CharonY

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.

Their genomes are quite different and critically, SARS-CoV-2 has a proof-reading enzyme that cuts down on replication errors and hence, mutation rate. It is utterly unknown. Could be between 0-100%.

There is little relation between these observations. For influenza a challenge is that there are numerous strains and the annual vaccines are designed around the modeling of which strains migh be dominant. There are years where the predictions fail or when something really unexpected happen. Now SARS-CoV-2, has a significantly lower mutation rate than influenza. While different variants have been detected to since the outbreak, the changes were fairly minor among the dominant variants. Most vaccines target conserved parts of the virus which so far did not seem to vary much. However, there are other challenges surrounding the development of a new vaccine, of course. So to re-iterate, I do not see any information from influenza vaccines that we could meaningfully translate to COVID-19.

There is a lot of false information there. -Without testing you do not know what you had. Making medical assumption based on gut feeling is really bad idea. -Influenza is not 100% symptomatic. Estimates are difficult (for obvious reasons). Longitudinal tests based on serological studies tend to estimate above 75% of asymptomatic cases (e.g. Hayward et al. Lancet 2014) . Note that influenza is much better investigated than COVID-19 and there are still a lot of unknowns and with influenza there are widely divergent estimates. The only thing we know with certainty is that your assertion is entirely unfounded. - Asserting that your feeling trumps actual data via testing is utterly ridiculous. Of course MDs should order tests. One might call it evidence-based medicine or just common sense. Acting on anything else is basically endangering oneself and others. - The unknown regarding immunity is actually correct. We only have limited data suggesting that there may be immunity, but we need to collect more. Also serological testing (but not, say gut feeling) can provide additional evidence of duration of immunity.

I think now with more information at the very least one can look at the responses based on different parameters. The first is how fast plans were developed and/or put in place. These would point to overall outbreak response readiness. Here only few countries distinguished themselves. The second is what type of responses were put in place once local numbers have been detected. Looking at outcomes is a bit difficult here, as the spread throughout the world was uneven. Some areas did not react faster, but due to lack of cases had much better outcomes who put similar restrictions in place.

Not to mention that GI issues are rather rare (though not unheard of) for COVID-19. Using anecdotes and opinion to influence decision making during times of crisis is very dangerous. Not only that, in the same post flu was mentioned- obviously there are influenza vaccines. Or measles and mumps.

It highly depends on how the respective health authorities collect their data. Some do not actually record symptoms and only provide hospitalizations rates, for example. Also note that you can asymptomatic when tested, but develop symptoms after. Recording these things accurately is difficult unless you have identifiers for each person (which is generally not the case).

The data are also only partially help to establish that. In almost all countries tests are administered after indication, which could include symptoms but also e.g. contact with positive persons. In conjunction with the fact that a positive person may exhibit not symptoms the data will mostly show bias in sampling procedure or of the cohort.

I suspect an easier explanation is a mix of volume of travel from infected areas and potentially incomplete testing. In Russia the number of detected cases are rising rapidly.

They are generally reported by each country's health agency (e.g. CDC, Health Canada, etc.).