CharonY

I do not have any real expertise on that, but the connection is complex and different pathways are activated (I'd have to ask my wife for more insights). But on the outcome levels there is evidence that if you are already suffering from inflammation, virus infection can have worse outcomes. Conversely respiratory diseases seem to make folks more susceptible to things like asthma (or at least worsen symptoms). But the immune system is notoriously complex. It is perhaps not surprising that we do not fully understand allergies yet, for example (with quite a few uncertainties regarding regarding the hygiene hypothesis, for example). It should also be acknowledged that immune responses need to be modulated properly. It is not a system that works better the stronger its responses are. In fact, certain aspects can result in damages themselves (cytokine storms have made the press a while connected with the swine flu pandemic, for example).

With regard to OP, I think it the different measures are useful for different purposes. The one outlined in OP would provide something like that relative health burden (as a count of deaths) though one would probably also want to see or at least try to account for secondary effects(e.g. whether there is also an increase in morbidity and mortality due to overburdening the health system). In addition, as iNow pointed other causes of mortality are way down. OTOH this year's influenza seasons is shaping up to be pretty bad (estimated at ~60k in the US and it is not over yet). So it is probably quite difficult. The crude number, on the other hand, are easy to generate but may not be easy for most folks to contextualize. Also, some countries have for some time not published all data (e.g. number of folks tested total) or unclear data (e.g. number f samples vs number of people tested). Often, because the reporting system was not centralized and clear. However, it is convenient for epi-folks to grab those numbers that come out and plug them into their models (say, playing around with Rt). It is one of the rare reasons where they can make predictions and see them unfold in real time. Wuhan data was used quite a bit to this end and as StringJunky noted, it is sad that much of the World outside of Asia has not taken steps once it was clear what was happening. I also do see the of some news articles indicating that China was fudging their numbers as if that would excuse inactivity (which I find worrying, as it clearly indicates that folks in the US are not trying to address their own shortcomings). So at least in that sense rapid release of numbers could help to at least appear more transparent.

I guess it depends on how many bacteria we count as pretty devoid (and probably also types of bacteria).

I have not really read it yet, but this article seems to reference some of the publications I have read on the subject: https://arstechnica.com/science/2020/04/should-you-wear-a-face-mask-heres-all-the-data-we-have/ So it could be a good read. A few seem to be missing, though. Not sure if I referenced it before but there is also a review that is mostly focused influenza but also has (and criticizes) some SARS data: bin-Reza et al. (2012) Influenza and other respiratory viruses 6(4), 257-267. Probably the overall outcome is that more studies are needed.

I do not think you can find then. Molecular biology is vast and has a lot of specialization even depending on what organisms you are looking at (animals? unicelluar? multi-cellular? plants? bacteria?). The list Dagl1 has clearly an eukaryotic slant, for example, and reading each of these points would get you a spotty overview at best. Say you want to do perform bioinformatic genome analyses. For that, you should first figure out whether for what purpose and which organism. Pro- and eukaryotic genome have very different structures and data availability for example. In other words, even a concise overview requires a focal subject, otherwise you will get hopelessly lost. Do you want analyze mass spec data? Whole different set of knowledge required. Again, Biology is heavily, heavily specialized. While there are disciplines that require some broader knowledge, you have to expand from a core.

From what I understand it is because of the risk of asymptomatic transmission coupled by the fact that there are a lot of undiagnosed cases in the US. I.e. it is not about not catching COVID-19, it is about not spreading it, which does not contradict what most have been saying before. That is one of the worries when I see folks casually wearing certain masks (or gloves). I am not sure how big of an issue it really is but it feels "wrong" (based on my training in biosafety environments). I am seeing masks, cloths etc. as a portable sneeze guard more than anything, which is probably a good thing. It is just wrong to thing (IMO) that casual use will have protective properties, especially if folks then take more risks (as they think they are protected).

You mean oxygenation? You cannot do with a dialysis machine, but you can use an ECMO system (which is being used for extreme cases).

Yes there are some conflicting results. A few studies from Italy and China indicate no difference in the load between asymptomatic and severe patients, for example. Another one suggests that the load is only different in swabs. Also animal studies with other coronaviruses suggest worse outcome with higher loads. As with anything, the knowledge is very much in flux.

AFAIK the minimal infectious dose for SARS-Cov2 has not been established yet. I.e. no one knows yet.

It is a common observation that pathogens with long evolutionary history tend to become less virulent. Our genomes are quite full with dormant viral sequences, indicating that at some point they just became part of us. There is an assumption that there is an optimum on what level is the optimum, depending on a variety of host-pathogen factors (e.g. resistance). There has also been experimental evidence in simple systems. However, due to the nature of interact there can be cases where virulence can increase (but again, the current outbreak does show how effective tempering virulence can be). It also means that pathogens jumping hosts are often maladapted and may have suboptimal virulence (e.g. too high).

Another random thought regarding SARS-Cov vs SARS-cov2 is that the latter is much less virulent. But in this case it does show how reduced virulence actually leads to far wider spread.

There are easier explanations. The first is that in some states there was earlier spread from folks that returned from holidays and there were carnival festivities resulting in major infections in NRW. In Baden-Wuertemberg folks travelling from Italy were diagnosed with COVID-19 in February for example. Another element is that aside from major cities the population density in East Germany is fairly low (unless it has changed in recent years) and I would think that together with spread pattern it could account for most of the differences. There are also differences in the length and time of winter holidays in the different states, so depending on when they are, there might also be different timing in when folks returned from holidays. Those coming back earlier might have evaded infection in Italy, for example, in addition to the point MigL made..

Essentially anything that can works as splash protection has a decent change of capturing the droplets containing the virus. I will re-iterate again that the data is very thin on whether widespread use is a good protection from getting it. Theoretical papers have looked on whether N95 masks can protect effectively from particles under lab conditions, and, well of course they do. As you mentioned, handling and other issues make them less effective under less ideal situations (e.g. no full seal). Surgical masks can also be penetrated, which kind of makes sense, as they are basically disposable splash protection. Take a look at some influenza data. A review is e.g. Cowling et al. Epidemiology&Infection 2010 138:4 pp/449-56 As mentioned, despite the fact that surgical or even cloth masks are way inferior as N95 masks in terms of protection and potential penetration with small particles, folks found similar efficiency with both masks when it comes to household transmission. That indicates that if they work, it might not depend on the material (or perhaps wearing them at all) per se. The one measure that throughout all studies reduced transmission was hand washing. However, since folks might be transmitting viruses while being asymptomatic, it does make sense to wear masks to limit spread. For that scenario you can find more literature indicating that it might actually help (see also references provide in the above paper). There are also other thoughts, folks wearing masks may be better in distancing themselves from others, for example, which can skew results. But as a whole, there is a distinct difference in efficacy when comparing professional (e.g. laboratory or clinical use) vs. household use.

Well there are good reasons to call the virus and disease the way it is called. First the virus name is not provided by the WHO but by the International Committee on Taxonomy of Viruses (ICTV). SARS-CoV-2 is short for "Severe Acute Respiratory Syndrome Coranavirus 2". Based on their approach the ICTV found that the the new virus is not sufficiently (genetically) different from the previously identified virus named SARS-CoV, the causative agent for the SARS disease. Naming it Wuhan Virus or something like that would essentially go against all naming conventions. The disease itself is named simple Coronavirus Disease 2019 (COVID-19).

Yeah, researchgate, Google scholars and probably a couple others do have that. For the most part I have more success with focused searches. But I also change my searches as my thinking on the problem evolves.

I disagree with that. The issue is that molecular biology has a lot of concepts with varying degrees of understanding. Any given list without proper context (i.e. being concise) is unlikely to be of a lot use for most students. What normally is more helpful is to specialize in particular question first. E.g. What do you want to model? For what purpose? What type of biological information do you want to analyze? What are the models you are comfortable using? If you develop your research question you can assemble the tools and knowledge to tackle it. After you got some foundations, you can expand and see what else is out there. If, otoh you just wand an overview, I recommend a textbook. They provide certain viewpoint and context (often still incomplete) that will help you to understand why folks look at and analyze things a certain way. However, even the broadest texts will be fairly incomplete. Biology is often a hot mess of different concept, approaches and thoughts, even when dealing with the same phenomenon. This really just mirrors the complexity of biology itself and I have yet to see a successful student project that starts overly broad.

To me it is preparedness after it became clear that there was widespread community spread. There was a weird lack of contact tracing, folks were (and as recent at two weeks ago) not asked where they came from, no test or even asking for symptoms (unlike e.g. during the ebola outbreak). A number of countries initiated these measures and increased preparedness and among the community there was a sense that CDC and other agencies were starting just that. But then there was quite a bit puzzlement among my colleagues that have been travelling. And then it became clear that even countries who were producing the test kits were not stockpiling them. Manufacturers of PPE have reached out and asked whether they need to ramp up production but got no response (sure there are also financial interest there, but it shows that there was no concern as of yet). Structurally, it also showed that many lacked a decent pandemic response team. The US dismantled theirs, Germany assembled theirs end of February. And this goes to my general point, pandemic response needs to become a regular element of public health and an ad hoc assembly late in the game is likely not going to cut it. Regarding swine flu, there was a pandemic in 2009 resulting in 100-500k deaths. Any good response will look overprepared, because that is what they have to be.

Actually I think that is fine. A surgical mask does not have filter capacities, either, it is more a splash protection. Considering it is about minimizing producing droplets it would still work. N95 or equivalent masks, are, when properly worn, very uncomfortable especially after prolonged use. If it results in fiddling with it, you may increase droplet transfer via your hands. Again, it is more about protecting others rather than just yourself.

Case mortality is about that. It is a fluid number of course, case-mortality of influenza for example is dependent on a variety of factors and in the US the death rate of symptomatic illnesses is somewhere between 0.1-0.2%. The case mortality for COVID-19 is estimated somewhere between 1-2% according to most estimates. The crude death rate is higher, but probably overestimates as undiagnosed folks are missing from the number. Contagious is also a bit difficult as often there are differences in interpretation. Typically a measure to compare diseases is the so called reproductive number, R0, which indicates how many cases are generated from a single case, assuming no immunity or other interventions. That number is often a bit difficult to assess, as for flu a certain (fluctuating) number of folks are vaccinated or naturally immune against a given strain. In case of COVID-19 there is no immunity, but isolation can curb the number. That being said, for COVID-19 the current estimates are around 1.4-3.8. The various influenza strains have a range of estimates from 0.8-2.2. It is roughly like SARS is but lower than MERS.

I have posted in this thread, so not making this statement as a mod. However, it would be great if we could stay on topic. Please open a thread in politics for example if other aspects are to be explored.

Airborne transmission is closely related to droplet. Essentially if they survive the drying process and remain viable in evaporated residuals. Quite a few are nasty (tuberculosis, measles, pertussis etc). In the studies mentioned, the mutations allowed ferret to ferret transmission, but the original was not lethal to them, either.

Well, there are certain diseases or conditions that makes it harder for pathogens to infect their hosts. Sickle cell anemia is such an example. However, the disease in question is an autoimmune disease. The antibodies in this process are specific to host components and therefore do not target pathogens. More commonly the reverse is likely true, an infection can trigger autoimmune diseases.

There are a few reports and comments that have raised the concern that non-symptomatic spreaders could be a bigger issue than previously anticipated, especially in countries which are still undertested (such as e.g. USA). In this cases adopting a broad facial coverage policy (scarves or surgical masks are fine and probably more comfortable) could be a benefit as it reduces the spread of droplets from unwittingly positive folks.

Well, we already had plenty that did not originate there (as well as a few pandemics) and we will have plenty of outbreaks within the next few years. It is mostly the confluence of factors that make a disease more likely become a pandemic, which includes e.g. effective human-human transmission, long incubation time, late/difficult detection, outbreak in areas with high connections to rest of the world etc. This time a lot of folks dropped the ball which resulted in a rather unprecedented situation. The question is whether the next one (which will come) will be contained better or not.

I think it depends a lot on the discipline and also how specialized one is. My work is, unfortunately, somewhat multidisciplinary, so my approach is likely very different from someone who works in a far more specialized area with more focused papers/reviews.