text:
What causes cells to inactivate one X-chromosome?
Normally, when a cell has two X-chromosomes (female genome), one is randomly inactivated. How does the cell detect that there are two X-chromosomes in the first place?
Is there some kind of protein that's coded in the X-chromosome, such that having two X's increases the protein concentration and a dosage effect causes one to become inactivated? I can't find any information about it in my textbook, nor on Google. A citation would be appreciated - especially for peer-reviewed research.

Even a male cell can count the number of X chromosomes. (Lee et al. 1996; Cell 86: 83-84)
When X inactivation is getting started the two chromosomes "kiss" - a process that lasts for a couple of hours (first shown by Jeannie Lee in 1996). The physical contact between two X chromosomes is over a small fraction of the chromosome but it's essential for triggering inactivation. (Xu et al. 2006: Science 311: 1149-52)
If it doesn't happen then the X chromosome assumes it's alone which would mean that Xist never gets switched on and inactivation never happens (a key stage in chromosome counting).

Chromosome counting is a process in which cells determine somehow
  their intrinsic chromosome number(s). The best-studied cellular
  mechanism that involves chromosome counting is 'chromosome-kissing'
  and X-chromosome inactivation (XCI) mechanism. It is necessary for the
  well-known dosage compensation between the genders in mammals to
  balance the number of active X-chromosomes (Xa) with regard to diploid
  set of autosomes. At the onset of XCI, two X-chromosomes are coming in
  close proximity and pair physically by a specific segment denominated
  X-pairing region (Xpr) that involves the SLC16A2 gene.

Take a look at Xist and Tsix. Some more papers worth taking a look at:
Xist regulation and function eXplored
Mechanism of regulation of ‘chromosome kissing’ induced by Fob1 and its physiological significance

Please note that this only applies to placental mammals. Drosophila, for example, has a different method for compensating for the two copies of the XX chromosome in females.


text:
how many times can a spitting cobra spit its venom?
exactly how many times can a spitting cobra spit its venom at a predator
it has a small venom sac, so I presume it can only spit once or twice only

I presume it can only spit once or twice only An unwise presumption.

These cobras exhibited distinct control of venom flow with spits averaging 1.7% of the volume of the venom gland, thus enabling the cobras to rapidly expel over 40 consecutive spits ... There was no significant difference in the amount of venom spat between the first few spits and the 20th spit, however there was a significant (Student's t-test with unequal variance, p=0.017) decrease in the amount of venom spat between the 20th and 40th spits.

--Protein variation in the venom spat by the red spitting cobra, Naja pallida (Reptilia: Serpentes)

so it can spray up to 40 times

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

sort: votes


text:
What percentage of individuals infected with COVID-19 don't have symptoms?
There are various statistics estimating mortality of COVID-19 infections, based on how many diagnosed people have died. These numbers are used by various media to extrapolate how many people will die if the disease spreads uncontrollably.
However, what is missing here are the undiagnosed infected (due to their immune system fighting the virus fast enough and thus only presenting with mild, or no, symptoms).
Do we have any data or estimates for the percentage of infected people that are asymptomatic?

I don't find the source right now, so this is only a comment for the moment. But as far as I read, there are not completely asymptomatic patients. They develop symptoms, but these are sometimes misjudged as a normal seasonal flu: Runny nose, headache, sore throat, fever (this not always).

Probably the best way to estimate this is based on molecular/phylogenetic data. I've seen a study go by on Twitter but can't put my hands on it right now (anyone know how to search Twitter for a tweet from the last few days with an image of an iceberg ... ??)

I'm voting to close this question as off-topic because it is not about biology in the terms of SE Biology but a request for statistics about the current outbreak.

SE Biology is concerned with the mechanisms of biological processes, and questions are generally answered by people with biological rather than medical or epidemiological expertise. Although I understand your concern about the coronavirus outbreak, your question is not about the biology of the disease but about statistics for the current outbreak. I advise you to consult more appropriate reputable sources for such information, some of which are listed here.

@David, I continue to disagree with you about appropriate scope ... I'm still planning to answer (if I get around to it before the question gets closed). (The answer actually depends on a lot of interesting molecular evolutionary theory.)

https://twitter.com/trvrb/status/1238643293103075329

the relevant thread is here, you can go there and read it while I get around to digesting it enough for a good StackExchange answer ...

The proportion of individuals infected by SARS-CoV-2 who remain
asymptomatic throughout the course of infection has not
yet been definitely assessed.

The COVID-19 epidemic, Tropical Medicine & International health (2020)

The asymptomatic ratio is thus estimated at 41.6% (95% confidence interval (CI): 16.7%, 66.7%) among evacuees. Because fourteen days have elapsed since their departure from Wuhan—longer than the 95th percentile estimate of the COVID-19 incubation period (Li et al., 2020; Linton et al., 2020)—there is very little probability that the five virus-positive asymptomatic individuals will develop symptoms. Should one of the five becomes symptomatic in the future, the overall asymptomatic ratio would decrease to 33.3% (95% CI: 8.3%, 58.3%).

Estimation of the asymptomatic ratio of novel coronavirus infections (COVID-19), International Journal of Infectious Diseases (2020)

Our estimated asymptomatic proportion is at 17.9% (95%CrI: 15.5–20.2%), which overlaps with a recently derived estimate of 33.3% (95% confidence interval: 8.3–58.3%) from data of Japanese citizens evacuated from Wuhan [13].

Estimating the asymptomatic proportion of coronavirus disease 2019 (COVID-19) cases on board the Diamond Princess cruise ship, Yokohama, Japan, 2020, Eurosurveillance (2020)

Table S1. Model parameters. All time periods are given in days.
Parameter                     Baseline              Distribution  Reference/reason
                              (alternative values)
...
Pr(Asymptomatic | Infection)  0.178 (0.1, 0.5)      Beta          Mizumoto et al. (13) (lower, higher)

Estimating unobserved SARS-CoV-2 infections in the United States (preprint) (2020)

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Are omeprazole and other members estrogenic and/or antiandrenergic?
As of 2020, omeprazole is a widely used OTC medicine for various types of acute heartburn and some other gastrointestinal disorders.
Almost every time I read about it I read that one of the possible side effects is gynecomastia, which Wikipedia defines as "noncancerous increase in the size of male breast tissue".
As a non chemist (let alone biochemist), it is unknown to me why should it at least theoretically cause gynecomastia.
Are omeprazole and other (chemical family) members estrogenic and/or antiandrenergic?

There is not a lot of evidence that the compound itself is estrogenic, but it may affect how estrogen is metabolized in the body, leading to feminizing outcomes.
Pubmed is a good source for information in the biomedical literature- here is a pubmed search that has more information on those terms.
Looking through some of the results of that search, I find that there seems to be a fair amount of evidence that omeprazole has something to do with gynecomastia, but the association is not strong:

A review of the literature has some conflicting information. One study of general practice in Britain suggested no detectable statistical relationship between taking omeprazole and gynecomastia. However, a smaller study suggested that in people who experienced gynecomastia who were also taking omeprazole, removing omeprazole helped in the majority of cases. I suggest reading the section of that review on omeprazole. The conclusion of the review is that omeprazole probably has a role in gynecomastia.
There is a literature of studies (mostly in Spain?) ascribing omeprazole a role in gynecomastia. One example.
There is evidence that omeprazole has a chemical effect on estrogen metabolism. However, it was much less strong than some other drugs examined.
There is evidence that omeprazole slows the metabolism of estradiol, an active estrogen compound (see Figure 2 in the review linked above).

Overall, people seem to say it (and related compounds) probably has something to do with gynecomastia, but it is not a principal contributor on average. Possibly it shows a synergy with some other drug or some lifestyle variable.


text:
If mutations are random, why do antibiotics 'cause' resistance?
Full disclosure: I am not a biologist and this is more of a general question about understanding antibiotic resistance of bacteria.
We are always told that careless antibiotics use is the cause of new more resistant bacteria, which can obviously devastate huge societies and even have global impact. At the same time from my knowledge it seems that bacteria mutates in a purely random fashion.
So, thinking about this concept probabilistically, the virus mutating and antibiotic consumption seem to be completely disjoint events such as:
$$P(M|A) = \dfrac{P(M \cap A)}{P(A)} =\dfrac{P(M) P(A)}{P(A)} = P(M)$$
Where $M$ is the event that the bacteria mutates and $A$ is the event of taking an antibiotic. I couldn't find any research online as to how $P(M)$ is actually modelled or what probability distribution it even roughly follows, but intuitively it would depend on time as the longer the bacteria spends inside the host the higher the probability of mutation would be. So from this train of thought it would seem that taking antibiotics would actually be a good idea as to eradicate the bacteria quicker and give it less chance to mutate down the line.
I am obviously not trying to discredit hundreds of years of research and understand that there must be a gap in my thinking somewhere. My question is, why are we told that antibiotics cause antibiotic resistance even though the mutations are described as 'random'?
(ELI5 explanations are preferred as I said I don't come from a biology background)

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, you are ignoring the effects of selection, which suggests to me that you would benefit from this introduction to evolutionary theory from UC Berkeley. ——— We also encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

Presence of antibiotic does not significantly affect mutation, but rather affects selection of variants.  You may find this Khan Academy page helpful.

Mutations are random. Selection of mutants (with use or overuse of antibiotics) is not random.

There are many models for mutation accumulation (Liò and Goldman, 1998). The simplest model (Jukes and Cantor, 1969) assumes mutations to be a Poisson process. With a given mutation rate, the number of mutations accumulated will follow the Poisson distribution.
This basic model has been extended to include non-uniform mutation rate across the genome and different rates for different kinds of mutations. You can check out the link and the works it cites to have a better idea.
However, the answer to your question does not pertain to how mutations happen. Although there is some evidence that some antibiotic treatment can actually increase mutation rate (Long et al, 2016; Meouche and Dunlop, 2017, Windels et al., 2019), the main principle pertains to selection and not actually the mutations. Improper antibiotic treatment can lead to some cells with moderate resistance to survive, which in turn can evolve strong resistance. Here, we assume that the infecting bacterial pool already has enough variation (or develops during infection) some little resistance. Moreover, there is another phenomenon called persistence (ability to survive antibiotic, Brauner et al., 2016). Windels et al (2019) report that persistence can increase resistance.


text:
What's the evidence against SARS-CoV-2 being engineered by humans?
A couple of colleagues suggested in a discussion that the virus that causes COVID-19 appears to be made by humans, since nature could not have produced such an efficient virus — that spreads so fast and whose patients are contagious quite some time before showing signs of infection.
Since my knowledge of biology is very limited, my only counterargument for such a conspiracy theory was along the following lines:

there is a consensus that the most probable source of the first infection was in an animal market in China.
since that animal market was actually composed of a plethora of animals belonging to various species (mixed with humans), a virus had a bigger chance of evolving a mutation that might infect an individual from another species (a thing that is way less unlikely in the wild since many of those animals do not sit close to each others or next to humans).

Clearly, I have made a little story that might be quite far away from how SARS-CoV-2 infected humans, so I am interested in a scientific arguments to support my cause.
Question: What are the main scientific arguments that can be used to debunk COVID-19 being engineered by humans?
Answers that also include explanations more accessible to laymen are greatly welcomed.

Comments are not for extended discussion; this conversation has been moved to chat.

At the moment, there is very little scientific literature about this, but I found two papers that address the problem and are fairly easy to understand. You can find them in the references. Reference 1 is probably the most interesting and is the basis for this answer.
Edit: It is also interesting to read reference 2 on the origin of SARS-CoV-2; the article also addresses some of the conspiracy theories.
As far as I can see, there are a few major points taken up by conspiracy theories.
1. SARS-CoV-2 leaked from a lab in which research on the Bat CoV (RaTG13) was done:
Unlikely, since the viruses share only around 96% sequence homology, which translates into more than 1100 sites where the sequence of SARS-CoV-2 viruses is different from RaTG13. The mutations are distributed throughout the viral genome in a natural evolutionary pattern, making it highly unlikely that SARS-CoV-2 is a direct descendant from RaTG13. For comparison, the original SARS-CoV and the intermediate host palm civet SARS-like CoV from which it originated shared 99.8% sequence homology, showing a much closer relation.
2. The S (spike) protein from bat SARS-CoV cannot be used to enter human cells via the human ACE2 receptor and therefore has been adapted in the lab:
This is untrue, since a 2013 study of a novel bat coronavirus was published showing the ability of the virus to enter cells via the ACE2 receptor. See reference 3 for details.
3. The spike protein of SARS-CoV contains a unique inserted sequence (1378 bp) located in the middle of its spike glycoprotein gene that had no match in other coronaviruses:
As shown in reference 4, the sequence comparison of the SARS-CoV-2 with closely related other coronaviruses shows that this sequence is not unique to the new virus but is already present in older strains. It shows some difference due to inserted mutations.
4. The claim that SARS-CoV-2 contains four insertions from HIV-1:
The paper claiming this has now been retracted due to severe criticism, and additionally a renowned HIV expert published an analysis (reference 5) demonstrating that the HIV-1 claimed insertions are random rather than targeted.
5. The claim that the SARS-CoV-2 virus is completely man-made:
To design such a "weapon grade" virus in the lab, the design would usually start from a known virus backbone and then introduce logical changes (for example, complete genes from other viruses). This cannot be seen in the genome of the virus; rather, you see randomly distributed changes throughout the genome coming from virus evolution and not directed cloning. It is more likely that this virus originates from the recombination of a bat CoV (to which it is closely, but not directly related) and another, not yet known CoV in an intermediate host, like the palm civet for the 2003 CoV.
References:

No credible evidence supporting claims of the laboratory engineering
of SARS-CoV-2
The proximal origin of SARS-CoV-2
Isolation and characterization of a bat SARS-like coronavirus that
uses the ACE2 receptor
Is SARS-CoV-2 originated from laboratory? A rebuttal to the claim of
formation via laboratory recombination
HIV-1 did not contribute to the 2019-nCoV genome

The mutations are distributed throughout the viral genome in a natural evolutionary pattern. I don't think this means it wasn't engineered per se. Aren't viruses in research labs often "encouraged" to naturally mutate in a certain direction? It could both be engineered and have a "natural evolutionary pattern."

Comments are not for extended discussion; this conversation has been moved to chat.

Could you please comment about this paper? "Using the SARS-CoV reverse genetics system, we generated and characterized a chimeric virus..." - this is from the abstract of https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4797993/

If you need more [counter]evidence, there's a newer paper "The proximal origin of SARS-CoV-2" by Andersen et al. (March, 17) that touches on the same topic.
The paper brings up two reasons why SARS-CoV-2 is not "made in a lab". The first is the (relative) [in]efficiency of its spike protein; the second is somewhat more complex to explain and is related to cleavage site in said protein that is usually an indicator of rapid (but natural) evolution; this cleavage site is actually not found in the most related relatives of SARS-CoV-2 (the B-lineage of the betacoronaviruses), but only in the more distant A-lineage. Features related to this cleavage site also suggest that it was probably shaped by an immune system, something unlikely to happen in mere cell cultures.

Our comparison of alpha- and betacoronaviruses identifies two notable genomic features of SARS-CoV-2: (i) on the basis of structural studies and biochemical experiments, SARS-CoV-2 appears to be optimized for binding to the human receptor ACE2; and (ii) the spike protein of SARS-CoV-2 has a functional polybasic (furin) cleavage site at the S1–S2 boundary through the insertion of 12 nucleotides, which additionally led to the predicted acquisition of three O-linked glycans around the site.
The receptor-binding domain (RBD) in the spike protein is the most variable part of the coronavirus genome. Six RBD amino acids have been shown to be critical for binding to ACE2 receptors and for determining the host range of SARS-CoV-like viruses. [...] Five of these six residues differ between SARS-CoV-2 and SARS-CoV. On the basis of structural studies and biochemical experiments, SARS-CoV-2 seems to have an RBD that binds with high affinity to ACE2 from humans, ferrets, cats and other species with high receptor homology. [cites 6 references in support]
While the analyses above suggest that SARS-CoV-2 may bind human ACE2 with high affinity, computational analyses predict that the interaction is not ideal [citing: Wan et al.] and that the RBD sequence is different from those shown in SARS-CoV to be optimal for receptor binding. Thus, the high-affinity binding of the SARS-CoV-2 spike protein to human ACE2 is most likely the result of natural selection on a human or human-like ACE2 that permits another optimal binding solution to arise. This is strong evidence that SARS-CoV-2 is not the product of purposeful manipulation.

Wan et al. indeed mention that

several other critical residues in 2019-nCoV RBM (particularly Asn501) are compatible with, but not ideal for, binding human ACE2, suggesting that 2019-nCoV has acquired some capacity for human-to-human transmission.

Basically what Andersen et al. say is that if someone made SARS-CoV-2 in the lab, they could have made it better in terms of human transmission by using what we knew from previously studied SARS-like viruses, instead of coming up with a completely new and somewhat inefficient solution.
Another argument of Andersen et al. (somewhat similar to Chris' #4), which they only mention briefly is that

if genetic manipulation had been performed, one of the several reverse-genetic systems available for betacoronaviruses would probably have been used. However, the genetic data irrefutably show that SARS-CoV-2 is not derived from any previously used virus backbone.

As I mentioned in my first paragraph, Andersen also discuss that SARS-CoV-2 "borrows" a fairly distant feature, namely a polybasic cleavage site, which is only found in more remote "cousins" of the A-lineage of betacoronavirues:

The second notable feature of SARS-CoV-2 is a polybasic cleavage site (RRAR) at the junction of S1 and S2, the two subunits of the spike [...]. This allows effective cleavage by furin and other proteases and has a role in determining viral infectivity and host range. [...] Polybasic cleavage sites have not been observed in related ‘lineage B’ betacoronaviruses, although other human betacoronaviruses, including HKU1 (lineage A), have those sites.

And if you think this was an international manipulation, the trouble is that we still have no precise idea what that cleavage site does in SARS-CoV-2, although cleavage sites observed in other coronaviruses are thought responsible for cross-species infectivity and also are thought to be related to rapid evolution in highly dense populations.

Neither the bat betacoronaviruses nor the pangolin betacoronaviruses sampled thus far have polybasic cleavage sites. Although no animal coronavirus has been identified that is sufficiently similar to have served as the direct progenitor of SARS-CoV-2, the diversity of coronaviruses in bats and other species is massively undersampled. Mutations, insertions and deletions can occur near the S1–S2 junction of coronaviruses, which shows that the polybasic cleavage site can arise by a natural evolutionary process. For a precursor virus to acquire both the polybasic cleavage site and mutations in the spike protein suitable for binding to human ACE2, an animal host would probably have to have a high population density (to allow natural selection to proceed efficiently) and an ACE2-encoding gene that is similar to the human ortholog.
[...]
The acquisition of both the polybasic cleavage site and predicted O-linked glycans also argues against culture-based scenarios. New polybasic cleavage sites have been observed only after prolonged passage of low-pathogenicity avian influenza virus in vitro or in vivo. Furthermore, a hypothetical generation of SARS-CoV-2 by cell culture or animal passage would have required prior isolation of a progenitor virus with very high genetic similarity, which has not been described. Subsequent generation of a polybasic cleavage site would have then required repeated passage in cell culture or animals with ACE2 receptors similar to those of humans, but such work has also not previously been described. Finally, the generation of the predicted O-linked glycans is also unlikely to have occurred due to cell-culture passage, as such features suggest the involvement of an immune system.

Nice paper, thanks for adding. It shows how fast science is moving.

"The (relative) [in]efficiency of its spike protein" does not make sense as a proof of the virus being of natural origin. By that standard, my first car also could not have been designed by humans.

A conclusive proof of CoV2's artificial origin would be finding lab records or samples dated before the epidemic, or finding an obvious unique marker sequence in the cDNA. To date there is no such conclusive proof.
All other "proofs" I have seen are just hypotheses, and they all can be explained by natural processes too. In fact, if your opponents refuses to consider natural causes, such hypotheses become infalsifiable, like the Russel's teapot: any naturally occurring coronavirus can also be recreated in the lab. Here's an article from 2003 in which researchers describe how they have recreated SARS-CoV using a panel of cDNA fragments, which produced a virus identical to the natural strain (except for marker mutations).
For instance, here's a closer look on the infamous "unique sequence in S protein" (called Receptor Binding Domain) of CoV2, compared to RaTG13 (bat coronavirus) and MP789 (pangolin coronavirus):

source
As you can see, the "uniqueness" of this sequence is questionable if we consider that RaTG13 could have combined with a part of MP789 (in the red frame) and accumulated some additional mutations to produce CoV2. The conclusion that such recombination happened artificially can only be drawn if you see no possibility those two viruses could have met in the wild.
There's also a philosophical side to what should be considered "artificial". Two viruses recombining in the wild is natural. How about two viruses recombining in a market? What about a lab cage or waste?

I'm sure if this claim of recombination is plausible, it would be published somewhere else than a Russian (science?) blog.

To help you with that, the same author has published his views here https://onlinelibrary.wiley.com/doi/10.1002/bies.202000240 This is of course no proof as to whom is right but Andersen's paper has 2000 citations by now,  Deigin's has two.

And by that I mean citations in Google Scholar. Deigin's paper has surely made more of an impact on the right-wing press, e.g. https://spectator.us/virus-causes-covid-man-made/


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Is it true that if a human lived long enough (up to 3-400 years), he/she would eventually develop cancer?
I have just studied DNA, but I am not so clear. So, I would like you to explain it more clearly.
This is what I think when a human grow older and older, his or her DNA repair mechanism would be weaker and weaker and eventually so weak that it couldn't repair the DNA damages and he or she would develop cancer sooner or later?
Is it true that if a human lived long enough (up to 3-400 years), he/she would eventually develop cancer?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, questions should not be speculative — such questions lead to opinion based answers and are off-topic for this site. ——— We also encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

Every year we have a risk of cancer.  With enough rolls of the dice they will come up snake eyes.
That said, https://www.cancerresearchuk.org/health-professional/cancer-statistics/incidence/age#collapseZero highlights an interesting issue.  The incidence of cancer increases greatly from birth to seventies, then decreases.  If you are being optimistic enough to suppose a treatment could make you live for 400 years, I suppose you could assume your appearance and cancer risk would remain comparable to that of a teenager for hundreds of years as well.  If your cancer incidence is 0.2% per year (200 of 100,000 on the chart, 25-29 year olds) then your risk by the time 400 years have passed will be a little over 50%.


text:
Can stomach acid destroy a virus?
I was reading about a viral list of dubious coronavirus tips on The Verge and reached this tip:

“Even if the virus gets into your mouth, drinking water or other
  liquids will wash them down through your throat and into the stomach.
  Once there, your stomach acid will kill all the virus,” one tip reads.
  Loren Rauch, an emergency room doctor in Los Angeles who has a
  master’s degree in epidemiology, told Mother Jones this advice was
  “totally bogus.”

I asked a friend, who has a PhD. in cell biology, about this and she said that it's true that a virus would be killed by the stomach acid (i.e. due to high acidity, or low pH value, of stomach acid which could easily break the structure of the virus); however, she added that it's NOT true to think that drinking water would wash the virus from your respiratory system (i.e. trachea or lungs) into your stomach, so drinking water regularly does not necessarily help if it's in your respiratory system.
I was a bit confused since the doctor referenced in the article considered the whole advice as totally false; on the other hand, my friend thinks at least part of the advice, i.e. the virus being killed by stomach acid, is true.
Now, my question is not limited to coronavirus and I am not seeking medical advice or treatment here. I just want to  know if my friend is scientifically correct, i.e. whether stomach acid is able to destroy the biological structure of a virus (any virus, and not necessarily coronavirus)? And if so, how does this work biologically?

Unless you only eat sterile food , your stomach kills a lot of stuff . I think the question is "what doesn't a stomach kill"?

Study on MERS coronavirus and HCoV-229E: "rapidly lost most of the infectivity in fasted-state simulated gastric fluid (FaSSGF; pH 2.0)" but "survived FeSSGF" (fed state, which is less acidic). See Figure 3. IOW, on empty stomach, the gastric acid rapidly deactivate the MERS coronavirus and the 229E coronavirus, but if there is food in the stomach then the virus survives.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5687858/

You know why rotovirus and polivirus vaccines are oral, not injected?
Becuase it's the immune system in your stomach that needs to be primed to kill those viruses, they are primarily GI infections (yes, polio is primarily a GI infection, it only sometimes infects nerve cells.)


text:
Difference between aerosol and droplet transmission for airborne diseases
I've been doing some pandemic reading and can't find why there is a distinction between transmission by aerosols and by droplets. Some articles give a size cutoff of 5 microns; how is that important?
Aerosols were also mentioned to be either wet (small droplets) or dry (dry remains from an evaporated droplet). Does that mean droplets can evaporate enough to count as an aerosol?

An Aerosol is a suspension of droplets or particles in air. A "suspension" means that the droplets or particles are suspended in the air and do not just fall down with gravity. Very tiny droplets can be suspended in this way by the Brownian motion of the air molecules: The air molecules move around randomly (their speed indicates the air's temperature) and hit these tiny droplets back and forth and prevent them from falling down as they would normally do because of gravity. But larger droplets are too big, the air's Brownian motion is not powerful enough to keep them suspended against gravity, so larger do fall down and do not create an aerosol.
So, if the coughed-up droplets are big, they will quickly fall down - and as a result the disease will be hard to transmit (the healthy person needs to stand close enough to the infected person to inhale the droplets before they fall down). However, if the droplets are smaller than some size, they form - as I described above - an aerosol. Such an aerosol can be suspended in the air for a long time, which can mean that a person who walks into a room where a person previously sneezed will get infected. It can also mean that the aerosol can float around the room, and infect a person standing pretty far away from the source.


text:
Do endocrine cells always lie adjacent to capillaries?
The circulatory system transports plasma contents to the body via the interstitial circulatory system, reabsorbed with the lymphatic system. Cell metabolism "waste products" are transported into the blood via this "sewer system", to for example be excreted by the urinary system. The lymphatic system provides a basic route for interstitial fluid to return into the blood stream. The endocrine system has to be relatively fast, and, lymphatic transportation is relatively slow. Do endocrine cells always lie adjacent to capillaries so that hormones are secreted directly into the blood stream?


text:
How can I get started in molecular biology?
I have a background in computer science and math and am interested in learning molecular / synthetic biology - what resources do people recommend?

Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In particular, opinion-based questions like this are not appropriate for this site. Thanks!

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

imo reference request and book recommendation questions are valid question. For people from one background may face tantalizing experience in someother discipline  while the required 'prior research' before asking question. so imo its okay to provide context dependent answers to help clear up confusions to asker and other people at similar situations.

@AlwaysConfused We have a tag wiki that addresses what we expect for "book recommendation"-style questions. https://biology.stackexchange.com/tags/book-recommendation/info This one does not seem to follow those guidelines, and I'd probably vote to close it as a regular user. I will defer using my diamond power, though, unless I see it gets 4 votes to close from others.

@tyersome: Also, if you prefer physical books and have a state university or community college conveniently nearby, many of them have "community borrower" options for their libraries.

First develop a background of basic highschool chemistry, basic biochemistry and basic genetics.
What is molecular biology: Molecular biology has 2 definitions. A broader definition is molecular basis of life. That is indistinguishable from biochemistry. The second definition is how does genetic information flows through
 molecular mechanism. The secod one is a more specific definition of molecular biology and how it differs from biochemistry.
Its good to develop some background in biochemistry and genetics because concepts of molecular biology comes from biochemistry and genetics.
A quick start through biochemistry:

Lippincott's illustrated review on biochemistry.
Harpers's illustrated review on biochemistry
Organic chemistry by Solomons and Fryhle (especially stereochemistry portion).

then go through gradually more detailed book, such as biochemistry by Lubert Stryer.
Parallelly go through Genetics book such as

Principle of genetics by Hartl and Jones
Gene IX by Benjamin Lewin
Principles of genetics by Snustad et al.
iGenetics by peter J. Russell
Concept of genetics by Benjamin pearce
Genomes 3 by T A Brown
Principles of gene manipulation and genomics by RM Twyman and Sandy B Primrose.

Each book has a different perspective. it will help a clearer picture of different concepts.
Some basic molecular biology books:

Molecular bioloy- principle of Genome function: by Nancy Craig et al.
Molecular biology by RF Weaver.
Fundamental molecular biology - Lizabeth Allison
Princiles of molecular biology by Barton and Tropp.

For a more cellular approach and bigger picture see cell biology based molecular biology books viz.

Cell biology by Pollard, Earnshaw et al.
Cell biology by Gerald Karp
Lewins' CELL by Plopper et al.
The Cell- a molecular approach- by Geoffrey M. Cooper.


text:
What are some good books on basics of Cell signaling?
I think the title says it all.
(self answered, although others' answers requested)

Why these close votes? Do you have any suggestion to improve this question?

Cellular Signal Processing (an introduction to the molecular mechanisms of signal transduction), by Frederich Marks, Ursula Klingmuler, Karin Muller-Decker;
Garland/Taylor-Francis.

Link: CRC book, Google books
.............

Structure and function  in Cell signaling by John Nelson, Wiley.

Link:  Wiley, Google books


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Why don't what I can define as "aerophilic viruses" establish colonies?
Throughout my life I have seen some bacterial and fungal colonies in various sizes and colors, mostly on food or in hot humid dirty environments.
Putting bacteria and microfungi as well as other microbiology such as microalgae and archea aside, I ask here as a non biologist:
Why do what I can define as "aerophilic viruses" (viruses that can live significant amounts of time in the air and especially on surfaces interacting with the air - around 12 hours or more) don't establish colonies?
If such "aerophilic viruses" are so common and constantly going through evolution (perhaps faster than any other organism), why a microscope is needed to see them and one cannot see gatherings of them in the macro level?

Virus cannot reproduce on their own; they can only reproduce by taking over a cellular organism. For this reason, the idea of a 'virus colony' does not make sense.
You could have a colony of mold or bacteria that is infected by a virus, but a virus by itself could never create a single offspring, let along a macroscopic colony.
If there were some type of mutated virus that could reproduce independently, then I would argue that it would be a new type of life and not a virus.

I'd argue that the plaques in a plaque assay (https://en.wikipedia.org/wiki/Virus_quantification#Plaque_assay) are analogous to colonies, since the author seems mainly concerned with visible phenomena caused by high concentrations.


text:
How does the immune system find the DNA code for antibodies
There are millions of possible antigens. To respond to each antigen, the immune system must quickly produce an antibody by modifying the DNA of a B cell.
I have no idea how this process works, but surely it can't be by trial and error.
So I thought how I would do it:

The part of the pathogens DNA that codes for receptors is copied
then an algorithm is applied that transforms this code into an antibody code.
This code is then pasted into the DNA of the B cell. So the B cell has antibody receptors that fit on the antigen.

But how does it work in reality?

Please read up on clonal selection and V(D)J recombination.

And yes, it happens through trial and error.

Thanks, that answers my questions. Apparently we have 10^12 B-cells predefined in our body generated by a random process. Amazingly that the correct antibody is found in relative short time of a few days.

@Jacq: consider answering your own question with what you found, that might make it easier for future users to use the answer.


text:
What is this blue insect?
I found this insect in my garden

It's the first time I see this insect, so I'm wondering what it is.
It has blueish, purplish reflections, a head like an ant or wasp but it's the size of a thumb (4-5cm)
I am located in Hungary if it can help identify it

I am pretty sure that this is an oil beetle (also known as blister beetle) of the family Meloidae. In this special case this is probably the violet oil beetle (Meloe violaceus), although this does not completely coincide with the size you mention. The slightly different color is probably caused by the different lighting.
See the image from this Wikipedia for comparision:

Be careful with them, as they can secrete a poisonous substance making blisters on the skin (hence there name) when they feel attacked. For more information see also here.

That's definitely the same as the picture just a big one. http://bugoftheweek.com/blog/2013/1/7/look-but-do-not-touch-blister-beetles-epicuata-and-meloe-spp


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Are all emerging viral diseases of the past 100 years zoonoses?
From my basic understanding: The viruses causing Ebola, Sars and Covid-19 are all the result of a zoonosis, meanings that the viruses have passed from animals to humans.
So my question is: Are all recently (let's say 100 years) emerged viral diseases, with potential for a global epidemic, the result of a zoonosis?

At least a lot of them. I don't like linking to Wikipedia for such matters, but they have a nice list of sybtypes of Influenza A that should give you an example of how many variations you can have on the same base. From H1N1 to H5N1 and beyond, some of those variations were endemic, some caused pandemics. Some of those that stayed endemic had the potential to become pandemic.

In general, viruses don't profit much from their host dying or becoming too ill to infect others. Viruses that "rely" on humans to procreate are often not lethal - the lethal variants of the virus have a lower propensity to spread, so the less lethal ones are "fitter". Zoonoses have not been culled to be less lethal to humans, and are often much worse for us. We are "dead-end hosts" to them, We are best killed off so the viruses can spread to the preferred host, in laymans terms. Fortunately, we have murdered most mammals larger than us, so we are safer now than before.

@StianYttervik, this is a somewhat naive/narrow view of virulence evolution. Smallpox circulated in the human population for many thousands of years with a case fatality rate of 30% ...

@BenBolker There are certainly exeptions, I am making a general case. And, afaik (and googled right now) smallpox was a zoonoses, and thus is not a contrary observation. It's lethality was supported because it had an alternate (preferred host).

Basically everything is a zoonosis at some point. I'm not aware that smallpox had a reservoir host: what was it? https://biology.stackexchange.com/questions/90636/is-covid-19-claimed-to-get-less-deadly-over-time-if-so-why/90672#90672 gives starting points for the modern literature on evolution of virulence ...

@StianYttervik: How would killing off humans help a virus spread back to (e.g.) bats? (And, given that evolution isn't intelligent/directed, how would the virus "know" this?)

@ruakh That was a bit of hyperbole, the virus certainly does not know this, neither does a mass of single cell pathogens have any desire or capability of making strategy. The point is that evolution tends to favor the pathogens that multiply, and being too deadly is not a favorable trait. Zoonoses on the other hand have other hosts (bats and rodents for instance) and strain as such is not limited much by being absolutely lethal to humans.

@BenBolker Rodents, I read. But I and a googled result might of course be in the wrong - I am merely an interested chemist - not a virologist.

@StianYttervik: Re: "The point is": Well, no, you made two points: (1) that human pathogens are better off being less deadly, and (2) that zoonoses are better off being more deadly. I'm only objecting to #2. It sounds like you're now retracting your second point (or at least, not interested in supporting it)? If so, then we no longer have any disagreement.

@Ruakh if (2) is how you interpret it, then yes. It's lethality is higher, but only because that lethality is no longer an important evolutionary stress.

To my knowledge, yes. A partial list of recently emerged/emerging viral diseases (I certainly could have missed some), with probable reservoir hosts:

Chikungunya* (birds, rodents)
coronaviruses/sarbecoviruses (SARS [bats], MERS [camels], COVID-19 [?? bats ?? pangolins ??])
Ebola and other filoviruses (Marburg): (bats?)
Hantavirus (rodents)
Hendra, Nipah (bats)
Ross river virus* (various mammals)
HIV (primates)
influenza (H1N1, avian) (birds/pigs)
Lassa fever (rats)
Mpox (formerly monkeypox: monkeys, rodents)
West Nile virus* (birds)
Zika* (? "a wide range of animals in West Africa")

Starred examples are vector-borne (so perhaps of slightly lower concern - might not fit your criterion of "capable of causing a global pandemic").
Omitted:

older zoonotic viruses (rabies, dengue, hepatitis, ...)
non-viral zoonoses (malaria, plague, anthrax, tularemia)

A list of zoonoses; another from US CDC
More generally, the only other place an emerging virus could come from would be from mutation or recombination of existing human viruses. I'm not aware of such an example.

Corrections and additions welcome (I could make this community-wiki)

there are human viruses, it is just a virus that evolves with humans is not going to be that destructive, killing your host is always a bad idea and viruses evolve away from it. https://www.ncbi.nlm.nih.gov/pubmed/14666532

@John evolving away from destructiveness includes cases where a virus evolved into something destructive anyway, but died out along with the population segment that was affected by it. So while destructiveness doesn't persist, there's always the possibility of a short-lived outbreak.

Should the hepatitis family be added to the list?

In the case of monkeypox, there was a 2003 outbreak traced to pet prairie dogs, who were themselves infected by African rodents (two African giant pouched rats, nine dormice, and three rope squirrels were found to be infected), suggesting rodents are a likely reservoir.

@Mast: are there recently emerged strains of hepatitis? A very quick search suggested that at least hepB https://elifesciences.org/articles/36709 and hepC https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0153761 are pretty old.  Pointers to papers on emergence in the last century?

In theory could a virus cross over from plants?

to the would-be editor: mosquitos are the vector of Zika, not its reservoir/original animal host

Tularemia is bacterial, not viral.

thank you .....

Hepatitis D emerged in the past 100 years, without being a zoonosis
Hepatitis D is a virus which is able to replicate only in the presence of a hepatitis B co-infection.  It causes the same symptoms as the hepatitis B virus, but with greater severity and lethality.  In developed countries, it is rare except among intravenous drug users.
It was discovered in 1977, although epidemics of Lábrea fever in the 1950s were later determined to be caused by the virus.  Comparisons of known strains and the mutation rate suggest a common ancestor around the year 1930.
Hepatitis D is the smallest known animal virus (less than 1700 nucleotides), and is the only species in the Deltavirus genus.  There is no known animal reservoir.  The most similar known animal virus shares only 32% of the nucleotides of hepatitis D.
According to its Wikipedia page,

It has been proposed that HDV may have originated from a class of plant pathogens called viroids, which are much smaller than viruses.

Even if indeed this virus originated in plants, is it really true that humans were the initial animal target? That seems exceedingly unlikely, and there are other similar viruses that infect other animals as well.


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Temperature to kill virus
Why do I see only high temperature advice to kill microorganism, and not low temperature?
Why isn't there any low temperature which kills virus? Are they more resistant to low temperature?

To re-create the spanish flu of 1918, they tried to collect it from graves from very cold countries like siberia, because cold temperatures stop most micro-organisms like pause on a TV, and when they wake up, they just keep going.

High temperatures means that lots of energy is available in the environment. This energy speeds up chemical reactions, and make possible some reactions that wouldn't happen at all at lower temperatures. In particular, proteins can adopt new shapes as temperatures get higher. It's the misshapen proteins rather than the temperature per se that kills the microorganisms.
Low temperatures mean there is relatively less energy available in the environment. This slows down or stops chemical reactions, including the ones that result in mis-shaped proteins. Extremely low temperatures may slow down a microorganism's metabolism and stop it from reproducing. That's why we keep perishable foods in refrigerators. However, if you warm the microorganisms back to a normal temperature, most of them will pick right where they left off. A few may be killed by the formation of ice crystals inside the cells that mechanically break the cell membrane.
If you walk into a microbiology lab you'll often see a wall of refrigerators, used to preserve microorganisms for later revival and use.


text:
Using decoy proteins to treat viral illness
As a non-biologist, my understanding is SARS-CoV-2 uses it spike protein to latch on to the ACE2 receptor on cells in order to inject its genetic material into the cell.
Questions:

What would happen if you flooded a person with exogenous ACE2 proteins?
Would the virus attach to these decoy proteins and thereby save cells from being infected?
Would the injected proteins cause unwanted side effects?
Has this approach to treating viral infections been tried before?

Reference:
https://f1000research.com/articles/9-72

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, each question should be posted separately — this improves the chances that you will get answers for each question and makes the answers more accessible for future users. In addition, if you are trying to "start a discussion" this isn't the site you're looking for. Finally, if you've read the linked paper you likely know whether these questions have answers and what they are as well as anyone here. Thanks!

I must admit your comment seems rather harsh. I don't have a biology background and included the paper as hopefully someone could use it to help me answer my questions (I was having trouble understanding it fully). My questions seem quite specific and don't see how I was inviting a discussion? Furthermore, prior to you commenting there was also an upvote.

A relevant article can be seen here.

SE Biology is a site primarily for questions about the mechanisms of biological processes that allow objective answers. Although I understand your concern about the coronavirus outbreak, your question is not about the biology of the virus but asks for comments on a proposal for treating the disease. Such questions about any disease are off-topic here. I suggest that you consult more appropriate reputable sources for such information, some of which are listed here.

This is indeed a reputable strategy (#1,2,4) for rapid response to novel pathogens.  See https://phys.org/news/2020-01-scientists-decoy-molecule-neutralizes-arenaviruses.html and the open access article it cites https://www.nature.com/articles/s41467-019-13924-6
In the case of coronavirus, however, there is an issue (your #3) in that ACE2 is an enzyme that catalyzes the breakdown of a circulating hormone, angiotensin II, which is responsible for maintaining high (or normal) blood pressure.  So the "bait" used would have to be at least somewhat altered from this.  You would probably have to take into account how it affected other protein interactions such as with integrin beta 1 ... (see articles like https://europepmc.org/article/MED/14754895 ) to avoid getting caught up in speculation, it makes sense that a neutralizing protein might be made from part of ACE2 just as a neutralizing monoclonal antibody could be made, but you still have to have something specific before you can test for safety and efficacy.

Thank you very much. This is very helpful!


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How can we calculate the constants of the SIR model?
I am not a biologist by profession, but I am attempting to implement a simple SIR model from the following paper. The paper assumes the following constants are known:
rc    = growth rate of susceptible group S
k     = carrying capacity of susceptible group in absence of infection
alpha = max value of per capita reduction rate of S due to I
a     = half saturation constant
gamma = natural recovery rate from infection
delta = death rate of recovered population
I found some coronavirus data from the following source, and I plotted the Italy data in particular:

Can I calculate the constants above from this type of data?
Is it a good assumptions for these "variables" to be constant?

Here is my attempt of the model with the constants given in the paper

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In particular, this question seems like it might be a better fit for [Bioinformatics.SE].  Thanks!

@tyersome Are you an administrator- can you migrate it please? Thank you

Sorry, I'm not and so don't have that level of access. Is there some reason you can't copy this and post on that site (and then delete from this site)?

I'm voting to close this question as off-topic because it appears to be a question about mathematical modeling rather than biology.


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Where does Embryo Implantation occur?
Where does the embryo get implanted? If it is in the uterus side wall, why is the embryo shown hanging from top in some pictures?

According to Minami et al. (2003)1 (open access) the early gestational sac can be located by ultrasound, and usually is high in the uterus, more often on the left or right than in the middle.  They provide an illustration of the distribution.

 1. Minami, S., Ishihara, K. and Araki, T., 2003. Determination of blastocyst implantation site in spontaneous pregnancies using three-dimensional transvaginal ultrasound. Journal of Nippon Medical School, 70(3), pp.250-254.


text:
Can you explain the behavior of this snake?
I just saw this video in which a snake is swallowing grapes.
 ("Whip snake eating grapes").
In the video, the snake just doesn't eat but goes on to swallow 2-3 grapes.
I did some research on the internet and in "bio stack exchange" but only to find that "snakes are obligate carnivores", which simply means they don't have the body mechanism to digest a vegetarian diet.
My guess is that it mistook the grapes for a prey due to the smell coming from the grapes, which may be left there by a rodent or any other organism the snake feeds on.
Can you provide a possible explanation for this snake's behavior? Regards

Hi, and welcome to the site!  Please don't just include links; they break with time.  Describe the behaviour, including pictures & figures as needful, with the link for reference.  Please [edit] so that this question would make sense even if the link were to break.  Thanks!

@rotaredom Hello, I didn't know about that. Made the changes.

Maybe that's an egg-eating snake that confused the fruits with eggs?

@Roland : Maybe, but my guess is that its something to do with the smell/odor of the grapes. Either the pray (like a small mouse) left its smell on the grapes or certain smell released by the grapes caught the attention of this snake. But I'm not sure..

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@tyersome Hello, thanks for the info. I made the changes to the post. I hope they are in alignment with the Biology.SE format. I also hope that the title and the content are more comprehensive to the reader.

You can convert up to 30 sec of a youtube video to a GIF file using gifs.com. If the resulting gif is > 2mb in size, then I recommend using ezgif.com to "optimize" it (e.g., cropping, reducing quality or size, etc.). In any event, it'd be best to have some stable evidence of your video on Bio.SE, which you can do by uploading the gif in the question editor. You can sill link to your original video, but inclusion of the animation on our site ensures that even if your youtube link dies, this post will still be "complete" and useful to someone in the future. Please [edit] accordingly. Thanks!

You're right, snakes rely on scent to capture their prey. The fact that snakes are carnivores may be the one constant among all snake species; absolutely none feed even partially on plant matter. So if plant matter is found in their feces, it must have gotten there accidentally.
Here, check out this post, which answers your question perfectly:

In most instances, these have been attributed to accidental ingestion, perhaps eaten with a prey item or mistaken for prey by scent...One interesting case was discovered by Harvey Lillywhite in a study published in the journal BioScience in 2008. Studying the scavenging behavior of pitvipers in the intertidal zone, Lillywhite observed cottomouth droppings that were composed almost entirely of seaweed. This was too much plant material to have been eaten secondarily or by accident, and he suspected that there was some other cause for the snakes to be eating it (it certainly wasn't for energy as the seaweed was passing through completely undigested. Lillywhite wondered if it was possible the snakes were feeding on seaweed simply because it smelled like fish. An interesting laboratory experiment proved their hypothesis correct; they offered various plants to cottonmouths, some with fish and others without. The plants without fish were investigated by the snakes, but ultimately left uneaten. Those that did contain fish were quickly devoured. Even when the fish was removed, the snakes ate the remaining seaweed simply because it smelled like their prey!

Thanks. The blog post, as well as the research (mentioned in the blog) conducted on such behaviors of snakes, answered my question very well. Thanks again.

I've seen a deer eating a live bird so a snake eating grapes doesn't surprise me.
My philosophy is that animals know better than us what they are doing, so if someone is mistaking it's probably us.
Anyway, my answer would be that this snake needs a substance (perhaps the acid since it's unrip) contained in those grapes, if it's not for feeding then it's for healing.

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an herbivore eating meat and a carnivore eating plants are very different, all herbivores can digest meat, meat is just far easier for an animal to digest.


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Is the CDC's reported drop today in COVID-19 cases by date of diagnosis meaningful?

I was waiting with bated breath for the CDC update on cases of COVID-19 in the U.S. by date of onset.  To my eyes this looks like absolutely wonderful news - that it means that the exponential growth of the virus has been "flattened" - but I'm still afraid I may be misinterpreting what I see.  It bothers me that the headline for the graph hasn't changed.  But it APPEARS that the number of new cases stopped increasing after 3/3.  Am I missing something?
Top: before noon on 3/16, bottom: after noon on 3/16.  Data from https://www.cdc.gov/coronavirus/2019-ncov/cases-in-us.html
Note: In today's update (the first in three days) the CDC page shows the number of cases with onset on 3/4 to be 159, and 3/9 is 307.  This doubled in five days rather than every two or three as other numbers would suggest, but given the dramatic changes in this curve, and their overall direction, I think the top answer below has been vindicated.

Did you read the text in the gray shaded area?

Yes I did.  And yes, I'm aware that on previous days some cases were added OUTSIDE the gray shaded area.  Nonetheless ... in many countries the number of confirmed cases has been growing about 33% a day.  So I was expecting to see the number of cases just to the left of the gray shaded area be something around 140 to 200 - instead, it is less than 70!  Is that a breakdown in the system ... or the system finally working?

The US has been adding more than 500 new cases a day over the last couple days; these data seem very incomplete. I would wait to have more information before interpreting them much. (There are over 4000 US cases but these data are based only on fewer than 800)

Well, there are more columns on the graph, and no cases were taken out ... yet it is still labelled as 800 cases.  So I don't think that headline is right.  Nonetheless, when I sum up their data table beneath in LibreOffice I get 970 cases, so it is still plausible this is unrepresentative (but if so, why?)

On the page those data are reported, the ** indicates: "Does not include cases among persons repatriated to the United States from Wuhan, China and Japan; does not include U.S.-identified cases where the date of illness onset has not yet been reported." I'm guessing that locations with high concentrations of cases are more concerned with reporting the cases as they come in than determining date of illness onset for everyone. They're probably quite busy.

This is against the experience of all other countries dealing with this disease. So this is most like due to under-testing.

Perhaps worth noting that the CDC is not keeping its public data current.

Any data you get from the CDC will not be current and so not accurately reflect trends. Further, lack of testing in the US means that any data that you do see will not accurately reflect true infection numbers or rates.

The information you show is meaningless unless it is also accompanied by the number of tests performed. If the CDC tested 2 people and got two positive results, that doesn't tell us anything at all about the actual rate of infection. And, indeed, the CDC has been testing a shockingly low number of cases:

‡ Data during this period are incomplete because of the lag in time between when specimens are accessioned, testing is performed, and results are reported.

(image source)
The last day they give data for, 2020-03-15, includes 0 samples from the CDC and 4 samples from other public health labs. Since only 4 samples are represented in the chart, of course we see a drop in cases, but that's because they are based on only 4 tests. As more tests for those dates and subsequent dates are reported, the numbers will change.
Date Collected  CDC Labs    US Public Health Labs
3/12            75‡         2302‡
3/13            0‡          1511‡
3/14            0‡          165‡
3/15            0‡          4‡

As you can see in the table above (from the same source as the graph), the past few days have seen almost no tests are being included in this analysis either from the CDC or elsewhere, so any drop in cases is completely meaningless.

The dates you highlight - from 3/12 on - are within the gray box, which we already know is incomplete data.  The days outside the gray box are the ones more at issue.  I see today's update increased the total cases in the chart from 930 to 1295.  The number of cases on 3/9 was 113, but all the others were less than the peak of now 90 (not 70 any more) for 3/4.  There is something complicated going on here and I think your connection to this other page IS on the right track but it is wrong to say no testing is happening or to link it with the gray box.

@mike what day are you referring to? The truth is, sadly, that the answer won't change. There is no way of looking at these data that could make them be representative of the real infection levels in the general populace, but if you clarify exactly what dip you are referring to, maybe we get get some more detail. – terdon 43 mins ago

Sorry to be confusing - I've gone back and edited the original question to add the third (current) version I was referring to.  Note that there have been cases added, but they have been added throughout the curve - so the 3/4 peak increased, yet 3/5 to 3/8 are still less than that.  So while the reported cases have been increasing exponentially, those at least might be OLD reported cases.  That means the total infected is much higher than we think ... but also leaves open the question of whether recent changes have actually reduced the spread of the disease.

@MikeSerfas any effect of the recent changes will only begin to be visible in a few weeks, not now. The main point, however, is that those data are not really helpful if you are trying to monitor the actual rate of infection because the tests being reported are way, way too few to accurately represent the rate of infection in the population. And, again, the dip isn't informative since there was a corresponding decrease in the number of tests whose results are being reported.

I added another graph from today that continues the trend.  The number of cases is not actually growing as fast as the cases reported for the country at large (the 792 is from before the weekend) but the later days seem like an exponential increase, yet the individual day of diagnosis still seems to have flattened out at 3/4.

@MikeSerfas you're still missing my point. You keep looking at the graph and ignoring the big grey warning on the last days explaining that "Data during this period are incomplete because of the lag in time between when specimens are accessioned, testing is performed, and results are reported." And you also don't seem to be taking into account the number of tests performed. Wait a few days and you will see the numbers for this period will change significantly. I understand the wish to see this flattening but there simply is no data to support that.


text:
Is a nightly curfew an effective intervention strategy for limiting the spread of an infectious disease?
The governing bodies of several geographic areas hit by disease outbreaks will sometimes impose a nightly curfew on their citizens, restricting or limiting the ability of their citizens from going outside during certain hours of the night (or day). As I write this, several United States local or state governments are implementing such strategies in March 2020 to contain the COVID-2019 coronavirus pandemic (Puerto Rico and Hoboken, New Jersey both have nightly curfews as of March 15, 2020).
My question is: does any data exist showing that these measures are effective, or counter-productive? My intuition is that a nightly curfew could actually accelerate the spread of an infectious disease, because citizens who have to leave their homes to do errands are all obligated to do them during a shorter time-window, thereby raising the number of people present in public places at any one time. I couldn't find any published research directly assessing the effectiveness of nightly curfews as an epidemic response strategy. (I only found articles such as this one discussing the failure of nightly curfews in Liberia during the 2014 Ebola epidemic, but those caused public rioting and low compliance). Considering how common this is frequently mentioned and attempted as an intervention strategy, what were the results? Is there any published data from real-world examples, or even results from model simulations?

I'm voting to close this question because it was cross-posted to Medical Sciences.

Cleaned up the comments since they are rather moot now that the question is closed; the discussion can continue on Meta. My personal view is this question is on-topic both at Biology.SE and MedicalSciences.SE, but I'm strongly opposed to cross-posting. A mod at MedicalSciences says it's fine there, so I'd rather close here and instead direct people to https://medicalsciences.stackexchange.com/questions/21448/is-a-nightly-curfew-an-effective-intervention-strategy-for-limiting-the-spread-o


text:
Are there any diseases that can harm and kill flies and mosquitoes?
For decades I have heard about how flies and mosquitoes carry diseases around and infect humans and indirectly kill them in mass numbers. Somehow these diseases do not appear to harm these insects, I am not sure why. This brings me to my question, are there no diseases that infect and harm flies and mosquitoes at any stage of their life? Are there really no microbes that are out to kill them? How is this even possible? I have not found anything related to this yet through my google search.
If the flies and mosquitoes are immune to harm from every disease on earth, then why is this so? Certainly we should be able to find out the secret behind this.

The top result of my search for "pathogen mosquitoes" was this abstract, which shows that there are (as expected) many disease that affect this group of flies. Adding "bacterial" as a search term yielded this article. Similar results are undoubtedly available for other groups of flies ...

My answer to a narrower question on insect diseases contains an example of a disease of the silkworm Bombyx mori.

There are plenty of diseases that affect insects, Dicistroviridae is one.
There are also plenty of fungal & bacterial ones, it's just that they aren't generally of concern to us so study of & information on them is somewhat light.
If you Google 'insect disease' you'll likely just get links for human diseases they're vectors for.
If you want to find links on diseases OF insects (rather than human ones they're vectors for) try refining your search to something that's important or useful to us like bees.
Diseases of the honey bee is the sort of thing you'll get hits for then.


text:
Does a higher body temperature slow the corona virus down?
The corona virus appearantly does not like high temperature:
High Temperature and High Humidity Reduce the Transmission of COVID-19
Also it seems that higher body temperatures helps the immune system to work better: Elevated body temperature helps certain types of immune cells to work better, evidence suggests
Should therefore someone who suspect they may have the corona virus or possibly another cold virus and do not experience fever try to elevate their body temperature slightly (say 0.5-1 degrees celsius) by dressing extra warm?
This is postulated here.
Does this sound plausible to you?

SE Biology is concerned with the mechanisms of biological processes, and questions are generally answered by people with biological rather than medical or epidemiological expertise. Although I understand your concern about the coronavirus outbreak, your question asks for subjective view on measures to avoid the disease. Such questions are doubly off-topic here. I advise you to consult more appropriate reputable sources for such information, some of which are listed here.

SARS-CoV-2 is believed to have spilled over into humans from a Rhinopholus (horseshoe bat) reservoir. During flight, bats' body temperature is maintained at levels associated with fever in other mammals. Rhinolophus bats are reported to reach skin temperatures of 41 C during flight. (From this review which describes why bats might be special sources for zoonotic viruses)
So, this virus is likely adapted to survive higher temperatures than a human host.


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Tools for modelling and visualizing growth of cells
I am looking for a program/GUI app/package that would help me do simulations for cell growth. I have a microscopic mathematical model, and the scenario is basically the following: I start with a rod-shaped cell characterized my its center and direction angle, it grows until it reaches a certain length, it divides into two identical cells whose angles change randomly and the process continues.
Is there any program or package that I can use for such a situation? I have found several on GitHub, but they were mostly for very complicated biological processes. I use Python/Julia/Matlab and can code, but I was wondering whether there are any tools for such simpler scenarios.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In particular, this question seems like it might be a better fit for [Bioinformatics.SE]. Thanks!

Hello, mathematical modeler here.  Some context about your model would be helpful.  It seems like a PDE model, for which, generally, people write their own code.  There are some packages that would help - such as finite difference (or other) numerical approximations for the gradient and Laplacian, but without details it is hard to know where to direct you


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Is Covid-19 likely to mutate into a deadlier form?
When the Spanish influenza hit in 1918, it struck in two waves. The first wave was typical for a flu virus, targetting mainly elderly people, but the second wave was far deadlier and killed far more young people. How likely is it for something similar to happen with the current coronavirus? Also, wikipedia states that people who contracted the virus during the first wave were immune to it in the second wave. I thought when a virus mutates it usually avoids detection, hence why we need to usually get an up to date flu vaccine annually. Why was this not the case for the spanish influenza?

Mutations can have differing effects - in the case of the Spanish influenza it sounds like it was a mutation that changed its symptoms. But not all viral mutations will change such that it gets around immunity.
Based on what little I know of the covid-19, I'd guess it's less likely to mutate than a strain of influenza, but it's hard to know at this point. It's certainly possible that something similar will happen, but I think it's less likely.

SE Biology is concerned with the mechanisms of biological processes, and questions are generally answered by people with biological rather than medical or epidemiological expertise. Although I understand your concern about the coronavirus outbreak, your question asks for subjective view on the future development of the virus. Such subjective questions are off-topic here. I advise you to consult more appropriate reputable sources for such information, some of which are listed here.

The two-wave claim for 1918 flu is getting a lot of airplay recently, but it is at best a hypothesis, not a confirmed truth.

This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology! I'm glad we encourage such questions from curious people who want to learn more.
Mutations are mostly deleterious to begin with. This means that mutant copies of virus only very rarely survive and proliferate. A virus that is deadlier will already be less likely to reproduce, having killed more hosts.
The current estimated mutation rate of the SARS-CoV-2 virus is 24 bases per year. Of those mutations, those to be most concerned about are those which would mutate the proteins specific to this virus. Vaccine development will aim to train the immune system to target those proteins, particularly the S or spike protein.
Mutations to those proteins can make potential vaccines less effective. This is why influenza ("flu") vaccines, which are produced ahead of the flu season, may not always line up against the more prevalent strains which result.
A recent comment was published in Nature, authored by life scientists and epidemiologists, which goes into your question in more detail, as regards to the novel coronavirus:

In this case and that of SARS-CoV-2, mutations consume the narrative, even though individual mutations seldom become fixed during outbreaks nor modulate complex virological traits. Rather, mutation is a humdrum aspect of life for an RNA virus. Because these viruses employ an intrinsically error-prone RNA polymerase for replication, their genomes will accumulate mutations during every copying cycle. Moreover, these cycles can occur on the order of hours, ensuring that a diverse virus population will be generated within a single infected host. While this amazing capacity to mutate fuels the engine of evolutionary change, most mutations adversely impact some aspect of virus function and are removed by natural selection. (emphasis added)

Further, and more to the original point of your question:

These warnings will probably not halt the question as to whether mutations will arise in SARS-CoV-2, enabling it to spread more efficiently between humans or generate a higher case fatality rate. In response, we can look to the 2002–2003 SARS-CoV epidemic. Large deletions in the open reading frame 8 (ORF8) region and mutations in the spike (S) protein were discovered during the early stages of the outbreak and eventually dominated the epidemic, suggesting that these were adaptations to humans12,13. Based on this observation, some hypothesized that virus genetic changes in part drove the SARS epidemic, but this claim is unsubstantiated14. So, could SARS-CoV-2 adapt in the same way? Yes. Will adaptation precipitate more deaths? Unlikely. (emph. added)


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what is this marine creature?
I found this creature floating in the Mediterranean Sea, probably dead.
I tried looking it up in the Marine Species Identification Portal but I couldn't find anything like that. It looks like some kind of jellyfish or hydrozoan.

This is a blue button jellyfish! they eat zooplankton and are usually found drifting along on currents
they aren't true jellyfish and just like a jellyfish have no blood, brain or nervous system. they aren't usually toxic enough to hurt but can cause irritation to the skin.
they live in warm waters off of Europe and in the golf of Mexico and the Mediterranean.
they are hermaphrodites and have both male and female reproductive parts. they lay eggs which turn into polyps
here is a website I found all about them as I'm not extremely knowledgeable on this species.
https://www.thoughtco.com/blue-button-jelly-porpita-porpita-2291819

Welcome to Biology.SE! While your answer seems reasonable, you are more likely to get a positive response if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion and (contrary to best practices) requires users to follow a link. ——— Thank you for taking the [tour], but please also consult the help pages for additional advice on [Answer] effectively on this site. Thank you!


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How does sunlight affect the longevity of SARS-CoV-2 on surface?
UV radiation is known to degrade most viruses rather quickly.  How does the UV radiation from sunlight affect the longevity of SARS-CoV-2 on surfaces.
Of particular interest to me is the virus' lifespan on gas pump handles, which are typically in covered but open spaces.

Please see here.

@David Thank you for the links, though they do not answer the question.  There was one FAQ question om the WHO which pointed out that UV light should not be used to sterilize skin, but that's because it irritates the skin rather than due to its effectiveness.  Another article from NIH points to it lasting hours-to-days on surfaces, but does not state any effect of UV.  I had seen both articles in doing research before posting, although I have to admit that was quite the nice collection of COVID-19 links!

I have no data on SARS-CoV-2 specifically, but for SARS-CoV UV radiation is an effective method of eliminating viral infectivity:

Irradiation of UV for 60 min on the virus in culture medium resulted in the destruction of viral infectivity at an undetectable level.
CONCLUSION: The survival ability of SARS coronavirus in human specimens and in environments seems to be relatively strong. Heating and UV irradiation can efficiently eliminate the viral infectivity.

Stability of SARS coronavirus in human specimens and environment and its sensitivity to heating and UV irradiation., Biomedical and Environmental Sciences (2003)

Yes, UV light is effective in killing all the viral and bacterial cells. And it is believed that UV-C  will be effective in disinfecting SARS-CoV2 which is responsible for Covid 19, as earlier it is reported that UV-C disinfection can degrade viruses which are similar to SARS-CoV2 virus (like SARS-CoV1 and MARS-CoV).
But, the effectiveness of UV disinfection is dependent upon exposure time and intensity. So, sunlight could not disinfect the gas pump handles which are not directly exposed to sunlight. Effect of heat due to sunlight is another factor which may be responsible to inhibit virus growth.
(Via: http://www.iuva.org/COVID-19)


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How is the protease inhibited by lopinavir different in SARS-CoV-2 compared to SARS-CoV?
The protease inhibitor lopinavir, originally developed as a cure against AIDS and HIV, has been shown efficient against SARS Coronavirus SARS-CoV.

Dayer M R, Taleb-Gassabi S, Dayer M S. Lopinavir; A Potent Drug against Coronavirus Infection: Insight from Molecular Docking Study, Arch Clin Infect Dis. 2017 ; 12(4):e13823. doi: 10.5812/archcid.13823.

Why is Lopinavir not efficient against SARS-CoV-2? Is there a difference in the gene encoding for the protease?

Is there a difference in the gene encoding for the protease?
This paper by Wu et al. annotates the SARS-CoV-2 genome and compares its divergence from other coronaviruses, which may help answer your second question.
This annotation includes 16 genes for non-structural protein ("nsp"). Supplemental materials for this paper indicate that all but two of these proteins (nsp7 and nsp13) have amino acid substitutions between SARS-CoV-2 ("2019-nCoV" in the paper) and SARS-CoV.
The gene nsp5 encodes 3CLpro (chymotrypsin-like cysteine protease), so there are differences there.
Literature suggests nsp5 and other non-structural proteins are potential targets for a number of antiviral therapies.
Another paper suggests further that lopinavir targets nsp3 products, among other proteins, in use against SARS-CoV:

Lopinavir’s possible target is Nsp3b, Nsp3c, helicase, NRBD or E-channel with the mfScores of –158.050, –189.140, –114.018, –171.127, and –221.785, respectively.

The nsp3 gene contains a papain-like protease 2 (PL2pro) domain. Supplemental materials from the first linked paper suggest nsp3 has a different amino acid sequence between SARS-CoV and SARS-CoV-2.
It might be worth digging into the Wu et al. paper and the raw annotation data to look at what those a.a. substitutions are, to see if that might help in determining why lopinavir is not as efficient at inactivating PL2pro and reducing levels of the novel coronavirus.
It may also be worth considering the target itself. Going back to the Nature Biotechnology article:

But Erik De Clercq, of the Rega Institute for Medical Research in Leuven, Belgium, says that in searching for or designing effective drugs against COVID-19: “We should stay away from antivirals known to be acting at targets not playing a role in the replication of coronaviruses.” Such drugs include penciclovir, which is targeted at the herpesvirus DNA polymerase, and lopinavir/ritonavir, which are targeted at the HIV protease. Instead, he would favor targeting a virus-specific protein such as the RNA-dependent RNA polymerase, noting that coronaviruses do not contain or use a reverse transcriptase.


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How exactly does DNA polymerase III detect a mismatched base?
How exactly does DNA polymerase III detect a mismatched base? I know how it removes it, via exonuclease activity, but how does it 'detect' it molecularly in the first place?


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Diastole/systole pressure in transcapillary circulation
The Starling equation factors in hydrostatic pressure and oncotic pressure. Given that the hydrostatic pressure in capillaries is pulsed, alternating between systole and diastole, does reabsorption tend to be favoured in diastole (low hydrostatic pressure, low volume from filtration in systole and therefore high concentration of colloids i.e. high osmotic pressure)?


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Viral mutation rates and replication
TL;DR
What's the relationship between the following?

Mutation rates (expressed as "mutations per year" for a virus like e.g. COVID-19 (SARS-CoV-2). E.g. this article mentions "The rate looks to be about 24 mutations per year"
Actual virion replication error rates in a single host cell, measured as e.g. error rates per released virion from the infected cell, i.e. (# of mutated released virions) per infected cell.

Assumptions
I would assume that mutations happen at a single virion-cell level because there are differences in e.g. nucleotides in RNA  between:

the virion infecting a cell (e.g. ACE2 for SARS-CoV-2)
the released virions from that same single cell

If so, wouldn't one argue that:

replication errors (at the nucleotide and thus released virion level) can easily happen, potentially billions of times during the infection of a single host organism
there is no "single successful" mutation or RNA variant within a host, rather, we have a distribution of RNAs, many of which could be simultaneously transmitted to another host organism?

Further context
I quote from e.g. this paper:

On a per-site level, DNA viruses typically have mutation rates on the order of 10E-8 to 10E-6 substitutions per nucleotide site per cell infection (s/n/c). RNA viruses, however, have higher mutation rates that range between 10E−6 and 10E−4 s/n/c

Again, wouldn't that mean that a single host could 1) easily generate many mutations of the same virus and 2) pass most of those uniquely generated mutations to another host? If so, how come we can simply say "24 mutations (over time) per year"?

Only those mutations which are themselves viable can be passed on. Most mutations are deleterious — evolutionary dead-ends, which do not reproduce. Thus you get a substitution rate calculated from the population of mutants that can reproduce.

Thanks @AlexReynolds but isn't it fair to say that on any single organism, you would still have a population (distribution) of viral RNAs, and not a single (even if dominant) mutation?

@AlexReynolds That sounds more like an answer than a comment.

Hi Amelio, I'd suggest taking a look at the difference between mutation rates and substitution rates, which is a subtle difference in terminology but which may help get a better comment to address your question. Hope this helps!

+1 I did here Thanks @AlexReynolds

Since no one else has done so, just gonna expand on what occurred here in the comments (mostly from @Alex Reynolds):
tl;dr: natural selection exists.
Longer version:

Mutations/replication errors/whatever will happen in the creation of new virus particles within a host cell. There is some distribution of number of mutational events that will occur as a function of the number of new RNA molecules created per cell and the replication error rate. Some subset of these RNA molecules will be packaged into new particles, yielding a new generation of viruses that get a chance to infect. Yes, this is potentially a large number of new mutations per infection event.
Some large proportion of these new particles will contain non-functional RNAs, due to inactivating mutations of one kind or another. Most of the new mutations will be worse at being a virus than the originally infecting virus (their immediate parent). So therefore, they will be outcompeted by non-mutated forms.
Among all those viruses which continue successfully infecting throughout the course of a year, on average we observe 24 substitution mutations in the genome over the course of that year. Every transmission chain included in the group of viruses at the end of the year must have remained viable for infection of hosts. In other words, it has survived natural selection.

In population genetics, this phenomenon is known as "mutation-selection balance"- e.g. new mutations arise in the population at a rate that is limited by the action of natural selection (at equilibrium).
Genotype-phenotype maps
What of course I am leaving unstated is exactly why "...new mutations will be worse at being a virus than the originally infecting virus..."
This is very hard to predict in many cases. In some cases it is very obvious why a mutant is bad at being a virus, if e.g. an essential gene is deleted from the RNA genome. But for many single mutations we don't really understand what their effect will be on virus function, we just observe that they drop out of the population due to negative selection.
If you are interested in this question, I recommend looking into genotype-phenotype maps. I know Jesse Bloom has done some work on influenza in this field, here is one example of such a paper. It is generally extremely laborious to do this kind of work, so relatively little is known about the functional effect of any specific mutation in any specific genome.
Hope it is helpful to have all that written out.

Thanks! This is perfect, and confirms exactly what I thought (the terminology here was confusing me so this is great!). Does the literature really use the term "mutation rate" to refer to both: 1) "population genome" mutation rates (for lack of a better term)  and 2) "per replicating virion" mutation rates?

There are many different mutation rates in the literature, and each of them has its purposes. For example, there is the "population mutation rate", https://en.wikipedia.org/wiki/Watterson_estimator, the rate at which new mutations arise at a site in a population. There is also the "mutation rate" which is closer to the "replication error rate", which is the rate at which mistakes/new nucleotide variants occur. There is also what is sometimes called the "substitution rate", handled elsewhere. And more. All have their proper domains, but figuring out which one to use can be confusing.


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Can COVID-19 affect a person a second time?
I keep hearing people are recovering from COVID-19 virus. Is there any chance that same person can become infected with COVID-19 for a second time?

Please see here.

Does this answer your question? Human Immune Response to COVID-19 Virus

Short answer: Although there are some reports on this, it is pretty unlikely. It is more likely that patients where released too early from hospital, developed further symptoms later on and got worse, was re-hospitalized, tested again for SARS-CoV2, which was positive and counted as re-infected.
Another possibility is that a false negative test happened, when people got re-tested later the test was positive again and the patient was counted as re-infected. Given the rising number of cases worldwide this should become evident pretty soon, if this is a real problem and not an artefact. For the moment, I don't think there is enough evidence for the re-infection of the same patient in such a short time period. If this holds, future will tell.
Long answer: There is now an experimental paper, which infected rhesus macaques with SARS-CoV2, tested if the infection was similar to humans happening in the upper airways (which it was), and re-infected the animals after 28 days with a really high dose of virus (which is much higher than what comes around in our environment), with none of the macaques getting re-infected or showing pathological signs of the infection. See reference 1 for details.
This article has its limitations with small sample size and the general questions if the chosen animal model is really comparable with human.
Additionally it looks very much like that patients who are recovering don't shed infectious virus anymore. The PCR test however does not discriminate between infectious virus and plain virus RNA, so it is most like much longer positive than people are infectious. They also show the rapid appearance of specific antibodies, which would at least temporarily protect against a re-infection. See reference 2 for a nice summary and reference 3 for the original article.
References

Reinfection could notoccur in SARS-CoV-2 infected rhesus macaques
People ‘shed’ high levels of coronavirus, study finds, but most are
likely not infectious after recovery begins
Clinical presentation and virological assessment of hospitalized
cases of coronavirus disease 2019 in a travel-associated
transmission cluster

Edit (24.11.2021):
Being 1,5 years further into this pandemic there are clear signs now that reinfections are possible, although it was first thought it should not be a concern. There are a few reasons for this, mainly the occurence of new, much more infectious viral strains (Delta variant), waning of the immune respone (in vaccinated and also people who got infected), weak immune responses at all (reinfection probably occurs in connection with the Delta variant). Following reference 4 (thanks to @bob1 for the hint) below, it seems that reinfections are less severe than primary infections.
For more information please have a look into the additional references below. This shows very well the problem with an unknown pathogen and the rapidly ongoing research on it.
Added references (24.11.2021):

Risk of SARS-CoV-2 reinfection after natural infection
The durability of immunity against reinfection by SARS-CoV-2: a
comparative evolutionary study
Prospects for durable immune control of SARS-CoV-2 and prevention of
reinfection
Severity of SARS-CoV-2 Reinfections as Compared with Primary
Infections

Update: Coronavirus reinfection has been reported in India for the first time. See this news: https://www.google.com/amp/s/www.timesnownews.com/amp/india/article/first-case-of-coronavirus-reinfection-reported-from-bengaluru-27-year-old-woman-affected/648563

And in US: https://indianexpress.com/article/coronavirus/first-us-covid-19-reinfection-case-identified-in-nevada-study-6574428/

@NilayGhosh I have read newspaper articles about this as well, but I would like to see a scientific paper first, before I update this answer. I am following this :-)

Good answer.  There's an interesting paper in NEJM today on severity of infection in re-infected patients, that might be worth including.

@bob1 Thanks for the hint, this looks indeed interesting. I will include this as well.


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Could blood transfusions from COVID19 surviver be worth researching as a possible form of treatment
As a general viral immunology question (rather than seeking personal medical advice).
Would a blood transfusion from a COVID19 surviver to a sufferer be worth researching as a possible form of treatment? There is evidence in other animals (elephants) that blood transfusions are beneficial against viruses.
BBC Chester zoo
More specifically would lymphocytes and other cells able to attack the virus from the donor outweigh the resulting increase in virus burden caused by adding the donors blood into the sufferer? and how does the is change over time from the time of the survivers recovery?
Needless to say this procedure risks crossing strains of COVID19 and other risks so would need thorough analysis of such risks before being practiced.

Please see here.

ok reworded they question

I don't know why this was closed; it is easily answered: https://www.nbcnews.com/health/health-care/doctors-push-treatment-coronavirus-blood-recovered-patients-n1158476  https://www.reuters.com/article/us-china-health-hospital-idUSKBN20B1M6  This is "convalescent serum" - a form of passive immunity


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Is it red blood cells or white blood cells that fight infection?
This article has me very confused;
https://www.dailymail.co.uk/science...-blood-likely-catch-coronavirus.html#comments
It's implying that red blood cells (ABO blood groups only affect the surface of red blood cells, but not white blood cells) fight disease, with type A being the weakest, and I've been reading that this is blatantly wrong, since it is white blood cells that are involved in the immune response, not red blood cells, and thus blood type would have no effect on the course of an infection because red blood cells aren't involved in fighting diseases and blood groups don't affect the internal workings of a red blood cell anyway.

That's bullshit. Red blood cells have only one function and this is the transport of oxygen. One advice: Stop reading Daily Mail as this is not a serious source.

@Chris the article referenced this study - medrxiv.org/content/10.1101/2020.03.11.20031096v1 I'd like to know your thoughts on the results.

It's one report so far, and the numbers are not so much different. Only because there seems to be a correlation doesn't mean there is a real causation. The study is also only descriptive without giving any hypothesis on a possible mechanism. It looks very much to me like a very fast publication to be the first. I would be very cautious here.

I somewhat like the Daily Mail - they vacuum up information indiscriminately and empty it out at your feet.  Provided you are willing to think critically, you should be alright.  This report is also found at https://www.scmp.com/news/china/society/article/3075567/people-blood-type-may-be-more-vulnerable-coronavirus-china-study and traces back to the preprint at https://www.medrxiv.org/sites/all/libraries/pdfjs/web/viewer.html?file=/content/medrxiv/early/2020/03/16/2020.03.11.20031096.full.pdf
Note that Medrxiv is a preprint server - the papers are not peer reviewed - hence it is another source of delight for the critical and skeptical thinker.  This preprint comes from a most respectable and prolific source, but one under great pressure to publish quickly for the sake of the world.  In my opinion, the authors err in their statistics - I think they assume that the odds of getting 42% instead of 32% type A blood in a sample is the odds of a group of individuals selected randomly from a large population having that much of a skew, so it seemed significant.  However, if the market at Wuhan was favored by people of certain ethnic extraction, or even if there were some extended family groups in the sample, the odds of seeing this effect by chance might be higher.  I won't fault them for publishing the study because people in other countries SHOULD look to see if there is a correlation in their hands.  But I don't think the paper would have passed a traditional peer review.