CharonY

Well, he flip flopped on China quite a bit, praising their strongarm responses (including some favourable views on the Tiananmen massacre), Now he is strongly against China because of his own mishandling of the COVID-19 situation. And I will re-iterate, folks had much more munition to blame China if they had actually had started implementing measures to stop it once it was out of the bag. But only a handful of countries actually did. Don't get me wrong, the information policy in China is abhorrent and it is clear that autocratic regimes are not good partners to combat such international crises. However, their failures should not be used to detract from own failures. It means that one needs to up ones own pandemic game and that the role of international agencies have to be strengthened and not diminished.

I may be going slightly off-topic here, but I like to chime in that while the historic elements are clearly directed against black folks in the US system, the undercurrent is not too different how most countries deal with immigrants. I have always been annoyed how folks, say in Germany, claim to have no systemic racism (or bigotry or whatever floats your boat) problem. But the the truth is that different folks experience the same society in different ways almost everywhere. This is obviously not only along racial lines, gender socioeconomic status etc. are also such elements. However, race (and gender) has always been a visible element at the intersection of these issues. Immigrants always had to work harder and make less mistakes and maybe (but only maybe) they might be seen as something approaching equals. This is something that many folks learn, and it makes sense when they arrive in a new country, but kids in the third or fourth generation get fed up with it. African Americans (and obviously indigenous folks) have been there since the beginning. And it must be way more frustrating to be part of the country for so long and still held at arms-length and still being being scrutinized and blamed for each misstep (which others are allowed to make). Some folks essentially summarized it as a breach of the social contract and ask the question why folks should adhere to it, if they are not accepted to be a full part of it. Edit: I should add that in the US the overall much higher lethality of the police force exacerbates all the underlying issues, whereas a more peaceful society would continue to simmer at a less dramatic level. Edit2: Another thing to add is that especially black communities are hit way harder by COVID-19 than white communities. Economically, health-wise and educationally. The whole situation has highlighted massive disparities.

The study exists it is a pre-print by Qian et al and it was actually one outdoor outbreak involving two cases. The study looked at 1245 confirmed cases and 318 outbreaks overall (the main list was over 7k but some where excluded from the final list) . One of the reason is also because outdoors folks have typically less prolonged contact. One known outdoor outbreak involves a person talking to an infected person, highlighting that prolonged contact can also lead to infection outdoors. However, the majority of outbreaks (~80%) occurred at home.

I may have missed it somewhere but I think it is worthwhile to re-iterate that current data suggest that COVID-19 spreads via droplets rather than aerosols. I.e. most models use a parabolic ejection. There are a few suggestions that it may exist as an aerosol, but most data is not terribly compelling at this point. As such, assuming droplet as the major source of non-contact infection, there are only limited options for ventilation to assist in that regard. Bottom up flow would likely increase the range where the droplets spread and the same goes for lateral flow. It has been discussed earlier that removing droplets before hitting someone is probably technically not feasible, which leaves downward flow. But that has to be mostly laminar otherwise we might get into turbulent mixing which would could keep particles longer afloat rather than dropping down.

Now contrast that with someone else: https://medium.com/@BarackObama/how-to-make-this-moment-the-turning-point-for-real-change-9fa209806067

There have been so many "last" straws, I have lost count. Just a few months earlier, a black jogger was murdered by gun-toting folks but that was not all, while he was jogging he accrued at least two 911 calls, one of them calling because a black guy was running down the street. I am not sure whether this incident will be remembered as extraordinary either. There have been so many mind blowing incidences. Remember John Crawford III? He was killed in a walmart after handling a BB gun in the toy aisle while on the phone. You know, in a store where they also sell real weapons in an open carry state. Police came in after an idiot made a 911 call about a black man brandishing a gun. He was killed before he could he could even react. No charges were laid. Philando Castille is another prominent incident. I submit that these incidences will imprint folks very differently. Even if it ends up non-violent, there have been a string of 911 calls on black folks who did nothing out of the ordinary. Sure, this case seems to be more gruesome than some of the others. And perhaps more importantly, it has been captured on video but many folks do see it as part of larger system of disenfranchisement. The police is not felt as protective agency, at best it is seen adversarial. A common interaction can turn lethal, with higher frequency for some folks (yes, not exclusively, but if embedded in historic experience it sure is heavily slanted). The measures of securing wealth have been systematically moved out of reach. Political powers have been and are continued to be minimized. And to add insult to injury, folks in power deny the experience of minorities, especially of black folks.

I wished that was true, but there are other groups (typically, but not exclusively on the right fringe) that share rather weird ideas and conspiracy theories regarding the pandemic.

The paper is out now (well yesterday): https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)31208-3/fulltext

In the early days (i.e. a few months ago) antibiotics were commonly administered as the damages in the lungs seemed to favour bacterial infections. Now, recommendation seem to be monitoring for co-infections and administer as needed. There is indeed no special consideration regarding viral co-infections that I am aware of (which does not mean much).

I took your comment as the assumption that folks in those times died well before they reached 60 years of age. However, after childhood, folks actually did get older. However, it would be true that there would be fewer persons of higher age (but it is just not true that folks barely reached 60). So that is another possible misconception. The health effects are not entirely age based, and certainly not "not a huge deal" for younger folks. Even among below 60 years old plenty of folks required modern treatment, ranging from antibiotics to ventilators. Without those, the fatality rate would go up significantly. But then there are other factors that appear to influence susceptibility. Lung and cardiovascular health seems to be a big one, and theoretically folks could be healthier in that regard. But that would be difficult to tell. And on the not a huge deal part, I should add that there is now significant evidence that even folks that recover from COVID-19 often show evidence of lung tissue scarring. There were expected reductions in lung performance, but so far it is not clear how much folks will recover. Also, it is not what precisely impacts the pathophysiology of the disease. But so far there are no strong indications of host factors that would help. In contrast, much evidence points to access to healthcare as a bigger determinant.

I think that goes a bit far. Horizontal gene transfer does indeed make certain things complicated, but there are conserved elements that can be used to re-create relationships somewhat reliably, even among prokaryotes. The issue is only there if you want to figure the history of a specific locus, rather than that of the whole organism. I.e. you can still construct neat (i.e. reconstruct relationship) if you want. The part that is probably the most problematic ones are likely the transition to eukaryotes. The high likelihood of endosymptiotic events makes their history quite messy at that point.

1) is a misunderstanding. Prior to the the bubonic plague folks that reached adulthood were expected to live well above 60 years. 2) yes that is a big one. But note that even if take a disease from modern times, such as the Hong Kong flu- in the US an estimated 100,000 folks died. For COVID-19 the US is at over 93k now. So responses are also a factor (I think some would also argue for population size, but in case of disease spread it is less of an issue, as folks do not stochastically become sick, they need to be in contact, which goes back to isolation measures). When it comes to the value of the graph, to me it says that despite all the tools of modernity at hand, we are still struggling with disease outbreaks. Not sure what else one could read from that, considering the pandemic is not even over yet.

Well they found a few more clusters in Wuhan, but in response they want to test everyone. If they do, there is good chance for further containment.

Pretty much. As the lockdown has reduced the number of active cases, an increase will be slower than before. Especially with heightened awareness. There are isolated reports of some local increase in cases, though. But if contact tracing can be maintained, it might be controlled.

I think I have mentioned that before but in order for a seroconversion to happen, you'd need a signficant amount of exposure (most commonly during actual infection). Or at least strong exposure to inactivated viruses. Licking body fluids form recovered folks does not seem prudent.

So while the issue with pre-/post-fusion proteins is an issue, I would like to note that in many cases one would frame it more about the conformation of the protein rather than overall energetics. There are several ways to stabilize a particular structure, independent on whether protein is ever part of a virus, or involved in membrane fusion or not. I.e. it is helpful when we think in terms of the dynamics and mechanisms of viral actions (as it needs to be performed within an energy gradient) but it may be less useful when we talk about other things, such as in this case recognition of structures. Specifically, a particular structure is formed in dependence on its milieu, its amino sequence as well as other elements such as chaperones that help in folding the protein a specific way. Perhaps more importantly, recognition of the molecule by the immune system is only dependent on a fairly small part- the epitope. Moving on to RNA vaccines, in other viruses it already has been shown that antibodies raised just by simply introducing the primary sequence has resulted in antibodies that are able to bind pre- as well as post-fusion protein structures. They also stabilized the pre-fusion structure by introducing additional sequences (not dissimilar to the wiki article linked above) but the overall titer did not shift much. This is not to say that this is not an issue with SARS-CoV-2, but it does not seem to be a fundamental issue, at least.

It is like the worst storyline of a badly produced soap opera. Only that folks are dying.

The Moderna vaccine mentioned earlier is almost done with phase I but preliminary results already indicate that some participants developed antibodies. This bodes well for the efficacy test.

Ha yeah. Poisoning ones voter base would seem like a bold move.

Typically you take the sample and apply it to a cell culture and see how many are getting infected compared to the reference.

In certain contexts it might be though I think most folk would actually state whether it is more or less infectious. Virulence refers the relative degree of disease caused by an organism. More commonly it could refer to e.g. severity or extent of infection (but I can see contexts where it might be used to minimal infective doses too).

Infections are to some degree stochastic, but there is the concept of the minimum infective dose, which indicates the minimum dose required to infect someone. However, it is actually a fair bit more compicated as folks rarely quantify individual virus particles, which is difficult. In practice, many virology labs use a tissue-based quatification system which cell destruction using dilutions of a a virus dilution. The dilution at which 50% of the tissue show damages or other cytopathic effects are then defined as the TCID50. I.e. the actual particle count is often not actually known. However, a single particle is highly unlikely to elicit any kind of meaning full effect, you need quite a few more than that. How many, depends a lot on virus and host factors. I seem to recall that I found an estimate of as low as ~200 virus particles in the cases of some coronaviruses, but frankly I do not recall it very well and may be mistaken. That being said, there is support for for single-hit models, in e.g. noroviruses. They are more theoretical and assume that the virus slip through all defensive barriers and reach their target fully functional. Effectively more than than one particle are needed for exposure, but this model have some what different dose response models compared to the more simple one which only looks at exposure and outcome. If the question is whether the mere exposure to a single virus is sufficient to create immunity, the answer is no. Acquired immunity requires sensing of a significant amount of antigens through a process called seroconversion. So it would only work if the virus in your body replicates sufficiently trigger first the primary infection (which is not associated with immune responses) and then persist enough to lead to to the buildup of immunological memory.

There is something to that. There have been observation consistent with observations of cytokine storm syndrome.

It is rather unlikely that it is a significant path. First of all, respiratory droplets are (hopefully) deposited much more frequently and broader than semen fluids. Second, I do not think that the receptor is found in significant abundance in female tissue. Now, as mentioned, vaginal tissue does not seem a likely target of the virus. However there are than the lung. One of them, the kidney is also a target and in some patients renal failure has been reported. That is obviously not good either. However, ACE2 receptors are found in the gastrointestinal tract. There is at least one guy who has speculated that potentially infecting folks through the GI tract might be a way to induce immunity with potentially less harmful symptoms. However, ultimately we know to little about the pathophysiology to make any calls at this point. But there is more research looking at GI infections now. As a minor point: note how fast research has been moving (relatively speaking). Beginning of the year we weren't sure what we were dealing with at all, now folks are exploring things on a rather broad front.

It is not 100% understood. Indirect (i.e. epidemiological data) suggest highest likelihood during symptomatic periods and it appears that respiratory titer go down or vanish after symptoms are gone (or ~10- days after onset of illness in mild cases). Shedding e.g. by feces seem to go on for longer, but it is not clear whether those are a source of infections. I do not think anything is known about potential of persistence at this point.