The fact is that immunological memory does not equate to having antibodies in the bloodstream all the time. The title of the article is pure clickbait, at the very least.
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> Thus, most convalescent plasmas obtained from individuals who recover from COVID-19 do not contain high levels of neutralizing activity. Nevertheless, rare but recurring RBD-specific antibodies with potent antiviral activity were found in all individuals tested, suggesting that a vaccine designed to elicit such antibodies could be broadly effective.
RECOVERY just posted their preliminary results on dexamethasone. The NIAID trials showed efficacy of remedisivir. But getting a trial right can take some time. RECOVERY started in March, and had to enroll 10,000 patients or so.
A lot of trials are running at this point, it is a matter of collecting data and drawing conclusions. Antibody based therapies are probably the ones going to be the most effective, but I worry about the cost (they aren't cheap).
> The false hope of a vaccine or cure has caused some US governors to announce waiting for a vaccine before ending lockdown.
That is misguided as much as saying that there is no cure (yet). In fact, I'd say that most governments focused too much on vaccines and too little on pharmacological interventions.
FTR, for SARS, a lot of programs were halted because it fizzled out, and so it was impossible to actually test them. For MERS though, there were vaccines in development (and still are), and that's why most of the stakeholders were this fast in getting candidates ready.
"Months of intense research" have yielded at least 200+ compounds being tested for various activities. Large consortia have formed. A lot of things are being done in parallel to speed up testing (see vaccine research).
It takes time to prove efficacy: remedisivir only showed its efficacy in a 800+ people cohort. At first the time to administration was not correct: lopinavir-ritonavir were thought to be not working, but perhaps they do if given earlier in treatment, and what not.
I don't know what the author's expectations are, but we're witnessing a very fast pace of drug development and testing (not without warts, of course). What did the author expect, a miracle cure in 6 months? Most of the drugs being tested at this point are repurposed: the new ones will be tested through the summer and early autumn.
And there are wins like with dexamethasone, which is effective and cuts down mortality.
I recommend (to the author) a thorough reading of what's going on before launching in such a pessimistic piece. Yes, we might still be in hot waters. No, it's not that we will be destroyed by this coronavirus.
By the way, indications from early data from vaccine development tells us that it immunity is generated. The open questions are the duration, and the efficacy in a diverse population. But that's what trials are for. The fastest vaccine ever made took 4 years, IIRC. We're close to having results in 8 months (positive or not, the data will tell).
P.S.: The cold is mainly caused by rhinoviruses. Coronaviruses only account for a small percentage of that.
See the discussion here[1] (from the person who wrote the open letter to Lancet on the now-retracted HCQ study).
[1] https://twitter.com/jwato_watson/status/1272734274823663616
I'm not expecting any different results than from this one, but we'll know soon enough.
The RECOVERY study is also studying azithromycin, a drug commonly administered with HCQ when used against this disease. It would be ironic if that one proves to be effective (study is still ongoing).
As you can imagine, it is quite variable in what it means, because it varies across countries and occasionally even hospitals (I'm sure the RECOVERY people have taken this into account, though).
It is different from a placebo study because in that case your control is something you know is inert and "does nothing".
This brings the list of currently effective pharmacological treatments to two:
- remedisivir (reduces hospital stay, might improve survival)
- dexamethasone (improves survival if requiring oxygen)
The screenplay was written by Sadayuki Murai, who put a unique touch on whatever he worked in (he also worked with Satoshi Kon in Perfect Blue).
Also not a film, but I found "Mōryō no Hako" (a short series adapted from a 1995 book) worth watching: at the heart it's basically a crime story, but the execution, with some "hallucinated" scenes, and also the characters are interesting.
How it is a lie? People talk a lot about the presence of asymptomatic transmission, but:
1. No one knows for sure if completely asymptomatic people are contagious, and the extent of such contagiousness;
2. People equate asymptomatic with presymptomatic, which is a totally different story;
3. The evidence is at best, inconsistent. There is one case report of a non-contagious "asymptomatic" (reading the paper, the symptoms were there, just not the usual ones), and Singapore contact tracing of a number of completely asymptomatic people did not seem to find infected people in contact with them.
Presymptomatic state is a different matter, and it looks more contagious, but again, a lot of it is speculation, because it's really hard to measure.
This transmission is there. The extent of it is not known.
What the paper says may be true, but I'd love to see more experimental data.
There haven't been many studies (to my knowledge) that actually try to see if surface transmission is a thing. The most sophisticated ones try to culture virus in cells from sampling on surfaces, but that's not sufficient anymore: cells in culture don't have an immune system, nor physical barriers like the nose and mouth. It is likely that animal testing is required at this point.
Turns out that those doing vaccine trials have actually thought of that, and most of them are making partnerships in different countries to prevent "bad side effects" from this (such as forced seizure).
Are there any hard data on this, or just predictions? Or are you talking about influenza, as you mention later?
In Bergamo it's closer to that from early data, but for example in Milano it might be from 4 to 10 (but in this case the sample was blood donors, so skewed towards younger and healthy).
> Nevertheless, rare but recurring RBD-specific antibodies with potent antiviral activity were found in all individuals tested, suggesting that a vaccine designed to elicit such antibodies could be broadly effective.
Very low levels, but still produced. (Note that I still have to dig through the paper.)
Are there any data available to support this claim? That would mean that the virus is cleared by the innate immune system and not the adaptive, but it is still a pretty bold statement.
The last I read (a Nature Genetics study, if I recall) was that the antibody quantity was lower in milder cases (but with a large inter-person variability).
Note that I don't mind a vaccine, but it's not the only solution.
The part with the "previous version" of the paper is also fishy, given that it is not shown.
Of course, the media kept on fueling panic, and also some non-government experts (one in particular saying until recently that masks and physical distancing were useless to reduce spread).
Yesterday even one of the people who handled the lockdown in one of the regions said that perhaps it was too heavy-handed.
Italy is not a good example of things done right. Not at all.
What about individual regions? I ask because most of the dynamics I've seen originate around hotspots, and thus it may be interesting to see how individual regions were affected (because it may drive different responses).
E.g., the Spain seroprevalence study said 5% country wide. But the estimates per regions can be as up to 3 times that (Madrid itself is ~11%).
[1] https://statmodeling.stat.columbia.edu/2020/05/25/this-contr... (one of the many posts there)