CharonY

Also non-coding DNA have numerous structural and regulatory functions.

Eugenics does have a different connotation relative the motivation behind abortion. There is the ideology that lives can be a priori divided into desirable and undesirable. While these may factor into individual decisions to various degrees, the idea of eugenics is more societal rather than individual. Of course if everyone in a society subscribe to an ideology that subscribes to that notion, it will become indistinguishable and I would argue that the society is pretty messed up.

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.

Check the updated CDC numbers https://www.cdc.gov/flu/about/burden/index.html. The have updated the data considerably, though it is true that that year was pretty bad. I will acknowledge that you actually did see the number somewhere, and did not make it up. My apologizes. Your propensity to make unsubstantiated claims have tainted my assumptions. It does how show that even with all the restrictions the US has outpaced some of the worst annual outbreaks. You can clearly see that not having them in place would make things worse, no?

Based on your second I suspect it is based on the observation that a phylogenetic tree using a given gene does not always 100% accurate reproduction of the relationship of different species. This is actually expected as not all genes are under the same selective pressure in the same organism. For example in some species a given gene may be more important and therefore does not mutate much, whereas in others there may less conserving pressures, allowing accumulation of mutations. These are expected and well known effects. There are are other issue that could complicate phylogeny, which is why folks do not use any random locus to reconstruct relationships. I other words, if someone thinks that the observation somehow disproves evolution, then it is pretty obvious that the person has no idea what they are talking about.

Please do not make up numbers.

Indeed. There are more studies looking into the potential benefits of large-scale mask wearing and the most promising one indicate that it might cut down transmission by a fair bit if every infected person wears one. This is especially important when there are many pre- or asymptomatic folks around. Categorically not wanting to wear a mask is therefore also on the selfish side (and obviously there is little benefit wearing it if alone and/or being in ones own personal space).

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.

! Moderator Note The same question has been asked, answered and locked after a stint in conspiracy land. Please do not bring it up again.

There is a good reason why abusive mentoring is falling out of favour.

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).

Generally that is just the purity indicator on the cylinder (ultra high purity) or so I though. But then I realize that I also have high pressure (HP) and ultra high pressure (UHP) tanks, so ...

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.

In addition, the documentaries are generally not prepared by scientists. They may feature the latter, but some may just use snippets or creative editing to make things more interesting at the cost of being factual (but potentially boring).

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.).