CharonY

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.).

In short, they identified a singular (monoclonal) antibody that binds to a conserved area in coronaviruses and found that if it binds, it interrupts the ability of the viruses to invade cells. It is at this point more a mechanical/functional study showing that presence of antibodies could at least fundamentally disrupt invasion by viruses. This gives hope to convalescent serum treatment for example. Of course it is not ensured that folks producing antibodies (they are always a mix, or polyclonal) will develop something similar. It is unlikely to influence vaccination development much I think, most target the spike protein anyway. It does increase the likelihood that immunization is feasible though (I think).

I vaguely remember that someone was looking into outcomes of folks with seasonal influenza co-infection but I just cannot remember the author. The only thing that I took away is that there was no indication that co-infections had a significant impact on outcome per se. Once the cases become severe, however complications from other infections become more problematic. That being said, I doubt that we have enough information to have definite answers- many of these studies were small in scale and quickly published (for obvious reasons) so conclusion may change once new findings pop up rather rapidly.

Basically that would not work. Adaptive responses react to specific antigen presented by a given causative agent of disease. The only possible scenario would be e.g. another coronavirus that has an antigen that is very similar to one from SARS-CoV-2. But that would be highly unlikely as a whole. Also co-infection is a bad idea, immunity (if it happens) is built during later stages of the response. Theoretically having multiple diseases is not a good situation especially if they can make things worse for the patient. I.e. you would want the immunization happen before getting the disease (which is the idea of vaccines and why vaccines cannot be used as a treatmen).

Most studies focus on COVID-19 but looking at the papers it does not appear to be common at all. The reason mostly being that in mildly symptomatic cases the person still would be positive, though one can probably not be absolutely certain which virus is the actual cause (or their relative contribution). After all symptoms for infections of lower respiratory tracts are very similar. The only other thing I can think of are infection with bacteria, which often indicates treatment with antibiotics. But at this point we are looking at more serious symptoms.

It is hard to watch that so many folks approve of Trump's flailing response. https://projects.fivethirtyeight.com/coronavirus-polls/ Considering that much of what worked out was more despite the interference of the WH rather than because of it. And with regard to the consultant:

I suspect the question is aimed at respiratory disease. I believe it has been asked and answered a few times, though knowledge is of course evolving. There are handful of studies who have tested COVID-19 positive patients for e.g. influenza, other coronaviruses an so on. In one study from Wuhan the co-infection rate was about 20%. In other regions such as Italy I have seen some higher estimates but with fewer tests. The general consensus seems to be that it co-testing does not change clinical practice and is probably not terribly helpful with few exemptions.

Yes there is a high prevalence of obese folks among the hospitalized folks. It is likely that obesity puts a strain on the cardiovascular system. However, there are also reports of many folks just being overweight, here it is a bit more difficult as in many countries there are a lot of overweight folks and it may be difficult to figure out whether the connection is spurious or not.

There is an interesting background to that, though. Throughout the years, certainly at least since Bush the response to outbreaks (I am talking about the US here, but one could exchange dates and it would somewhat also apply to many other countries) the common reaction is to have an outbreak, build up response capacities, then forget about them and slowly defund them up until the next one occurs. The playbook was one (possibly the most comprehensive) attempt to solidify these measures. But it is also true that when Obama came into office he initially disbanded an office for global health security (which was first disbanded by Bush but re-instated sometime after 9/11). So in a way Trump is doing the same mistakes as his predecessors (there is more nuance to it, but leave it a that). What seems to be massively different is that in this case there is no indication that there will be any lessons this time around. So basically the classic way is that we forget the lessons learned, get surprised by it blowing up, learn something from it and then over time forget again. This time we forget things, refuse to learn and double-down on ignorance. Can't wait to see what happens after that (ideally from the inside of my locked lab).

It has been employed against different viral diseases, incl. SARS, MERS Ebola and a few others. Don't recall respective efficacy, though. You are also correct that recovery time was the major effect.

To some degree. But unless you have quantitative coverage, you generally want to design your cohort so that they are representative in terms of your research questions (e.g. in terms of age, gender, area etc.).

Ehem: https://www.vox.com/2020/4/30/21243117/trump-blames-obama-coronavirus-broken-tests-jim-acosta