lbeltrame

Gilead was said to be working on an inhaled version (it can't be administered orally, because it is completely destroyed in the liver).

It may be worth noting that remedisivir was never associated to lower mortality, not even in the first NIH-led study. The primary endpoint of the trial was, in fact, time to hospital discharge.

Association with mortality was not significant.

I assume The Guardian means "natural" (non-pharmacologically caused) herd immunity? Because vaccines end epidemics exactly through that.

A quick look through the paper doesn't leave me very impressed. The data is lacking, and the categorization of the antibody assay signal is arbitrary at best.

There is also little to no information on the test. It seems that the authors did not try to actually validate it, or they did not write the results of such validation.

I wouldn't trust this study, to be honest.

Can someone familiar with the Netherlands situation comment on the state of the hospitals? This is far more important than the case numbers alone (which, without context, can't be interpreted correctly).

This is the combination trial with remedisivir, not the one with this drug alone, as far as I can read from the article.

Given the rise of "zero covid" ideas, which are unfeasible in the long run or even medium term (even with New Zealand's success, all it takes is an error... and of course, we all make mistakes), some countries are mistaking lockdowns for treatments.

OTOH, I'm not aware, at least in the EU (where I am located) of large pharmacological efforts sponsored by governments: most of the results have come, for good or bad, from the USA's Warp Speed or the UK. Yes, BNTech and CureVac are German, but they are exceptions, rather than the rule.

It isn't even proven that lockdowns can actually save lives, although the last study touching this among a whole load of other risk factors (from U of Toronto) can be now considered old (data up to early May).

Unfortunately the paper describes for the most part the genomic and sequence analysis. It would've been better to have additional biochemical data, and in particular immunological data, to determine what was the reason for the escape from the immune system.

P.S.: we still have 5 confirmed reinfections over a million cases. Very short lived immunity may (may, in absence of data, at this point) be an exception rather than a rule. It will be far more interesting to see data from a few months onward (1+ year from early infections).

I didn't say just vaccines. I said pharmacological interventions, which are more than just vaccines. No one worries about a disease if it can be treated. There are two approved drugs so far, with a third under emergency use authorization review right now. These are the way out (with an eventual vaccine afterwards).

There were a couple of studies with artificial sunlight published a few months ago. On non-porous substances, viable virus does not last more than 6 minutes if exposed to light (25 C and 70% humidity, IIRC).

Yet another study that doesn't take into account cellular immunity (T-cell based).

Also, antibodies aren't always present in the bloodstream: memory B cells can start producing them when needed.

That said, the study provides interesting findings, from a quick look. In particular, there is no cross-reactivity of antibodies against other coronaviruses. This is the exact opposite of what was observed with cellular responses, which IMO means that cell-based immunity plays a larger role with coronaviruses. It's a pity the discussion section of the paper doesn't mention this.

It is much easier to use pharmacological means for that. You don't fight bacterial pneumonia with good discipline and stern words, you use antibiotics. What will ultimately get out of this problem are drugs (and vaccines).

All these non pharmacological interventions are just bandaids.

The serology studies in Italy are unfortunately underpowered because of a dumb decision: any person positive with IgG (which appear after or very close to the end of the infectious period) would have to quarantine then wait for a double negative PCR test. Thanks to this, only half of the expected people participated.

There are a few, but mostly don't show transmission, but persistence on objects in hospital settings. That said, most of them seem to exclude the fomite hypothesis.

That said, it is highly unlikely that it is a prominent way to get infected, assuming it occurs: with the numbers of positive people in the world, it would've become known by that.

But is it enough for infection? Current data say that infection through fomites is low, or even unlikely. Also the experiments were carried in the dark, so I wonder if they can be readily applied to everyday situations.

I wonder why at this point no one is doing studies in animals to see whether these concentrations equate with infections.

I find this difficult to believe. The figure of 60% needing infection to reach the so called threshold is debated within the scientific community, due to the fact that pre-existing immunity (or factors which downplay severity) may have been underestimated. See this editorial by the British Medical Journal which argues this point, including analogous lessons from the swine flu pandemic[1].

Also these statements:

> There is nothing about test and trace or mask-wearing – two interventions that we know are effective at stopping the spread of Covid-19 and don’t require any curtailing of our individual behaviour.

"We know"? About mask wearing, the literature (yes, the scientific literature) is largely inconsistent and unclear[2][3]. Which does not mean masks do not work, but the answer is not "we know", it is "we don't know yet".

[1] https://www.bmj.com/content/370/bmj.m3563

[2] https://www.cebm.net/covid-19/masking-lack-of-evidence-with-...

[3] https://www.cebm.net/covid-19/covid-19-evidence-is-lacking-f...

Clarification: for hospitalized patients, because that's what the RECOVERY trial does (it is about testing drugs in patients who are hospitalized).

It does not mean does not work elsewhere (in early symptom, non-hospitalized patients, as they were out of scope for the trial), as this editorial[1] makes IMO very clear (it's from August).

Key sentence from that editorial:

> Although both trials [SOLIDARITY and RECOVERY] provide convincing evidence for patients requiring hospital admission, these findings cannot be translated to other disease states.

[1] https://www.thelancet.com/journals/langlo/article/PIIS2214-1...

> My daughter is 3 weeks after first symptoms

She should be fine, unless immunocompromised. RT-PCR tests do not tell, in absence of symptoms, if you are infectious. If you have symptoms, the presence of a positive test correlates with actual, infectious virus in your throat until 7 days with milder symptoms and 15 days with more severe symptoms.

See https://www.cebm.net/covid-19/infectious-positive-pcr-test-r...

Also bear in mind, in particular for your daughter, that viral RNA takes a lot to clear, even when her immune system has already defeated the virus (IOW: you're seeing the "debris after the battle" and not the virus): the milder the symptoms, the longer it takes to clear.

tl;dr: Your daughter should be fine at this point, in general terms.

Of course, as an obligatory disclaimer, IAAS (I am a scientist), IANAMD, this is not medical advice, etc etc.

There are places that keep on doing "open evidence reviews" that summarize key finding in transmission, cures, etc.

Oxford's CEBM is one (https://www.cebm.net) and someone else has posted another for transmission in children here.

The paper says that children are more efficient in transmitting to people of their same age range, so perhaps the title as you edited it can be misleading.

Some key limitations to keep in mind from the study:

> The contact tracing data analyzed included only 20% of all reported cases as index cases and represented only 19% of all contacts traced

So the observations, while important, are probably just part of a more complex picture.

> Another limitation was the lack of data on timing of exposure and symptoms onset in relation to testing dates; this necessitated assumptions about identification of true index cases.

This is important: some cases may not be "true positives" in the sense that the PCR test alone does not tell if you have the disease, or had the disease if you did not develop symptoms. Given the size of the population tested, admittedly doing that is difficult.

> Finally, while comorbidities data collected as part of COVID-19 mortality surveillance revealed clinical and epidemiological attributes of fatal cases, the fact that such data were not collected for all diagnosed cases prevented inference of the contribution of comorbidities to fatal outcomes.

I found the arguments lacking. I don't think there was any plan on preventing infection on the first batch of vaccines, and even the FDA does recommend a minimum of 50% efficacy.

Infection prevention or preventing severe symptoms, are however part of the secondary endpoints of the trials, something that it is not mentioned in the article.

For a counter argument, see https://mobile.twitter.com/nataliexdean/status/1308474303810...

Not necessarily. It might be out of precaution to make sure prompt action is required if needed.

This was hot off the recent information that it can cut duration of symptoms in half in people that have not yet mounted an effective immune response.

I find this talk of first/second wave misleading. This is not the flu for mortality, and it is not an influenza virus. It spreads differently.

Some people at my institution in fact have argued that you should not use flu-derived models, but instead model the spread and the outbreaks in similar ways to SARS and MERS, which rather than big "waves", had a series of spaced outbreaks. At an internal seminar they showed that at least their models for the Bergamo area seemed to be consistent with the actual data.

If you count cases by specimen date (when they were taken) and not by reporting date (when the results were known), the picture is a little different: while high, cases seem (too early to be sure) to have plateaued around the end of August.

See https://www.cebm.net/covid-19/spains-outbreak-updated-on-reg... for some discussion (two weeks old though, so beware).

Pneumonia can do very similar stuff. It is not widely known because of antibiotics usage, but even if treated it hits your lungs really hard and you can take up to a year before recovering.

A family member had the misfortune of getting one twice (at a distance of many, many years), and it took quite a while to recover.

It is actually hard even to make sense out of hospitalization numbers. In my country, hospitalized people are counted as "positive hospitalized" even if they are positive (due to mandatory test prior to admission) but had to go to the hospital for a completely different reason.

Likewise, a region during August mandated mandatory hospitalization for most of the people positive to the virus, therefore inflating hospitalization numbers.

Unless reporting is either standardized (unlikely) or harmonized (possible) it is always going to be hard to make sense of the numbers.

Common cold: not worth it, and is caused by a lot of different viruses, making vaccination even harder.

SARS1: the virus was eradicated before trials could complete.

MERS: There are several vaccines in testing, however MERS comes and goes randomly, so it takes a lot of time to gather events.

HIV: Apparently there's a trial in Uganda going on since quite a while, which looks better than the past ones (which were failures), but with HIV, it takes years to see if it works or not

That said, betting all your options on a vaccine is not what I'd call sound policy. In fact, there are several drugs in the pipeline, but few if any report that.

When I used to do RT-PCR for research, 40 cycles would mean (to me) that I had nothing in my solution and I had to redo the experiment.

The precautionary principle (anti-scientific, because it assumes the worst even without evidence of such) is what drives such decisions, even if, according to Oxford's CEBM, there is little to no correlation between a PCR positive sample at 37+ cycles and actual presence of an infectious virus.

That is why antigen testing, although less sensitive, is important. A PCR test without symptoms does not tell if you have the virus you had the virus, and if you are infectious (assembled virus present in the respiratory tract) or not. Also, RNA in the throat can degrade slowly, and be present for a long time (this is not unique to this virus).

An antigen test will identify the virus proteins, and as such, a higher probability that a positive test detects an infectious virus.

> This is a novel virus - meaning noone initially has natural immunity to it.

This has then been proven to be an incorrect assumption, due to cross-reactivity with existing coronaviruses. While this does not prevent infection (or it is likely it does not), it may explain why some people did not experience symptoms, or very light symptoms.