CharonY

That is a bit tricky. For coated viruses folks often see seasonality and it is suspected that at lower absolute humidity the viral particles stay infectious for longer (there are various hypotheses as to why, incl. osmotic pressure, staying longer in the air as aerosols etc., but no definitive answer AFAIK). While seasonality have been observed in various coronaviruses, there have been (as you noted) sustained transmission in humid regions. So folks by now assume an at best modest slowdown, but not a sharp decline.

Different markets in various countries have taken a range of measures, including limiting the number of folks allowed in, reserving hours for vulnerable persons, waiving delivery fees and so on. Not every country has a system for online pickup delivery and trying to implement it now is likely going to go badly. Some supermarkets in Germany are looking for help restocking since they cannot keep their shelves full.

I am not sure what you are seeing there, the first unbolded part is also true, as most folks are probably not handing them correctly thus providing no benefit (or in some cases increase risk) but those who could put them to good use then don't get them either. Edit: Do you mean the increase risk part? In my mind it makes sense - per standard biosafety procedure inproper use of face protection is a common risk (i.e. you should only use it when properly fitted, for the right application etc.). But do you mean that folks can misinterpret it somehow?

I read up in German articles in case of mistranslation and it does not look much better there. As usual nativism and cruelty go hand in hand (not to mention stupidity, as if nature adheres to borders).

Coronaviruses are RNA viruses. On the RNA strand they encode everything they need to replicate and form the capsids. I have mistyped earlier (ironically i did not proofread) and one of the genes it encodes a proof reading exoribonuclease. It excises mismatched nucleases. Other proteins required for basic processes such as ribosomes are hijacked from the host rather than being encoded in the viral genome.

I think it is too early to calculate mutation rates. However, coronavirus have something that is called a proof-reading polymerase. These reduce errors in while they replicate and thereby cut down errors (and hence, mutations). Right now we are pretty much past the point of containment. Even without draconian measures it can be possible to contain it, some countries managed to achieve that. However, what one need to do is quick testing and near perfect contact tracing. While Singapore, Taiwan and also South Korea did well on that end, many countries (incl USA and Europe) botched that, even with the time bought by China.

Iirc the Spanish flu put the immune system on overdrive, resulting in massive inflammation, which caused damages. Personally, I think with Covid-19 the issue is less about immune responses alone, but comorbidities. Preexisting conditions are highly correlated with worse outcomes and my guess is that those in conjunction with Covid-19 mediated lung damages are what is causing the fatalities. I.e.younger folks with those issues might also be vulnerable.

This is the basic idea for attenuated vaccines. However, ascertaining how is not trivial. That is unclear. If the dosage is too low it may not result in disease, but may also not trigger immune responses. Again, same idea for attenuated vaccines, but without studying what levels of inactivation and required dosages, it is rather risky (or useless). You can think in terms of inactivation. If you destroy their structure they become ineffective. As discussed before, cold is a not a specific disease and given the wide range of viruses causing such mild symptoms there was little incentive to develop a vaccine for each of these viruses. However, there have been work on SARS and from what I remember it was difficult but they were close. But funding effectively dried up as outbreaks were small and there was no sufficient economic incentives, I imagine. Any level of immunization as well as immune population reduces the transmission rate. Even if no perfect herd immunity is achieved it would make other measures (such as contact tracing) more effective.

So the paper discussing the use of cholorquine (and Remdesivir) is authored by Wang et al. (Cell Research volume 30, pages269–271 2020). The mechanism is not actually known but based on other viral data it is suspected to work by increasing the endosomal pH and interfering with glycosylation. The authors also speculate that modulating the immune system may also play a factor. Edit: apparently some studies with SARS suggest a role of zinc in inhibition, but from the looks of it most are in vitro data and I am not sure whether there are more studies out there.

Note that the spread was predominantly along trade routes. While there is decent evidence supporting the use of (black plague) bodies (which, btw. were already spreading in Asia and the Middle East), the entry of the plague was likely independent of that (or it may have contributed it, but was not the major driver). The narrative of the use of cadavers and the spread of the bubonic plague to Europe following the the siege of Caffa was strongly based on the account by Gabriele de' Mussi. Historians disagree whether he was actually physically present during the siege, but it appears that they think it is at least plausible that cadavers were hurled into the city. There is also the possibility that the plague arrived with the army and was subsequent transmitted by rodents, but despite overall uncertainties it is (from what I have read) not the favoured explanation. In the accounts de' Mussi also said that those escaped from Caffa were bound to Genoa Venice and so on and thereby spread the disease. However that clashes with what I think is now fairly well established understanding how the plague spread into Europe. It is well established that the plague spread over the Crimea, but cases in Genoa and Venice appeared well over 2 years after the siege of Caffa. Since even under unfavourable conditions the voyage should have not taken more than a few months, the timeline does not line up well. Another aspect that even if that timeline would have worked out, the time required would still have resulted in a substantial outbreak on the ships themselves. But again, around that time, there were no records of something that must have been considered to be a significant event. There are also folks who dispute that corpses were used in the first place (as there are no reports from folks fleeing from Caffa describing it aside from de' Mussi's account) or that there is no indication that it was knowingly used as a bioweapon (some dispute that bodies would be effective, they should have flung rats instead...). There is for example the speculation that the plague may have entered Caffa via the waterways. The Mongols were not able to fully block those and this where Caffa was getting resupplied. Also historians report that a step-wise entry of the plague into Europe is more likely which makes a spread over trade routes via Crimean ports even more likely. Well established reports pinpoint spring 1347 as the start of the plague in Constantinople, for example. I.e. there are quite a few reports that contradict the strong narrative of warfare-mediated spread, which is quite fascinating actually as not only historians have been working on it, but also epidemiologists and microbiologist, who use the documents to establish timelines and spread, not dissimilar to modern epi-studies (just with scarcer data). What is rather neat is that a fairly recent PNAS paper actually described genome evolution in Yersinia pestis which is consistent with repeated introduction via migratory and trading routes.

That is indeed a cause for concern. And to me, nationalism and unilateralism are going to make things worse. It should be noted that the graphs are specifically to spread awareness regarding COVID-19. Coronavirus while all respiratory (to my knowledge) can have different suites of symptoms. The discussion with cold is complicated by the fact as it is not a specific disease (as e.g. COVID-19) but rather a descriptor of symptoms that can be caused by a number of viruses and some of them belong to the family of coronaviruses. A number are endemic and responsible for a significant fraction of upper respiratory infections. Up until SARS, they were considered mostly harmless and often symptoms would fall under the "cold" bracket.

Historically bioterrorism has been very unsuccessful (a large scale food poisoning was the most known even, but even that is dwarfed by "regular" food poisoning events) . And even so, regular outbreaks have had higher impact than human designed ones. As whole bioweapons are difficult to implement, near impossible to control often inefficient compared to chemical or nuclear warfare. What it is efficient in, however, is having reasonable doomsday (or equivalent) scenarios. Undetectable spread high but delayed mortality, for example. There are oodles of novels around of terrorist groups creating designer pathogens for their purposes, but technically it is very difficult and more often than not a crapshot. There is the fear that they are easy to isolate and spread. But, as noted, common spread is often on a far larger scale than a group can orchestrate. So what about state actors then? Well, here the issue how are they going to control it (and what benefit would it have?). It is not total fantasy, of course, and there us bioterrerrorism research and prevention in place. At the same time we see that in a globalized world diseases spread at a much larger speed that we are accustomed of. So given that COVID-19 is around and possible join the ranks of circulating diseases such as influenza I am not sure what the bioweapon potential would be here. A more systematic (but slower way) to erode public health is to boost antivaxxer campaigns and otherwise reduce public preparedness. At this point I would take bets that these would end up in more fatalities in the event of a natural outbreak than what folks would achieve by actively trying to implement a doomsday scenario. And how is it different impact-wise from what is happening right now? Also note that for this disease asymptomatic spreading is very rare. There seems to be an overall correlation of spread and severity of symptoms. But of course there are plenty of (younger in this case it seems) that don't care too much about a little cough. By overall point though is that while it is always more frightening to thing in terms of an intelligent driver to some crisis, the truth is that there are plenty potential catastrophes around that can and will occur eventually (even just regarding disease think climate-change driven rise of diseases, demise of antibiotics etc.) that will likely to be more impactful than most bioterrorism scenarios. While I am not saying it is a zero-sum game, I do feel an imbalance in terms of risk and how afraid folks are about a given scenario.

Technically the virion refers to a whole virus particle. Practically it is the same as a single (complete) virus but it is typically used in structural context. Also just to be sure: the causative agent of flu are influenza viruses. These include members of Swine and bird flu for example belong all to the group of influenza viruses (classification are provided in Studiot's link). COVID-19 is a specific disease caused by the strain SARS-COV2, which belongs to the family of coronaviruses. Other notable diseases associated with members of this family include SARS and MERS.

The plot revolves around a group of highly trained professionals who break into homes of elderly folks and aggressively cough into their faces for a few minutes. In a heartwarming twist one of their presumptuous victims confuses the terrorist with their grandchild to whom she had lost contact. After a furious intermezzo consisting of baking and copious amount tea the terrorist realizes that deep inside he is just longing for the love of a family. Meanwhile the grandparent realizes that the nightly visitor in stealth suit is indeed not her grandchild (the climbing hook on the balcony being a crucial hint- as well as a flashback highlight that the real grandchild had a fear of heights). But she enjoys the moment too much to care.Tragically, this human moment is also what ultimately resulted in successful infection. The terrorist becomes guilt-ridden when it becomes clear that the lonely grandma is not long for this world and he tries to reach her a last time to say his farewells. Meanwhile, his terrorist buddies consider him a traitor and try to stop him resulting in a highly choreographed fight scene involving lots of offensive coughing and running noses in slow-mo (the filmmakers did not consult experts as per usual and did not realize that this is not part of the symptoms). Finally, he survives all these ordeals and reaches the grandma, who turns out to be a special CDC/Homeland security agent in disguise (Jason Stratham) who have been delaying a rollout of coronavirus testing in favour of sting operations to catch corona-terrorists. PS: can anyone tell that I really, really do not want to read those student reports?

Well, if you wanted to actually kill someone with the coronavirus you'd have to try to sneak into homes for the elderly to be efficient. Assuming you get in contact with 100 folks above 80 you may have caused somewhere between 8-14 fatalities. You could contribute to overall spread, but if it is already spreading as it is now, it is unclear whether it would amount to more. But to do so, you will have to spend significant time with each person as casual contact seems to inefficient. So in other words you may have made the situation worse, but it is unclear how much you contributed. That, is typically just the opposite of what most lone wolf types have in mind. Part of their motivation is some distorted desire for notoriety and striking fear into folks. A "regular" mass shooting or other attack is likely to be more satisfying to them. On top, this is only likely going to work during an ongoing outbreak as there is a decent likelihood for vaccines eventually and/or most folks will develop immunity (due to infection). So all they are doing is accelerating things perhaps a little bit. Perhaps worse than any of that, poor public health responses are likely to create more fatalities than any level of deliberate act of terrorism is going to achieve. Think about that for a minute. Let's say hypothetically that testing for the virus is going to cost more than you can afford and you have the choice between going to work or lose the job, what do yo do? You cannot self-quarantine since you live paycheck to paycheck and have no food stocked up because of that. How many are in that situation compared to say ten deliberate spreaders? Now combine that with a slow roll out of tests even if they are affordable.

Also there are more folks spreading it around due to lack of knowledge or care. There are quite a few students, for example who said that they want to travel to hotspots due since the prices are now low. They do not care much about infection since they think they are in low risk group. As such the folks in OP are probably not contributing much.

Looks like typical choloroform/phenol extraction protocol. I have not experienced myself but in general there a couple of theoretical effects that one might need to control to make sure that good phase separation happens. This includes having enough ionic strength of the aqueous layer, control of pH or sometimes even just the addition of another organic solvent. I suspect that bad phase separation can happen due to excess amounts of compounds that in a given poorly separate into either phase, which includes certain proteins and lipids.

Look, I know it is amusing in a way an accident between clown cars might be. But underneath all that there is real tragedy and one should not forget that. The administration has cut funding to critical health and disease prevention/monitoring systems and the uncharacteristically slow response may be the result of that. It is not the first time either, NOAA, EPA and FEMA all are cut or in the process of being dismantled with serious consequences for affected folks (and especially EPA issues will only be visible when it is far too late). One can only hope that damages are still fixable but for now folks will suffer unnecessarily.

OP is quite vague in their concerns and waffling quite a bit between issues more connected to undergrad vs grad situations. There is a focus about getting things done, which may mean different things and priorities for undergrads vs grads vs postdocs vs PIs. What I do read is that OP is ultimately unhappy in their position and thinks about them in structural terms (i.e. departmental issue, Western vs Eastern education system etc.). If that happens, one should ask oneself what are the precise reasons for the unhappiness. The complaints listed above appear to be very diffuse and it may be important for OP to sit down and think more specifically what the issues are. Being unhappy about how things are run is often only be symptom of other issues. One important bit that has not really been mentioned is the relationship with the PI. Ideally a PI is a mix between a boss and mentor, switching between these poles as need be (ideally mostly the latter as much as possible, the former as much as needed). What is needed is a sit-down to discuss expectations goals and develop plans how to reach them. What a student may think is an important next step may not be in the mind of the PI. Is it the only project? Or one of many? If work is self-directed, what are the hurdles? Often students overestimate their ability to work independently and have to be reigned in. This is a time consuming process for the supervisor, but sometimes the only way to ensure that usable results are being produced (or at least allowing the student to graduate in time). Ultimately, the PI has to ensure that the funded project progresses and pays the grads to do so. Unless they are swimming in money, there is only so much one can let a student play before it becomes a drain on the finances or otherwise endangers success of the project. There is a shared interest between PI and student- successful execution of the project helps obtaining further funds and pay for the student. However, there can be disagreements on how to best execute the project. Here, it is relevant to acknowledge that students are still in training and for most it will take a while until they obtain the knowledge to be able to properly evaluate progress and adjust accordingly. Again, if one is unhappy with the PI it is time for a sit down. There, it is important to discuss specifics and not make it personal. It is not your business what lifestyle your supervisor has. Rather think about what you need to achieve, what your common goal with the PI are and how you both can achieve them. But also try to have a broader view on the situation or project and don't have a tunnel view where only your perspective counts.

So if we are talking undergraduate degree costs, there are a few things to consider. The first is that generally speaking each student is heavily subsidized. Increase in tuition fees are often connected with a reduction of school funding, of which typically state and federal funding are the highest chunk. Cost has also been associated with increase in student services. Schools with lower fees often have fewer amenities. In addition, public schools tend to have much lower fees than private ones. The salaries of faculty is fixed, so an increase of tuition fees as such does not e.g. result in higher salary. The latter is more often than not connected to obtaining grants, which in turn results in overhead for the university, which then also helps covering the cost for students. Thus more funds can in theory actually reduce tuition fees. In addition, research grants are a major source to pay graduate students. What you describe seems to me a common concern of mostly undergraduate students. While I am not saying that it would apply to you, many expect a high-school like environment and think that faculty are only there to cater to their specific learning needs. It often takes a while to realize that university is mostly self-directed learning. And the role of faculty is a bit different from that of a teacher.

So you have one example and extrapolate from there? That is often not representative. And it apparently is quite a bit different from your earlier characterization that the younger faculty (which are more likely to be on TT) are slacking off. The other thing to ask yourself is: do they have an active externally funded research program? If so, how can they maintain it by slacking off. If not, then you may have found an example of someone resting on their merits. Of course they are differences and if anything I found most of the slackers in the full Professorial area, folks that have accomplished much in their career and are also at an age where spending even more energy feels like have a lower return. Younger and hungrier folks are around and compete like crazy, one might as well cut down. I suppose (but then there are those who literally need to be carried out from their jobs). However, the example with thy Gym is really weird. Most folks I know get scolded by their MDs to work out more. We spend way too much time sitting and it really is bad for health as well as productivity. I still get to use the bench, and when I do, do actually feel better. If I need to spend extended time sitting down for paper/grant writing or lectures I do feel myself tiring out much faster.

See, that is exactly what I expect from folks that are overcomitted. Most younger faculty need to establish their research, balance their comittee duties, create new courses as well as engage in outreach. Older faculty tend to have settled in their research (and those closer to retirement may ramp down their labs) and have established their teaching duties. On top, there have been a lot of discussions with labs and while I am somewhat dismayed by it, the truth is that most universities are starving for money due to budget cuts by Fed and State. Labs are the most expensive parts- they require more instructors and eat more resources. While I personally like them as a teaching tool, they are also often not well-liked by students, as they can quite a chore. As such many universities have starting cutting them as a cost-saving tool. That seems to imply an intimate relationship with faculty which seems odd. Just to be sure, are you talking about college-level? There is a a certain frequency of things like dinners with colleagues, which often are a kind of networking sessions (we do talk about shop quite often, especially if partners are also researcher and/or faculty). But I have a hard time believing that folks would go out partying on a regular basis. At least I have not seen that anywhere. The only possible exception are sessionals (i.e. non-tenure track folks) who are probably drowning their sorrow on a semi-regular basis. What you should realize is that teaching, especially at research unis is but one of the many duties faculty have to fulfill and considering the competitiveness in other areas (especially in attracting grants) it is often not considered the most important bit, especially for younger faculty. In order to get tenure many institutions require some level of success in obtaining grants, which is a highly competitive process. Unfortunately just spending a lot of time teaching won't get you there.

If you are talking about faculty I can only assume that you are a student? Usually there is a ton going on for faculty and if there is no sense of urgency in things you are involved in, it is usually because there are more urgent matters to attend to. From my experience and those of my colleagues, unless you are one of the lucky folks where things miraculously seem to go your way, (so that e.g. you can buy yourself time) folks to keep too many balls in the air. Most of the time your decision is not what to keep up, but what you are able to let fall to the floor.

Yes, they are called opportunistic pathogens. However, it is not specific to viral infections but can be any situation that negatively affects host defense mechanisms or otherwise create situations that are allows certain pathogens to strive. A famous example of a genetic disease is cystic fibrosis, which creates a lung environment allowing Pseudomona aeruginosa to cause harmful opportunistic infections.

Typically two distinct epitopes are selected (one for coating, one for capture) to avoid competition effects. Often a control is added which interacts with the labelled coating antibody.