread should aim at droplet-, rather than fomite-based transmission.The prolonged viral shedding in sputum is relevant not only for hospital infection control, but also for discharge management. In a situation
characterized by limited capacity of hospital beds in infectious diseases
wards, there is pressure for early discharge following treatment. Based
on the present findings, early discharge with ensuing home isolation
could be chosen for patients who are beyond day 10 of symptoms with
less than 100,000 viral RNA copies per ml of sputum. Both criteria predict that there is little residual risk of infectivity, based on cell culture.The serological courses of all patients suggest a timing of seroconversion similar to or slightly earlier than in SARS-CoV infection18. Seroconversion in most cases of SARS occurred during the second week of
symptoms. As in SARS and MERS, IgM was not detected significantly
earlier than IgG in immunofluorescence, which might in part be due to
technical reasons as the higher avidity of IgG antibodies outcompetes
IgM for viral epitopes in the assay. IgG depletion can only partially
alleviate this effect. Because IFA is a labor-intensive method, ELISA
tests should be developed as a screening test. Neutralization testing
is necessary to rule out cross-reactive antibodies directed against
endemic human coronaviruses. Based on frequently low neutralizing
antibody titers observed in coronavirus infection26,27, we have here
developed a particularly sensitive plaque reduction neutralizationassay. Considering the titers observed, a simpler microneutralization
test format is likely to provide sufficient sensitivity in routine application and population studies.When aligned to viral load courses, it seems there is no abrupt virus
elimination at the time of seroconversion. Rather, seroconversion early
in week 2 coincides with a slow but steady decline of sputum viral load.
Whether certain properties such as glycosylation pattern at critical
sites of the glycoprotein play a role in the attenuation of neutralizing
antibody response needs further clarification. In any case, vaccine
approaches targeting mainly the induction of antibody responses
should aim to induce particularly strong antibody responses in order
to be effective.
I think you are correct. I just read the entire study, (disclaimer: I’m not a scientist and struggle to understand a lot of scientific writing), and have no idea where the article drew that conclusion from. Here is the paragraph in question from the study:
Full study: https://www.nature.com/articles/s41586-020-2196-x_reference.pdf
Hopefully one of our scientists can read the study as well.
Edit: Jesus H Christ my pony died on the cross
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Apparently people have been getting swabs jammed into their eyeballs for no reason when throat swabs will work fine.
Why can’t you just lie and say you’ve been to China recently?
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California seems to be kicking everyone’s ass at corona management. same number of cases as Florida.