CharonY

Well, to be precise it leads to lung damages. While that can make the patient more susceptible to secondary infections, it is not necessarily connected. It ultimately depends on what the patients dies from first (if they die). I also do not think that folks have actually a consensus on whether the 1918 influenza epidemic actually caused things like cytokine storms. There are papers out there that have argued that the vastly different outcomes in various subgroups of patients indicates that host immune intensity actually plays a role (and would also be in agreement with the dominant role of secondary infections. I know that folks like to pick up the Spanish flu due to the large number of deaths, but for a variety of reasons it is not a good reference point (not least because we only have limited pathobiological information from that time). A cytokine storm in itself can be deadly. In the case where we have good data (as obviously the assumption on the 2019 pandemic are based on forensic reconstruction and indirect evidence), such as the 2009 swine flu pandemic, severe alveolar damage and signs of capillary damages were observed, these then can to lead to organ failure. In addition, the cytokines can also spill into circulation which can cause multi-organ dysfunctions. Either way the patient is gets in a really bad shape, which also makes the vulnerable to secondary infections. However, even if isolated in a sterile room, there is a risk of organ failure. The latter usually happens fairly fast, those that survive beyond that point are usually those that are at risk of getting infected.

Ah, no. Cytokines are signalling molecules produced by your body. Some of them are proinflammatory and are produced as response to infections. If they get too high while reacting to an infection the inflammation response of your body can start to cause damage. These responses tend to be stronger in younger folks (or conversely, in older folks immune responses are often muted). In very bad cases theses pro-inflammatory responses can lead to death, which has happened during the Spanish flu as well as Swine flu, which caused many of the deaths among younger folks.

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).

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..

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).

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.

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.

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, 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 would reduce one source. Though again, the same could be said about most animal farming. Several aspects make those market more likely to be a threat, but what I fear is that folks will just say think that banning those practices (especially those that they do not engage in, as it is the least annoying for them) is enough. For example, the current US administration tries to lay blame of the pandemic entirely on China, mostly to distract from their own failings (which had plenty of warning beforehand plus the active dismantling of mechanisms that could have given them even more intel). If we phrase overall pandemic readiness in terms of "those guys need to do XYZ" I fear that the overall result is that folks then lapse their own preparedness. I think this is what has happened now. Too many countries thought they were immune from biology and waited up to the last minute to get prepared. Countless folks suffer from it now and in the foreseeable future. Also, it creates the illusion that own practices (and I feel a little bit about that in the initial question) are somehow safe and sanitary. Yet, intensive animal farming does carry significant risks of spreading disease to the environment. In fact, the rise of antibiotics resistance bacteria is largely driven by agriculture. Certainly, it is not a zero-sum game, but regardless whether those markets are banned or not, it must be done in addition, not instead of disease preparedness.

Even if feasible, one should not believe that this would remove the threat of zoonotic or other diseases. It is not a matter of if just of when new diseases will emerge. As such implementing mechanisms and plans to stop their spread are crucial and one should not assume that removing single sources (wet market or even animal farming as a whole) would magically erase the risk.

There is also several fundamental misunderstandings of the methods, it is a RT-PCR (which along with viral cultivation is considered a gold standard but has mostly replaced the latter),primers provide target specificity, detection of antibodies is useful for rapid testing (but suffers more false negatives than RT-PCR), current tests look at two targets and inconclusive tests are validated via Sanger sequencing.

I think by now interactions will or should be severely limited. As others have said, it should be taken seriously, if not a a risk to yourself it poses to those you interact with. There are already a ton of good advise posted basically everywhere (keep distance, wash hands, do not touch your face etc.). Trying to remove infectious material should also help. One should try to avoid touching things with our hands (e.g. opening doors hands-free if possible, use elbows to operate switches or doors etc.). One of the habits I picked up during lab work is to use the non-dominant hand as designated "dirty" hand (assuming that you are less likely to touch yourself with that hand, which might not be true for everyone) and then make a fist with that hand whenever you are not using it (I often imagine holding something in the fist). I try to keep it up until I disinfect/glove/whatever needs to be done. What I also train students is to lock their hands when they are not supposed to touch anything (e.g. when they are gloved) to keep them from touching themselves, their clothes and so on.

So there is a preprint that predicts about 80k deaths in the USA over the next 4 months with large uncertainties, though (MEDRXIV/2020/043752). See also https://www.reuters.com/video/?videoId=OVC6U1U23&jwsource=cl Edit: If true, it be more deaths than the deaths attributed to influenza (at least since 2010).

Yes it is a possible treatment. If the recovered patients produced enough antibodies against the pathogen, it can help in alleviating the disease. It has been attempted with SARS and Ebola, mostly with modest success. And there are ongoing trials (i.e. treatments of patients with this approach) in China and Italy. (side note- antibodies should be directed toward external targets, such as viruses and bacteria. Sometimes they react to host cell components, which can result in auto-immune diseases). I think that this is useful to limit. However, even conditions that we consider sanitary, we run risk of spreading zoonotic diseases. Animal farming is not a sterile process and pathogens are constantly evolving. In my mind, better processes can slow down the rate, but not stop the process.

No, I am not sure whether the community actually proposed a name (I think the evidence is not strong enough to warrant it, but folks still may have done so). Radiata is a historic term deep in the animal group. The idea was to group all animals with radial symmetry. However, as it turned out, animals with such body plans are not monophyletic (i.e. share the same common recent ancestor). On the comment I made above, when we go away from viruses, I should also add that the various Cholera epidemics throughout history (including the one that is going since the 60s) have origins largely in India. Though due to the mode of transmission this is actually a sanitary issue (specifically lack of access to clean water).

I think there may a couple of wrong assumptions but I am not read enough in those areas to provide an immediate in-depth response. Let's talk about zoonotic diseases first. One thing of note is that at high population densities and contacts with animals there is a higher likelihood of a pathogen crossing species barriers. But even then they may not cause large outbreaks, as they may have low transmission or low virulence and either exist invisibly in a given population or do otherwise do not garner a lot of traction. Many viruses re-assort in pigs transfer to humans and then change further (e.g. by grabbing genes from other viruses in their hosts) before they cause outbreaks. Take the H1N1pdm09 (swine-flu) pandemic, for example. That particular strain has a bit of a mosaic structure, probably originating from three parental pig viruses and emerged into humans somewhere in North America, some assume in Mexico. There is also the MERS epidemic, that came likely from camels but were sufficiently contained not to cause an epidemic. Hantavirus is a deadly virus that has a case fatality of ca. 40%. However, it is spread by mice and not human to human (luckily) and was found in the USA. There are also plenty of zoonotic diseases found in India, such NIpah virus and has been slowly spreading. However as there is no human-human transmission the spread is not as rapid. Likewise, we had a Zika pandemic not so long ago, a mosquito borne disease, originating from Africa. Japanese encephalitis likely originated in the Indonesia-Malaysia region and while it is also transmitted by mosquitos, it causes outbreaks every couple of years with about 13-20 thousand deaths each year. Again, lucky break that they need mosquitos as vectors. So in a way to me the question is whether it is by chance that those originating from China have larger impact on global health and economy or whether there are factors contributing to it. I think one needs to think beyond sanitary issues, as you mentioned. One question could be for example how connected China is compared to India. But also for example how the meat industry looks like. Another perhaps simple question is also what types of potential zoonotic diseases are there that could for example mix with animals that come into close contact with humans. In India many are mosquito borne, but perhaps they are less relevant in China. In Europe and US industrial pig farming has a huge potential to recombine and spread viruses in pigs, but there are perhaps fewer animals around that can spread novel viruses into pigs. Regulating or closing those market can likely close some of the risk factors. However, ultimately my thinking is that the world is shrinking, for better or for worse. There will be more contact between each of us and there are diseases that not zoonotic. What it means is that otherwise local disease have a much easier to become epidemic and even pandemic. Without the willingness for rapid responses to detect human-human spread, I think that most of the measures will be insufficient. And I think it is somewhat wrong to think that in the Western world our measures will keep us safe indefinitely. We had prion disease entering the food chain (sure it is not an infectious disease per se, but still). Farm animals often have to be culled due to various disease outbreaks. So far those have not managed to jump the species barrier, but it is not something that may so forever. On the other hand of course there is the tendency of diseases to become less virulent over time (as killing the host is generally not a good long-term strategy) but in the meantime a lot of harm can be done. Other man-made reasons for outbreak are for example anti-vaccination campaigns. HIV/AIDS now is well controlled, and we get complacent again (in the 90s it was for a time the leading cause of death in young adults). We have tons of pathogens that can mix, mutate and while there may be area with larger reservoirs than others, I do think it is dangerous to think it as an "elsewhere" problem. I think this is what lead to complacency when China was facing COVID-19 and that is why despite ample warnings the Western world only reacted when they had deaths in their midst. It may not be quite what you are thinking of, but I do think that this change in mentality is necessary to combat the inevitable occurrence and re-occurrence of diseases (and I apologize for all the typo and rantiness, it is more flow of thoughts without proper editing, may try to express it clearer when I got time again). Edit: had so many unfinished thoughts but wanted to include that global warming is going to increase the likelihood of many, especially mosquito borne diseases, so that has to go in there also somewhere.

Yes, cardiovascular issues are associated with worse outcomes, for example (based on Wuhan data). But also note that all age groups can have more severe outcomes requiring hospitalization. The US is still undersampled but initial info shows almost all brackets affected except 19 and younger based on CDC data a couple of days ago:

Also pre-existing conditions.

Well, there are recommendations for decontamination of hospital bedding and clothing. Heat alone is seemingly insufficient for full decontamination based on above data, but a combination of heat/detergent/bleach might be. For sun light one might calculate the output for UVC and see whether that may be high enough, I suppose.

I am not sure, ozonation, UV treatment and disinfectant fogging are being used in certain biocontainment facilities, but I don't know whether they would work and/or may be harmful in patient care facilities. The latter are often more crowded than biological workspaces and patients are more vulnerable to ozone, for example. I know that fogging is not allowed but I don't think that there are recommendations regarding UV and ozone in patient care (to my knowledge). Theoretically one could establish a protocol with thorough ozonation followed by quantitative ventilation or quenching to ensure safe levels. But again, I do not know if folks have tried or studied that.