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What gene targets associated with the new coronavirus (SARS-CoV-2) have been identified so far?
One hypothesis for which we have some supporting evidence is that the new virus (SARS-CoV-2) "enters human cells through an interaction with angiotensin-converting enzyme 2" see here. Although it is still unclear what genes to target in order to prevent the infection (entry or reproduction).
Is there empirical evidence suggesting what genes can be modulated to fight the infection?

The linked article does not suggest "targeting the gene that modulates ACE2"...I think you've misunderstood.

Hi thanks for your comment. Could you please expand

"The researchers concluded that their research could contribute to structure-based designs of decoy ligands or antibodies able to specifically target ACE2 or coronavirus spike proteins to prevent viral infection." - They're talking about making decoys that look like ACE2 (virus binds these rather than real ACE2), or antibodies that bind ACE2 or the coronavirus spike protein. Antibodies that bind ACE2 sounds like a horrible idea to me and one they probably didn't think through too much.

This is an interesting question. A recent study published on bioRxiv by researchers from Xi'an, China (pre-print) argues that CD147 can also be an entry receptor for the virus. They showed virus entry can be blocked by an antibody to human CD147.


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Why are victims of Covid19 being wrapped in plastic?
Several articles describe the unique ways Covid-19 patients are being buried.
For example, in this Reuters article about Israel:

These included decontaminating and hermetically wrapping bodies in
  double layers of polyethylene. For Jewish dead, ritual washing of the
  body would be conducted in one of four special stations in the
  country, the document showed.

And this LA Times article about Iran:

Nor are they wrapped in traditional white cloth. They are covered in
  hospital plastic, marking them as victims — both young and old — of
  the coronavirus.

People die from viruses all the time but I've never heard of victims being buried in this way. What is unique about Covid-19 ?

The WHO guidelines for VHF victims (Ebola etc.) do say that they should be buried in body bags, and if those are not available, in plastic sheeting.

If body bags are not available, wrap the body in two
  thickness of cotton cloth and soak with 1:10 bleach
  solution. Then wrap the body in plastic sheeting. Seal the
  wrapping with plastic tape. Spray the body bag as in
  Step 3. Place the body in a coffin if one is available.

Obviously some are treating covid-19 victims with the same amount of caution. I can't tell you at the moment if this is justified or not.

I suppose we might see copper-lined coffins soon.

source: Stack Exchange

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

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Why don't anti-viral drugs like "Acyclovir" work against coronaviruses?
I've always used Acyclovir to treat cold sores, why doesn't it work on other viruses?
How do coronaviruses differ from herpesviruses?

Aciclovir specifically targets HSV-family viruses.
It is metabolized by a viral-specific enzyme into an inhibitor of the specific DNA polymerase expressed by the virus:

in infected cells, HSV or VZV coded thymidine kinase facilitates
  the conversion of aciclovir to aciclovir monophosphate, which is then converted to aciclovir triphosphate by cellular enzymes. Aciclovir triphosphate acts as an inhibitor of and substrate for the herpes specified DNA polymerase, preventing further viral DNA synthesis.

https://www.ebs.tga.gov.au/ebs/picmi/picmirepository.nsf/pdf?OpenAgent&id=CP-2009-PI-00595-3
Other viruses don't express these specific enzymes, and even if they have similar enzymes they may not interact the same way with the drug. Even within the herpesvirus family, the drug is not equally effective against every virus.
Coronaviruses are RNA viruses, so even though the drug is not effective for DNA viruses outside the herpesvirus family, coronaviruses are definitely not going to be affected because they don't even have a DNA polymerase to inhibit.

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


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Large study showing that attraction to only the same sex has to do with your genes, published where?
Can someone please help me out and find and link me the study from a couple of years ago that showed how only same sex attraction, when the male cant become attracted to a woman, it has to do with genes?, it was a large study and a first of its kind, maybe from 2016-2019, i am not talking about the big study from 2018 by Andrea Ganna about not finding any single gene that explains sexual orientation.

Is it this? https://www.nature.com/articles/s41598-017-15736-4

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

No thats not the one. They said that it was the largest study of its kind, and i think they might have mention DNA besides the word genes also but i am not sure, i know it was a very big studie that looked at genes/DNA in a new way. It seems like not many places wrote about it and then the other study by Andrea Ganna came and everybody wrote about that so its hard to find it now i have looked a long time.

Have you looked at the references section in the Ganna study? If this is as large a study as you say, it may well be referenced there, and the date range may help you drill down to what you're after.

Nope its not there, i think the both studies where done very close in time and thats why. Only the Ganna study got any real news.

I'd suggest scanning the reference sections of as many related papers as you can. You have a known time window to limit your search to some reasonable possibilities.

Possibly https://science.sciencemag.org/content/365/6456/eaat7693.long is what you were looking for?  It implicates a few specific genes - the connection to olfaction is interesting (I would suggest it could be fun to look up the vomeronasal organ, terminal nerve, and GnRH).  [Alex Reynolds' suggestion of https://www.nature.com/articles/s41598-017-15736-4 is highly useful for those reading, even if it wasn't what you were looking for.  https://www.sciencedirect.com/science/article/pii/S0091302219300585?via%3Dihub is also potentially useful]


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Where can I find the genome of the L-strain coronavirus and the S-strain coronavirus?
I read an interesting article about two strains of the coronavirus:
https://www.newscientist.com/article/2236544-coronavirus-are-there-two-strains-and-is-one-more-deadly/
I would like to know how the scientists used to classify a coronavirus as l-strain and s-strain.
And more specifically I would like to have the genome(The DNA) for a l-strain and a s-strain.

“Two of the key claims made by this paper appear to have been reached by misunderstanding and over-interpretation of the SARS-CoV-2 data, with an additional analysis suffering from methodological limitations ... Given these flaws, we believe that Tang et al. should retract their paper, as the claims made in it are clearly unfounded and risk spreading dangerous misinformation at a crucial time in the outbreak." —Response to “On the origin and continuing evolution of SARS-CoV-2”

Article links to this publication which has all the information needed:
https://academic.oup.com/nsr/advance-article/doi/10.1093/nsr/nwaa036/5775463
It is mentioned in the paper that:

Although we found only 4% variability in genomic nucleotides between
  SARS-CoV-2 and a bat SARS-related coronavirus (SARSr-CoV; RaTG13), the
  difference at neutral sites was 17%, suggesting the divergence between
  the two viruses is much larger than previously estimated.

Their results highlight evolutionary changes in the development of new variations in functional sites in the receptor-binding domain (RBD). These developmental variations have a spike in changes to the RBD of SARS-CoV-2 and viruses from pangolin SARSr-CoVs
How do they define S and L variations?
They did population genetics on 103 available SARS-CoV-2 genomes.
These two major types are well defined by two SNPs which show complete linkage across the viral strains.
It also important to mention that SARS-CoV-2 was found to have 96.2% similairty to a bat SARS-related coronavirus (SARSr-CoV; RaTG13) but not very similar to SARS-CoV (79%) or MERS-CoV (50%).
How do we know that there's two type?
We know there's two types because from the 103 sequenced genomes two SNP locations show significant linkage. These are SNPs at location 8,782 (orf1ab: T8517C, synoniumous) and 28,144 (ORF8: C251T, S84L).
If you have a "CT" (as in base pairs) haplotype SARS-CoV-2 you've got the L-type ("L" type because T28,144 is in the codon of Leucine). Otherwise, if you've got a "TC" haplotype you have the S-type (C28,144 is in the codon of Serine).
They found that S-type is the ancient (less aggressive version) by aligning it with other older viruses. In fact for each variant of the virus the ancestral state was inferred by alignments of SARS-CoV-2 (NC_045512), RaTG13, and GD Pangolin-Cov.
So to be more precise on my answer for finding S and L types. You sequence the genome of an infected individual (you can find these online on NCBI) align it with the current reference sequence (MN908947, NC_045512), look at the SNPs and figure if they have a "CT" or "TC" haplotype to determine S or L type.

I downloaded the complete genome of MN908947 and NC_045512.
They are both identitical.
Aren't they supposed to be different?

The paper was a little confusing on that. I aligned them and you're right. I changed my answer to reflect your question better.

I downvoted this answer because it doesn’t point out that the notion of two biologically significant strains is nonsense, the product of incompetent researchers messing with things they don’t understand. See genuine experts’ opinion in Response to “On the origin and continuing evolution of SARS-CoV-2”

Understandable, I'll read the linked page and see if I can add more clarity to the answer with more correct research. Feel free to edit/modify my response or add a new one.

Hey you were really useful in answering this question. Could you help me with another similar question? I would really appreciate it!
https://biology.stackexchange.com/questions/92383/how-can-i-classify-the-3-cladess-g-v-of-the-coronavirus-that-are-found-on-gi

I know it's been a while, but in case anyone comes back to this: since the beginning of the pandemic, many tools have been developed to help identifying lineages and clades.
L-Strain corresponds to Pango lineage B and descendants including all VOCs like Alpha, Delta and Omicron.
S-Strain corresponds to Pango lineage A and descendants (and Nextstrain clade 19B).
To find out if something is A/B, just drop them into Nextclade and check the Clade column. Everything is L, unless it says 19B:

In this example, the sequences with id #2, #3, and #4 are S, everything else shown is L.
Disclosure: I'm a Nextstrain/Nextclade developer.


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Are there any detrimental effects to long term electrical muscle stimulation?
I know that different types of electrical stimulation can be used in fields such as physical therapy to get muscles to contract. However, these electrical stimulation sessions are not prolonged and contiguous.
Does anybody know if stimulating muscles to contract and retract for an extended and continuous period of time has negative side effects? Does it damage the muscle? Nerve?


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Absent gene expression from one of two vectors co-transformed into the BL21(DE3) strain of E. coli
I've been trying to express two proteins in the BL21(DE3) strain of E. coli.
One gene is in a pCR2.1 vector and the other in a pET-expression vector. When I induce with IPTG and run on an acrylamide gel I only get the protein encoded in the pCR2.1 construct. If I transform the BL21(DE3) cells with each vector independently (only one of the plasmids in the cells) I can get expression for either protein.
Does anyone have any Idea why I wouldn't be able to induce expression from the pET vector in the double plasmid strain but can induce expression from either vector in single plasmid strains?

I edited you post in a way that I hope makes things a bit clearer. ——— Some suggestions for [edit]s to your post that may help you get a better answer would be to include answers to the following questions: 1) How are you ensuring that both plasmids remain in the co-transfected cells? 2) What are the proteins you are expressing and are they known to interact with each other in any way? 3) Would the way you prepare your protein samples for PAGE effectively solubilize proteins that were in inclusion bodies?

the use of two antibiotics kanamycin and  chloramphenicol, 2)the proteins being expressed are NPR1 in the pCR2.1 (protein related to systemic acquired resistance in arabidopsis) and TGA3 a transcription factor in the pET vector. The two proteins have been shown to interact in Y2H. But didn't interact in the pull down assay since the TGA3 wasn't induced. 3) I don't think it has anything to do with insoluble aggregates since in the single plasmid strain we see the TGA3 protein. Thanks @tyersome .


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Why does Porous-tube Nutrient Delivery System cultivation improve nutritional quality of Okinawa spinach (Gyruna bicolor)?
I wrote a review paper and it involves in growth system of a plant “Okinawa Spinach (Gynura bicolor)”. A research of (Wang, Fu, & Liu, 2015) reported that Porous-tube Nutrient Delivery System (PTNDS) cultivation enhanced calories from 139.5 to 182.3 kJ/100 g dry matter, and carbohydrate from 4.8 to 7.3 g/100 g dry matter and reduced the amount of protein from 7.3 to 4.8 g/100 g dry matter and ash from 1.4 to 1.0 g/ 100 g dry matter, compared with hydroponic culture. PTNDS cultivation also accumulated the nutrition elements of Ca, Cu, Fe and Zn, and reduced Na concentration.
The reviewer asked me that “why the plant grown in PTNDS reduced the total ash but why improved accumulation of Ca, Cu, Fe and Zn.? “My major is food engineering and I’m not expert in this field.
If this area is your expertise or someone knows the answers? Please help me out with it. Thanks very much.
Wang, M., Fu, Y., & Liu, H. (2015). Nutritional status and ion uptake response of Gynura bicolor DC. between Porous-tube and traditional hydroponic growth systems. Acta Astronautica, 113, 13-21.


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What differentiates diseases like Covid-19 and Polio from the common cold
Why are vaccines required for our body's immune system to destroy viruses that cause the likes of Covid-19 or Polio, while viruses that cause the common-cold are self-limiting (go away on their own)? What is so different about viruses that cause diseases requiring vaccines?

"..while viruses that cause the common-cold are self-limiting (go away on their own)" You heard of the human immune-system and antibodies - right? But to partially answer your question: Certain strains and their mutations are more 'contagious' and more 'viral' (have a higher virality) than others..

"Why are vaccines required for our body's immune system to destroy viruses"...no, vaccines are not 'required' for anything.  Most people infected with Covid 19 are recovering fine with no special medicine, so it is self-limiting in most people.

@swbarnes2 Thanks for the response! Sorry, you're right that a vaccine isn't necessary for the viruses. However, viruses that cause the common cold doesn't cause a pandemic, while the virus that causes Covid-19 does. With relation to the human's immune system, what can be attributed to that difference? I'm sorry if this question sounds silly...

It's not that polio &c don't "go away on their own" - or more accurately, are defeated by the immune system, it's that they cause lasting damage that persists even after the active infection is controlled.  The common cold just causes a bit of sneezing and runny nose, but the polio virus damages nerves.

There is not really an inherent difference between these viruses.  Polio is a run of the mill enterovirus - some of its closest relatives are "common colds", while others are less pleasant - see https://www.slideshare.net/TarekMahbubKhan/enteroviruses-and-polio for some examples.  Note that some "common cold" viruses have uncommon but nonetheless devastating polio like effects; a leading culprit for acute flaccid myelitis (polio-like paralysis) was the common cold enterovirus D68 ( https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(18)30094-X/fulltext but I haven't checked for updates lately).  But for that virus, damaging replication in nerve tissue is at most a rare complication rather than a frequent one.
Coronavirus has long been known for several strains of "common colds"; they were just not as frequently deadly.  Unfortunately, we did not see the "cold and flu season" as a demonstration of defenselessness against viral outbreaks, and did not use the opportunity to practice exterminating them.


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What's the difference between mutation and substitution rates?
The Wikipedia section on substitution rates (shown below) isn't clear to me. What's the precise definition and difference between mutation and substitution rates, and how do they relate to each other?

Substitution Rates
Many sites in an organism's genome may admit mutations with small fitness effects. These sites are typically called neutral sites. Theoretically mutations under no selection become fixed between organisms at precisely the mutation rate. Fixed synonymous mutations, i.e. synonymous substitutions, are changes to the sequence of a gene that do not change the protein produced by that gene. They are often used as estimates of that mutation rate, despite the fact that some synonymous mutations have fitness effects. As an example, mutation rates have been directly inferred from the whole genome sequences of experimentally evolved replicate lines of Escherichia coli B.

Further context behind this question here.

@Tyersome's answer is correct if you consider that the only mutations that occur will result in substitutions. This is false for biology, if true for how the subject is commonly talked about. (I realize that I'm in the uncomfortable position of saying that Rich Lenski is being imprecise about his evolutionary terminology). In fact probably a rather larger proportion of mutations will result in other kinds of DNA modifications.
For those unfamiliar with the different kinds of mutations, substitutions (also called point mutations) are only one class of mutation. Other kinds include transpositions, inversions, insertions, deletions, and many many more.
In other words, the "mutation rate" is probably >2X higher than the "substitution mutation rate", and I suppose since I'm getting very involved with my terminology, we could then say that there is an "accepted substitution rate" (the same as the "substitution rate" that people talk about) and an "accepted mutation rate" which includes all substitutions but then also all other kinds of mutations that are incorporated as laid out in the quote above. (I have made up all the terms other than "substitution rate" and "mutation rate" to emphasize that I think the usage of terminology from the Barrick and Lenski article is extremely misleading).
We tend to focus on substitutions because they are easy to understand and our math works well for them. Thus when people write about the "mutation" rate they have a tendency to use it to mean the "mutations that lead to substitutions" rate. But that's an approximation for mathematical convenience rather than reflecting real biology.
It's good to recall that when Hugo de Vries wrote "The Mutation Theory" >100 years ago the mutations he was talking about were not substitutions but changes in ploidy- those are absolutely mutations, but they have nothing to do with substitution. In plants changes in ploidy are among the most phenotypically dramatic class of mutation, but those are invisible to analysis of substitutions.
Of course, the approximation for mathematical convenience has more or less taken over the field, so from that perspective @Tyersome's answer is perfectly correct, and it does directly address your specific question. But I think that there are problems with how the field in general thinks about this.
(Forgive me for being pedantic, I wrote a review on the topic: https://www.cell.com/trends/genetics/fulltext/S0168-9525(19)30012-5)

Thanks Maximilian. Very helpful. I noticed you introduced several terms here that would be great to define more precisely (e.g. you mentioned "substitution mutation rate", "accepted substitution rate",  and "accepted mutation rate", not sure if there are others). Perhaps this could be an answer with a preamble that describes the basic entities, mechanics and steps involved, followed by definitions with their corresponding Eqs. I would love to help if you can point me to the right info. This is a good time for people to learn more and become more interested inabout virology / genomics :).

updated answer to reflect that these are terms that I made up on the spot, to underline how Barrick and Lenski's "mutation rate" is actually just one way people use that term.

(I also clarify that "substitution" has a very specific meaning in terms of the kind of modification to DNA that occurs)

Ok thanks. That's helpful. I think I get it now. From what you are describing a substitution is just one type of change (a single point nucleotide change specifically). I somehow understood "substitution" to mean directly the "acceptance" (i.e. take over) of an entirely new chain, i.e. a whole new chain   "substituting" (displacing) a chain (e.g. a viral strain) that is prevalent in a population. What you are saying makes sense, i.e. there many other types of changes that can take place in replication that don't need to be simple single nucleotide substitutions.

BTW - This whole question spawned from a comment I got to this other question which still remains unanswered. I wonder what you think of it!

Ok, glad to have cleared that all up! I will take a look at the other question.

The mutation rate is the rate at which mutations happen — i.e. the rate at which "mistakes" are generated.
The substitution rate is the rate at which mutations are accepted — i.e. the rate at which "mistakes" become incorporated into a genome.
The difference is due to selection — if a mutation happens that results in an essential protein becoming non-functional that mutation will tend to be purged and thus won't be "accepted".
A relatively clear discussion of these differences:

Box 1
Mutation rates versus substitution rates
  It is important to distinguish between the rate at which spontaneous mutations occur and the rate at which genetic changes accumulate in a surviving lineage. The MUTATION RATE reflects the probability of a change in genome sequence between a parent and its offspring. It is the compound result of unrepaired DNA damage, polymerase errors, intragenomic recombination events, movements of transposable elements, and other molecular processes that introduce errors during the transmission of genetic information. However, only those mutations in lineages that persist — typically in the face of selection — contribute to the SUBSTITUTION RATE measured by whole-genome sequencing. The failure to carefully distinguish between these two types of rates is a persistent cause of confusion and misconceptions about whether mutations are random. In the same vein, the frequency of a mutant allele in a population generally does not equal the rate at which the corresponding mutational event occurs.

From: Barrick, J. E., & Lenski, R. E. (2013). Genome dynamics during experimental evolution. Nature Reviews Genetics, 14(12), 827-839.
You may also find the following article to be of interest:
Yi, S. (2013) Neutrality and Molecular Clocks. Nature Education Knowledge 4(2):3
.

When you say "accumulate", or "become incorporated into a genome", you obviously mean the genome of an entire population (e.g. species of virus in this case), not a single virion, right?

Also, is it fair to say that the substitution rate is the rate at which the mutation in question increases its population share (%) over the entire population? If so, what are the units for it?

Yes, you could think mutations as being accepted in the "gene pool".  2) No, I don't think that is correct. These are measures of new mutations either being generated (mutation rate) or being accepted (substitution rate). {I'll change the wording in my post since I see that accumulation is open to misunderstanding.}

Thanks - but on #2 - if the substitution rate is not the rate at which a mutation increases its population share (%), then what do you mean by a measure of "mutations being accepted"? Wouldn't the substitution rate be a measure of how successful a mutation is, where success would be defined as a fraction or growth over this fraction of the resulting (genetic) population?

This answer is not accurate. Probably only a minority of mutations that occur in any given genome would result in a "substitution" if "accepted"- a much larger proportion consist of expansion and contractions of satellite DNA. There is a bit of an ascertainment bias in how we think about mutations because substitutions are easy to "see" using most sequencing technologies.

I downvoted this answer because I was feeling grouchy and it touched on a pet peeve of mine, but upon reflection I decided that I was wrong to do so. The time window for changing that has passed, nonetheless I wanted to comment a symbolic +1 back in.


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What is the maximum/minimum temperature humans can survive at for an extended period of time, and what rate does the body temperature change at?
3 questions:

At what rate does the body temperature of a human change at? That is, assuming the outside temperature is x, is there some sort of formula that can determine how long it takes for the human body to reach any temperature above or equal to x? I understand this is quite variable, but any data will be useful.

a) What are the harshest conditions currently on Earth that we can survive at (That is, the maximum temperatures people actively live at every day for a period of years, and the minimum temperatures they do so).
b) In what ways have their bodies adapted to allow them to do so?

Thanks!

Hopefully you're not asking this because of the covid-heat-yourself-to-56C-cure nonsense.

Why would that be the reason .... starts sweating because he's in a 60C home and doesn't know if he's going to die so he hoped the bio stack exchange would

This depends a lot on what kind of clothing and tools the human has.

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. ——— 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!


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L strain of SARS-CoV-2?
Early in the epidemic, Chinese researchers (Jian Lu, et al,) reported in the National Science Review earlier this month that there was an aggressive more virulent L strain compared to the older S strain of the virus. Of the 103 viral genomes they scoured, 70% were of the L-type variant using phylodynamic analysis of samples taken during the earliest phase of the outbreak that began in Wuhan late last year.
But subsequent later samples taken later in the course of the epidemic were mostly of the S strain.
Peer review by researchers at other institutions have recently called this study into question.
Does anyone know where this stands currently? Has an aggressive L strain been confirmed? Do current rRT-PCR tests make any distinctions between L and S strains?

Are you referring to X Tang et al, On the origin and continuing evolution of SARS-CoV-2?

Related if not duplicate (given the comments there)  https://biology.stackexchange.com/questions/90892/where-can-i-find-the-genome-of-the-l-strain-coronavirus-and-the-s-strain-coronav?rq=1

As you may already be aware, there are some interesting comments on this paper on PubPeer.  The authors' response may be found here

One and a half year later we see that the L strain (corresponding to Pango lineage B and all of its descendants, and to all Nextstrain clades except 19B) was winning the evolutionary race, mostly because of the emergence of Pango lineage B.1/Nextstrain clade 20A with mutations ORF1b:P314L and S:D614G that had a decisive advantage over the other virus variants. The S strain is still extant in form of Pango lineage A/Nextstrain clade 19B and its descendants, but marginalised numerically.

S/L refers to the amino-acid at ORF8:84. Also this split is more interesting than it seems because this mutation ORF8:S84L plus the other one C8782T it comes with are found in bat viruses, so it is believed that the ORF8:S84L lineage (or A or 19B) is ancestral. The problem is that all the market samples were from the S84 lineage (or B or 19A).

@reuns Indeed the split is interesting, as there are no published sequences with just one of the two differentiating mutations, which suggests a double introduction to Wuhan city from a yet unknown source.

@reuns You probably got the news that now also the A or 19B clade can be traced to the seafood market, and even to the same area inside that market.

Yes, thank you, I'm following it closely


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Is ampicillin a good choice of drug to treat a urinary tract infection caused by E.coli
Is ampicillin a good choice of drug to treat a urinary tract infection (cystitis) caused by E.coli? How does the environment of the urinary tract effect its ability to treat the bacteria.
When cultured on a CLED agar plate and an ampicillin disk is placed in the centre it appears to work well, but will it work this well in the human body?

Hi ! This seems like a homework question. The users of this site will gladly help you, however we will not do your homework for you: it is required that you show your attempts at answering the question first.

In this instance, the question text should lead you down the right path to the answer: try to summarize the difference between the in vitro antibiotic test (CLED agar) and the in vivo conditions in the urinary tract, and consider the consequences of these differences.


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Why does increased humidity decrease coronavirus "survival"?
All news I can see scientist telling that the SARS-CoV-2 virus survive more in cold and dry weather. I can understand cold as hot weather will desiccate virus, but why dry  weather.
Would not dry weather dry droplets of saliva sooner also desiccate virus, would not humid weather support virus?

So I found this information regarding humidity from an article by MIT on corona:
1) High humidity leads to condensation of sneezing cough saliva particles sooner, so it does not spread to farther distance
2) Low humidity leads to less condensation and higher range of movement of saliva particle, hence more spread area.
Apparently it has to do with physics and range of infection not on survivability.

The statements about humidity are based on cultures from surfaces, see for example http://downloads.hindawi.com/journals/av/2011/734690.pdf (this paper is about a previous coronavirus, not the current strain, but still likely applies for qualitative data). These are specifically measures of survivability, and not infection.

I found an answer to this mystery in the literature, but it is a somewhat tentative explanation from a relatively recent (2012) paper by Yang et al. In a nutshell, [respiratory] viruses do worse in small droplets compared to large/unconstrained ones. Even being "totally" dry is apparently somewhat better for them than being trapped in a small droplet. So you get a V (or U)-shaped survival curve as a function of relative humidity.

There appear to be three regimes of IAV [influenza A virus] viability in droplets, defined by humidity: physiological conditions (∼100% RH) with high viability, concentrated conditions (50% to near 100% RH) with lower viability depending on the composition of media, and dry conditions (<50% RH) with high viability. This paradigm could help resolve conflicting findings in the literature on the relationship between IAV viability in aerosols and humidity, and results in human mucus could help explain influenza’s seasonality in different regions.
[...]
After release from the respiratory tract, where RH is ∼100%, a respiratory droplet shrinks by 40–50% in diameter at RH below 90% due to evaporation [16]–[18]. As a result, concentrations of solutes in the droplet increase by up to 15 times, and solutes such as salts (e.g., sodium chloride (NaCl)) that are harmless at physiological levels may become harmful to the virus. For example, avian IAV has been reported to be less stable at salinities greater than 25 g L−1 [19]. Evaporation induces changes to IAV’s microenvironment inside droplets that may affect the virus’ viability, and the toxic effect of solutes may be enhanced at lower RH due to higher concentrations that result from greater loss of water.

Yang et al.'s paper has been positively cited in a couple of subsequent reviews  Lowen and Steel (2014) and Paynter (2014)
So it seems to be a fairly credible explanation as far as influenza is concerned. Paynter's review also discusses similar observations on RSV:

One study examined the effect of humidity on RSV survival in 1 μl droplets of tissue culture medium on polythene at room temperature. Over the first 5 h, RSV survival was highest at the highest humidity, while over the next 67 h, RSV survival was highest at the lowest humidity. The explanation of these findings may lie in the droplet drying time in this study. Droplets exposed to 77% RH were still wet at 18 h (no data were given for drying times at 32% or 52% RH). The relatively high survival at higher humidity over the first 5 h was probably due to the fact that the droplets remained wet in these conditions. The survival over the final 48 h (when all droplets were dry) was progressively reduced with increasing humidity. Consistent with this explanation, only 1% of RSV was lost over the 72 h when stored in liquid culture medium, and in addition, the authors noted that RSV survival was increased with increased droplet size. Similarly, in another study the survival of RSV on countertops was reduced if the virus was in droplets that were dried quickly. These results are consistent with the studies examining influenza survival on surfaces, suggesting that while the virus remains ‘wet’ in droplets, high humidity prolongs its survival, by reducing evaporation.

There might be more recent advances in this area though, especially regarding mechanisms of the "middle regime".

Great answer.There's much to be discovered in how viruses spread through droplets, and these studies probably involve physics too.

Increased temperatures and  humidity slows down the spread of virus, as warmer air holds more moisture it prevents viruses from traveling through air in comparison to the dry air conditions. As humidity increases, the size of water droplet is larger which settles out of the air quickly. This the reason why influenza-like viruses spread more in winter season.
The SARS CoV2 (strain of coronavirus presently causing COVID 19 disease) has the basic reproduction number (R0) approximately 3, which means each infected person can pass virus to about 3 other people. And researchers have found by increasing temperature by one degree Celsius and one percent increase in relative humidity decreases this R0 value by 0.0383 and 0.0224, respectively. This means less number of people are infected further by single infected person.
Checkout this review: https://www.ncbi.nlm.nih.gov/pubmed/32196426


text:
Is COVID-19 more deadly than swine flu?
I have a question about the novel coronavirus and swine flu.

How do the death rates compare between the two diseases?
How do the transmissions and rate of transmission compare?
Was a vaccine developed quicker for swine flu?

I ask because I don't recall this level of global disruption during the swine flu outbreak.

SE Biology is a question and answer site — not a discussion site or a site for floating ideas. It is concerned with the mechanisms of biological processes, not medical or social aspects of biology. For one of these reasons I think  that your question on the coronavirus outbreak is off-topic here. Question of a medical nature might be on-topic at SE Medical Sciences. Otherwise you are advised to consult more appropriate reputable sources for such information, some of which are listed here.

“Swine flu” is an obsolete name.  The official name for the virus that was briefly called “swine flu” is “H1N1pdm09”.
H1N1pdm09 has a mortality rate of around 0.01-0.1%. That’s roughly 10- to 20-fold lower than COVID-19. Its R0 was estimated at between 1 and 2, which is roughly half the estimates for SARS-CoV-2 (the virus responsible for COVID-19].
A vaccine for H1N1pdm09 was available in the fall of 2010.  It was possible to make it that quickly because it’s just another influenza strain, and the normal techniques for for vaccines against influenza strains worked fine.
Most importantly, H1N1pdm09 never went away.  It is still one of the main influenza strains circulating today, and if you were vaccinated for influenza since 2010 you received a vaccine against it.

CDC info here: 2009 H1N1 Pandemic (H1N1pdm09 virus)
WHO info here: Evolution of a pandemic:
A(H1N1) 2009, April 2009 – August 2010, 2nd edition


text:
If the covid-19 appeared once, could it reappear anytime?
Governments are imposing confinement measures on their populations, trusting that if there is no more transmission the virus will die out.
But since this coronavirus appeared a first time, what could prevent it from reappearing any number of times ?

SE Biology is a question and answer site — not a discussion site or a site for floating ideas. It is concerned with the mechanisms of biological processes, not medical or social aspects of biology. For one of these reasons I think  that your question on the coronavirus outbreak is off-topic here. Question of a medical nature might be on-topic at SE Medical Sciences. Otherwise you are advised to consult more appropriate reputable sources for such information, some of which are listed here.

Frame challenge answer: you are jumping to the conclusion that they really hope the virus will "die out". But it's more likely they adopted those measures to slow its progression to a manageable degree. See e.g. this conceptual image from ECDC

Even if there are new outbreaks of COVID-19 in the future, when they happen is not irrelevant, as we could be much better prepared given the current/ongoing research on both (antiviral) treatments and possibly a vaccine as well.
Regarding the "meat" of the question, it's a matter of probabilities, not certainties. It was and is generally assumed that other [bat etc.] coronaviruses will jump hosts to humans in the future.
Besides SARS, another (much) lesser known cross-species jump actually occurred in China in 2016 with SADS-CoV, which killed thousands of pig[let]s, but was not infectious to humans. Annoyingly enough for the Chinese pig farmers, SADS-CoV re-emerged in early 2019 despite the fact that there were no cases reported between May 2017 and January 2019.

I wish the (probably high-rep) users who downvote answers here, would put the effort into closing questions instead, if answering off-topic (??) questions  is the reason for downvoting answers. Otherwise please explain why you are downvoting answers...

Why close a question that, even if poorly worded, is likely to be of interest to many people?

@jamesqf: I guess you meant to ask David that.

No, I meant it as a general comment to anyone who cares to read it.  Of course it's rhetorical, because we can easily guess why certain questions are closed, and lots of interesting comments deleted.

This recent article explores the origin of the current covid-19 by performing comparative genomic analyses: https://www.nature.com/articles/s41591-020-0820-9
One of the main point of the article is that to be able to answer your question one would need to know how the virus started to emerge in humans in the first place.
The authors describe 3 main hypotheses:

Natural selection in an animal host before zoonotic transfer
Natural selection in humans following zoonotic transfer
Selection during passage

The first two hypotheses are probably more likely to be an explanation the 3rd being very unlikely (I leave the details to the article).
Here is a scheme coming from a different article (Source: https://www.nature.com/articles/nm.3985.pdf?origin=ppub) explaining graphically hypotheses 1 and 2 as emergence paradigms:

Now your answer to your question is in the conclusion of the first mentioned article:
"In the midst of the global COVID-19 public-health emergency, it is reasonable to wonder why the origins of the pandemic matter. Detailed understanding of how an animal virus jumped species boundaries to infect humans so productively will help in the prevention of future zoonotic events. For example, if SARS-CoV-2 pre-adapted in another animal species, then there is the risk of future re-emergence events. In contrast, if the adaptive process occurred in humans, then even if repeated zoonotic transfers occur, they are unlikely to take off without the same series of mutations. "
Essentially if it is hypothesis #1, it could be likely. If it is hypothesis #2 less likely. I don't think there is enough evidence yet to prove or disprove any of the two.


text:
Why doesn't copper affect human skin?
It's been known for a long time that copper has antimicrobial properties, but if it is so potent, why does it seem to have no effect on human skin or really any large animal?

https://en.wikipedia.org/wiki/Copper_toxicity

That's like if you ingest copper, not if you merely touch it.

Copper does affect human skin.  If you're in contact with it for a while, it will turn the skin bluish-green.

One possible reason is that humans are eukaryotes, while most microbes are prokaryotes.  There are significant differences in the cell chemistry, which explains things like why antibiotics work against (some) bacteria without much affecting the person that takes them.  See e.g. https://www.livescience.com/65922-prokaryotic-vs-eukaryotic-cells.html for more.

@jamesqf: Why does copper turn the skin bluish-green? Can you give a reference? Is the bluish-green color come from oxidized copper?

@Hans: My "reference" is having worn copper jewelry, and having seen other people wear it.  If you want to know more, typing "why does copper turn skin green" into a search engine redurns about 37 million hits.

@jamesqf: OK. My first reaction to your first comment was the greenish blue substance was copper carbonate Cu2CO3(OH)2 https://en.wikipedia.org/wiki/Basic_copper_carbonate.

The outermost layer of your skin consists mostly of dead cells, the Stratum corneum. Copper can't kill what's already dead.

Seems reasonable, but why doesn't it corrode the dead skin fast enough to cause more significant burn damage if it kills microbes quickly?

@Bangarang copper doesn't doesn't burn cells it poisons them. Dead cells aren't affected by being poisoned. The Status corneum is not just one layer, it's 15-20 layers. The cells are constantly being shed and then replaced from below.


text:
what is the role of granulation tissue in bone fracture repair
When a bone fractures, let's say with a large enough gap that repair has to occur through secondary healing, vessel rupture will result in a hemorrhage that then coagulates, there's inflammation that removes tissue debris, and granulation tissue forms as capillaries and fibroblasts infiltrate, using the hematoma as scaffolding. Next is the formation of the soft callus. What is the composition of this soft callus?
I understand that chondroblast precursors are activated, and cartilage forms to bridge the fracture ends, but what happens to the granulation tissue from earlier? The fibroblasts that infiltrated the site of the fracture, do they lay down fibrous connective tissue or do they differentiate into cartilage cells and lay down cartilage matrix as well? I've been reading from multiple sources, and none of them really specify it well enough for the ambiguity to not remain.


text:
Does the zeta potential of a nanoparticle generally take into account ligand charge?
For example, if I had a quantum dot nanoparticle with conjugated linker peptides capped with polyarginine tracts.
Would the localization of negative charge from arginine change the zeta potential of the overall np-peptide complex?
Or does the polyarginine tract have its own stationary layer and its own zeta potential separate from that of the QD? Especially if it extends outside the slipping plane of the QD?

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 doesn't seem to have a biological component — is there some reason you think this question belongs in Biology.SE? Thanks!

I'm voting to close this question as off-topic because it doesn't seem to have anything to do with biology.

Sorry I'm new and this is my first ever post.  How related to biology the question has to be? I suppose the question is more of a literal chemistry or physics question.  However, I posit that zeta potential is critical to how effectively nanoparticles and drug delivery systems interact with any biological model?

The links put in my first comment contain the official guidelines. I agree that chemistry or physics would seem more appropriate, but lack the background to suggest which would be more appropriate — I suggest searching for terms like "zeta potential" on both of those sites and see whether anything remotely similar to this turns up. If they do then try there. Good luck!


text:
How can a virus be determined to cause a disease?
How can a virus be determined to cause a disease?  From other posts I have read here, humans carry hundreds of different strains of viruses.  How is a study structured and carried out to determine that one virus is the cause of a disease, and not any of the other viruses present?  Any examples of studies are greatly appreciated as well.

A modified form of Koch's postulates is used to guide experiments that establish that a particular virus causes disease.
As a specific example of such a study, the SARS-CoV virus was determined to cause the SARS disease by fulfilling these criteria:

SARS virus is found in people suffering from SARS, and not found in those who are healthy.
The virus can be isolated from infected people and grown in cell cultures (here, Vero cells).
Viruses grown in culture can be reisolated and compared with (and found identical to) the suspected pathogenic virus.
This isolated virus can re-infect people (or infect model organisms; in this case, a species of macaques).
Virus in reinfected organisms can be isolated, grown in culture, and found identical to the original pathogen.
The immune system is observed to respond in similar ways to the infection (pneumonia and lung tissue lesions).

That's right, Koch's postulates have undergone adaptations over the years. Still, for some pathogens, the original postulates still succeed in proving causality. Above, I cited some more modern models, such as the Falkow criteria (which you cite as Koch's molecular postulates) and the Bradford Hill criteria; but they are all based on Koch's originals.

I'm going to submit an article, from 1996, written by Fredericks and Relman, which presented the most important updates to the original postulates:
Sequence-based identification of microbial pathogens: a reconsideration of Koch's postulates.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC172879/


text:
Unidentified Spider
Apologies for the rubbish quality of the image, but I found this spider while in the shower. I’m not exactly sure what species it is and wonder if someone can help me out.
I live in southeast Michigan, it was a relatively humid day and it is 1 degree Centigrade presently. It is 9:29 PM EST. I’d say the body of the spider is about a centimeter long. Any help is appreciated.

This is Cheiracanthium sp. with common name "Yellow Sac Spider." It is very common in North American homes, distinctly identifiable by having a homogenous colour that is almost an translucent yellow (sometimes yellow-green or yellow-brown) with no particular markings (no stripes or dots) aside from the cardiac mark (the dorsal line on its abdomen).
It often has black feet like in this photo and is sometimes alternately called a 'black footed sac spider.'
There are two species of this genus widespread across North America: C.mildei and C.inclusum which are difficult to separate from photos like this. It is generally understood that C.mildei is commonly found indoors while C.inclusum is commonly found outdoors.


text:
Can you be infected by two coronaviruses at once?
E.g. could you be infected by COVID-19 as well as a different strand of coronaviruses (e.g. those that circulate in the population every flu season)?

SE Biology is a question and answer site — not a discussion site or a site for floating ideas. It is concerned with the mechanisms of biological processes, not medical or social aspects of biology. For one of these reasons I think  that your question on the coronavirus outbreak is off-topic here. Question of a medical nature might be on-topic at SE Medical Sciences. Otherwise you are advised to consult more appropriate reputable sources for such information, some of which are listed here.

I honestly don't think this is a bad question... though I think you'll need to be a bit more detailed and probably have to do more research and [edit] to show exactly what research you've done and what is confusing you.

Yes:

Coinfections involving multiple HCoVs were also detected (Table 2).
...

Human Coronaviruses HCoV-NL63 and HCoV-HKU1 in Hospitalized Children with Acute Respiratory Infections in Beijing, China, Advances in Virology (2011)


text:
Did bilateral symmetry evolved just once?
If I understood correctly, all bilaterians come from a single organism (the Urbilaterian) that showed this type of body plan for the first time at the end of the Ediacaran.
Does that mean that bilateral symmetry evolved just once in the entire history of life? Is it correct to say then that bilateral symmetry is not a feature of convergent evolution? That this is indeed a thing that evolution explored just that time in history and never again?

It's currently hypothetical. pre-cambrian fossils are necessary from the 1bn-600 million region to find protostome - deuterostome ancestor. Genetic data is also inconclusive. some information if you search for bilateral common ancestor. i.e. https://dev.biologists.org/content/129/13/3021 indeed the common view is that there is a common ancestor.

@com.prehensible Let me see if I got it right. One can then say that bilaterality is a feature that appeared only once in life's history and that this is what we think right now? Even if there is no enought evidence to flasify this idea yet and we wouldn't be very surprised to see that it happened twice or more times during the evolution of life.

Yes, all the baliteria are classed in the common clade which have a similar cell attributes and physiology, they all have hearts whereas starfish and jellyfish don't, there are various genes that suggest common ancestry. There is currently no evidence of bilateral from parallel evolution, although it's very possible or probable that there were some previously and perhaps even today, i.e. tardigrades don't have hearts, so perhaps some species one day will be found to be convergeant species.

@com.prehensible I'm not a biologist at all so I would like your opinion on this. I've found that the Sea Cucumber has "weak bilateral symmetry" while been an Echinoderm (and thus a descendant of radially symetric creatures). Could this be considered bilaterality? If so, then we have some evidence for convergent evolution right? Source: https://en.wikipedia.org/wiki/Sea_cucumber#Body_plan

Sea cucumbers and sea anenomes both have a bilateral juvenile stage, so they have perhaps evolved from bilateral ancestors, check google scholar for "bilateral sea cucumber". https://www.researchgate.net/profile/Taha_Soliman4/publication/262415405/figure/fig6/AS:281720105521180@1444178715416/Light-microscopy-image-of-larval-development-of-Apostichopus-japonicus-red-variants-a.png A new fossil of a bilateral animal has been found from 550mn years ago: https://phys.org/news/2020-03-ancestor-animals-australian-fossils.html squids are starfish with mollusks on them, there are hybrid symmetries.

@com.prehensible Interesting, If you are willing to make of this a full answer I would accept it.

Ok, i collated the comments to an answer. thanks

A lack of strong evidence causes the field to be mostly hypothetical. Detailed pre-cambrian fossils are necessary, from the 1bn-600 million years ago, to find a protostome - deuterostome ancestor.
Genetic data is also inconclusive. A search for bilateral common ancestor gives i.e. dev.biologists.org/content/129/13/3021 It's a summary of research, where the accepted view is that there is a common ancestor to all known bilateral organisms.
All the baliteria are classed in the common clade which have a similar cell attributes and physiology, they all have hearts whereas starfish and jellyfish don't, there are various genes that suggest common ancestry. There is currently no evidence of bilateral from parallel evolution, although it's very possible or probable that there were some previously and perhaps even today, i.e. tardigrades don't have hearts, so perhaps some species one day will be found to be convergeant species, although they are thought to be miniaturized lobopodia.
Sea cucumbers and sea anenomes both have a bilateral juvenile stage, so they have perhaps evolved from bilateral ancestors.
researchgate.net/profile/Taha_Soliman4/publication/262415405/…
A new fossil of a bilateral animal has been found from 550mn years ago: phys.org/news/2020-03-ancestor-animals-australian-fossils.html squids are starfish with mollusks on them, there are hybrid symmetries.


text:
Species Identification : Worm like insect but broad at back
Can anyone help me identify this insect
Location: Southern India
Size: About 2cm
It looks like a worm but has a broad back, it seems like (not very sure) it tucks it's thin head inside the broad shell like body to ward off.
Here is the picture,

Please always include your location and the approximate size of your specimen

Related: Identifying a creature that appears to be a worm wrapped in a cocoon, What is this black and white worm in a white case?,  Help in identifying an unknown arthropod, What insect is this? (India), Identify this smooth-cocoon worm from Southern India, Small worm living in some kind of cocoon......

Related:  What is this animal that hides in dustlike structure?, What in the world is this critter?, What is this hard shelled insect in my house?, What is this insect found commonly in coastal India?, Insect identification - pantry moth vs clothes moth

That actually looks like some sort of caddisfly larvae in its case to me.

Are you sure that's it's 'body' & not a case?
Did you find it in water?
Or a Case Bearing Clothes Moth (Caddisfly are closely related to moths).
This one (a clothes moth larvae) looks very similar to your image.

This is not a caddisfly. Caddisflies are only found in water. Also note the bulging shape of the case -- such non-hydrodynamic shape would be quite challenging for the caddisfly to stay in place. The OP's specimen does in fact look like a case-bearing moth
(similar to the many linked posts I added in the comments above). In the future, please make sure that images and sources you use are reputable. Alamy stock photos are VERY often mislabeled and wrong, so using them as a form of evidence should be avoided or at least corroborated by better info. Also note that your link does not work.


text:
What is the formula to calculate $R_0$ (basic reproduction number)?
What is the mathematical formula for $R_0$ and what does each variable represent?
I have tried searching this to no avail.

$$R_0 ∝ \left(\frac{\text{infection}}{\text{contact}}\right) · \left(\frac{\text{contact}}{\text{time}}\right) · \left(\frac{\text{time}}{\text{infection}}\right)$$
More specifically:
$$R_0 = τ · \bar{c} · d \quad \quad (1)$$
where $τ$ is the transmissibility (i.e., probability of infection given contact between a susceptible and infected individual), $\bar{c}$ is the average rate of contact between susceptible and infected individuals, and $d$ is the duration of infectiousness.

Notes On $R_0$ (2007)

Further reading:

https://en.wikipedia.org/wiki/Basic_reproduction_number
Complexity of the Basic Reproduction Number (R0), emerging Infectious Diseases (2019)
Theory versus Data: How to Calculate R0?, PLoS One (2007)
The R0 package: a toolbox to estimate reproduction numbers for epidemic outbreaks, BMC Medical Informatics and Decision Making (2012)


text:
How do substances for gene expression work?
How does amplification of gene expression work?
I often find in various articles expressions like "Using substance X or peptide X, we enhanced the expression of gene Z, which led to a certain therapeutic effect.
How to find out which substance enhances the expression of a particular gene? Is there a law, a pattern for this, or, if all this is found out empirically, a summary table of expressing substances?

Try being more specific; Gene regulation is a very broad topic, with lots of intricate mechanisms. Where did you here this? What substances did they use, and for which gene?


text:
Is there any biological evidence corroborating a historians' claim that the 1918 "Spanish flu" originated from China?
A 2014 History article says

According to new research by a Canadian historian, the 1918 flu outbreak that killed 50 million people originated in China. [...]
Humphries found medical records indicating that more than 3,000 of the 25,000 Chinese Labor Corps workers transported across Canada beginning in 1917 ended up in medical quarantine, many with flu-like symptoms. The influenza ripped through the Canadian guards and soon took root in North America. [...]
The mystery of the origins of the “Spanish flu,” is not totally solved, however. “Only DNA testing of samples from these earlier outbreaks can truly confirm or deny the theory,” Humphries acknowledges.

His evidence/argument seems based entirely on the movement of people and occurence of these outbreaks of some kind of flu among Chinese Labor Corps. Has there been any biological research on these earlier outbreaks, proving or disproving a link to the later "Spanish flu"?

I see there's a (more recent) 2016 paper by GD Shanks which disses the idea, to the extent that it might have been the source of the Spanish flu in Europe

Laborers and soldiers from China and Southeast Asia recruited during the First World War by Britain and France have been suggested as the origin of the 1918 influenza pandemic in Western Europe. This study aimed to review the available data to better understand the sources and origins of the 1918 influenza pandemic, and clarify whether, in fact, there was an Asian connection to its onset. We reviewed official mortality lists from the Commonwealth War Graves Commission and the French Ministry of Defence for all-cause (Britain) and pneumonia/influenza (France) mortality, respectively. The results indicated that influenza mortality (estimated 1/1000) in Chinese and Southeast Asian laborers and soldiers lagged other co-located military units by several weeks. This finding does not support a Southeast Asian importation of lethal influenza to Europe in 1918.

I also see that a 2019 review by Worobey, Cox and Gill is more directly dismissive of the idea that Chinese laborers could have transported it through Canada, but again on a historical argument:

Our view is that attempts to pin down the exact location of the first cases of any influenza pandemic are fraught with difficulties, and, for at least two of the three hypotheses noted above there exists strong contrary evidence. The simplest objection is to the idea that Chinese labourers were responsible for the spread of the pandemic virus. Crucially, Shanks [16] showed that influenza cases among Chinese and Southeast Asian labourers and military recruits lagged, rather than led, cases among other groups in the same locales. Moreover, Chinese labourers were also shipped to Europe from the East via Suez or the Cape, although these routes were rapidly abandoned in March of 1917 in favour of transporting them across Canada [10]. Finally, although the Chinese workers were reportedly transported across Canada in sealed trains, it seems unlikely even under this harsh scenario that the virus would not have initiated detectable spread in Canada if these individuals really were the original hosts of the pathogen.

In their 2019 review, Worobey, Cox and Gill also point to the 2014 genetic analysis of Worobey, Han and Rambaut as the "state of the art" in terms of genetic knowledge on the Spanish flu, in which they argue it was more probable of "Western hemispheric" origin.
More reserved, a 2019 review in Science Translational Medicine (by Taubenberger, Kash and Morens) says

Phylogenetic analyses have also been used to model 1918 virus origin but have yielded different dates for the estimated origin of the pandemic virus (36, 76, 79, 80). Until pre-1918 influenza A virus sequences become available, reconciling
the dates of the origin of the 1918 virus phylogenetically will remain difficult. It seems highly unlikely on epidemiological and biological grounds that a virus expressing the pandemic H1 HA, with its inherent virulence, could have widely circulated in humans much before 1918.

(In there, ref 80 is Worobey et al. 2014.)
I guess that means there's no other/biological research on this putative China link presently, but I'm leaving this as an "open question".

I see someone voted to close this "homework question" for showing "no effort" when it basically contains its answer... and I'm pretty sure I've put far more effort into it than the average question here does! The "usuual welcoming" on Bio SE is amazing!

@David: Ehh?? This is not even about the coronavirus. I guess TLDR...

@David:  I'm not seeing the problem.  The question is if there's proof based on DNA or other medical evidence that the 1918 Spanish influenza originated in China.

SE Biology is a question and answer site — not a discussion site or a site for floating ideas. It is concerned with the mechanisms of biological processes, not medical or social aspects of biology. For one of these reasons I think that your question regarding virus epidemiology is off-topic here. Question of a medical nature might be on-topic at SE Medical Sciences. Otherwise you are advised to consult more appropriate reputable sources for such information, some of which are listed here.

@David that strikes me as a quite restrictive definition of what SE Biology should be about! Viral epidemiology, even for a human virus, is squarely within the domain of a big-tent discipline like "biology". This isn't a question about medical aspects of influenza, but a question about evidence for different interpretations of available data, and a request for other sources of data. It isn't Fizz's fault that some of the available data are historical in nature.

“What SE Biology should be about.”  Your or anyone else’s opinions on that are not to the point in this instant. I refer to what the site IS about — defined by others, but to which all users are beholden. Please read my meta post if you wish to understand my motivation.

Hm, not finding a specific post of yours on meta. And I'm not sure what the restrictions on what the site is about are, if they're not these: https://biology.stackexchange.com/help/on-topic. I would put this question squarely in the "on-topic" category based on what it says there, maybe there is something else I'm supposed to be looking at. Yes, this is just an opinion of mine. But with all respect, I don't see the value in gatekeeping a topical and well-researched question, even if it's on the edge for the site (which I don't believe this one to be).


text:
Design primers for PCR from given DNA sequence

Given the sequence: 5’-ACTGACTATGTAGAA………GGCCCTAAGGGCCAA-3’ (1)
You wish to do PCR of this dsDNA to add “overhangs” on the ends of it. On the 5’ end of you will put
  the restriction site for NdeI enzyme (5’-CATATG). On the 3’ end you will put the restriction site for
  MspI (5’-CCGG).
Write the sequences for the “forward” and “reverse” primers to do this. Each primer should be
  16-18 nt, with 12 nt for hybridization and 4-6 nt for “overhang.”

I am a little confused as to how to write the forward and reverse primers for the sequence. From videos I have seen that I should write the complementary strand of my giving strand. Which would be:
3' -TGACTGATACATCTT........CCGGGATTCCCGGTT-5' (2)
Then from sequence (1) I should get the reverse primer and from sequence (2) the forward primer. However, this doesn't allow me to add both restriction enzymes because both primers would be from 5' to 3'.
Or should I simply take the given sequence and write the primers only from that? So that the primers would  be:
Forward primer:
3’-GGCCTGACTGATACAT
Reverse primer:
GGATTCCCGGTTGTATAC - 5’
where the bold nts are the restriction sites.
Thank you!

This question is a bit confusing, in part because the convention is to always write DNA/RNA sequences left to right as 5' --> 3'. Is this a homework question?

Also, where you write "Should I simply take the given sequence..." You appear to in fact be using your complementary strand for both F and R primers, rather than the given strand, I'm not sure if this is intentional.

As alluded to in the comments above, remember that you are amplifying double-stranded DNA, so two new reverse-complementary strands should be generated from each cycle (so that they can hybridize with eachother). As written in your answer, both of your primers would hybridize with your given strand, and the amplicons would not overlap (one binds at each end, but both would amplify in the same direction).
To fix this, you need one primer that binds to the target sequence, and one that binds to the reverse complement strand, which you have already generated. The new amplicons extend 5' -> 3' (from the 3' end of the primer not the template), so your primers need to bind at the 3' end of their respective strand. This link has a good visualization of that.
The 3' end of the primer needs to hybridize tightly with the template, since this is where extension happens (discussed in this guide). So your flanking restriction site sequences will always be on the 5' end of either primer (notice that the question actually hints at this by indicating the 5' end of each flank).
The primer given as your "reverse" primer will actually bind to the 3' end of your given sequence in the appropriate orientation, but you may want to put your 3' flank onto the 5' end of that primer sequence, as this will be theoretically be the 3' end of your amplicon. Your other primer will need to bind the 3' end of your reverse complement (which is the 5' end of your target), so it will have the 5' restriction site flank.
By convention, primer sequences are always given in 5'---3' format. So make sure your answer follows that convention. (i.e. 5'-Flank-primer-3').
If all of this sounds really confusing, that's because it is. I do this for a living, and I still always double check my primers in a program like Primer3


text:
Would symptoms differ from eating virus contaminated food versus breathing in virus?
Would symptoms differ from eating virus contaminated food versus breathing in virus?
The COVID-19 causes respiratory symptoms and I guess that is because people are breathing in virus droplets in their lungs.
But if you would swallow COVID-19 contaminated food and avoid breathing in the virus would that cause other symptoms like stomach pain or diarrhea?

SE Biology is a question and answer site — not a discussion site or a site for floating ideas. It is concerned with the mechanisms of biological processes, not medical or social aspects of biology. For one of these reasons I think  that your question on the coronavirus outbreak is off-topic here. Question of a medical nature might be on-topic at SE Medical Sciences. Otherwise you are advised to consult more appropriate reputable sources for such information, some of which are listed here.

@David Can I remove the COVID-19 from my question and only keep "Would symptoms differ from eating virus contaminated food versus breathing in virus?". I believe that question is about biology but I could be wrong.

Does the virus genetic code decide which organs to infect or does it depend where it infects initially?

Please transfer your question to a site that deals with medical questions. Or read the Sources I suggested. And the virus uses the same genetic code as its host. The complete genetic information for an organism is termed the genome. The genetic code is a 64-word cypher used to transcribe the mRNA for that portion of the genome that encodes protein. Check it out on Wikipedia.

@David I posted the question now at https://medicalsciences.stackexchange.com/questions/21741/would-symptoms-differ-from-eating-virus-contaminated-food-versus-breathing-in-vi but I need to think how I can make this question non medical and more biology oriented.

If you have posted it on Medical Sciences you should now delete it from here according to SE policy.


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How effective is spraying disinfectant on streets?
I always wondered how effective spaying disinfectant onto outdoor ground is.

Source: Wikimedia
I understand that viruses and bacteria will sink down to the ground. I further understand that pedestrians may transport it across the area via their shoes, which shall be prevented.

Is the outdoor concentration of virus/bacteria particles really that high, that it helps to approach them with disinfectant?
Wouldn't it dilute too quickly?
Will the disinfectant droplets effectively touch the particles to inactivate them?

To me this looks more like this done to show "something" is done.

SE Biology is a question and answer site — not a discussion site or a site for floating ideas. It is concerned with the mechanisms of biological processes, not medical or social aspects of biology. For one of these reasons I think  that your question on the coronavirus outbreak is off-topic here. Question of a medical nature might be on-topic at SE Medical Sciences. Otherwise you are advised to consult more appropriate reputable sources for such information, some of which are listed here.

Thanks for your advice, I'll look into that. Though, of course, the SARS-CoV-2 outbreak pushed me to write this today, I wondered about this in the past too. And I don't want to discuss, I seek answers, so I thought my Q's nicely fit the Q&A scheme.


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How are antibodies specific for a disease detected in the blood if everybody produces a different antibody for the same antigen?
To break the title down into parts:

There exist serology tests that detect the amount of an antibody (Ab)
against a specific pathogen/antigen.
Every human produces their own Ab for a specific antigen by
(relatively) random combination of different gene segments in their B
cells, until one that recognizes the pathogen is found and produced
in massive amounts.
One portion of every Ab is constant, whereas the portion that
recognizes the antigen is variable. Even for antibodies (in different
humans) that recognize the same antigen, albeit to a lesser degree.

What exactly does an antibody titer/serology test detect in the blood so that it can accurately measure the amount of antibodies against a specific antigen? I am assuming they use antibodies against the antigen-binding/variable portion of an antibody. But if the variable region differs from person to person, how can a universal antibody (to be used in serology tests) against it be generated?
Is the variable region not that variable, so that any lab-generated antibody against any functional antibody against a virus works well enough for an accurate measurement of antibodies against that virus? But even so the concept sounds hard to believe since even a single antigen can have multiple epitopes, and one person might have an Ab for epitope 1 of antigen X, while the other would have an Ab for epitope 2 of antigen X. And they would still be immune to the same virus, while a universal Ab titer test for the virus would be unable to detect antibodies from one of them.
Do they perhaps employ multiple lab-generated antibodies against most of the possible variations of human-generated antibodies in the tests?

Specific antibodies are typically detected using ELISA.
The way you make a test for an antibody to a particular pathogen is not by using secondary antibodies to the specific part of the target antibody, but by using the antigen.
Different kits work differently, but the general idea is that you have antigen stuck to a surface, you put the sample on that surface. If there are antibodies to the antigen, they stick to it. Then you wash everything away and add a tagged antibody that binds to generic human antibodies.
See also https://www.sciencemag.org/news/2020/03/new-blood-tests-antibodies-could-show-true-scale-coronavirus-pandemic

ohh, using an antigen-coated surface makes a whole lot more sense. I don't know why I had such an extreme roundabout way of thinking.


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Does Rough ER (RER) produce phospholipids?
I have found out that rough endoplasmic reticulum (RER) produces membranes. Therefore it has to produce phospholipids, but I thought that the smooth ER was where the synthesis of lipids occurs.
What specific part of the ER produce phospholipids?

Could you substantiate your statement about the site of synthesis of phospholipids with a reference to your source of the information. I'm not sure that many of us are experts in that area, but our experience may help us to assess it. Also, please, one question at a time. Your general question about the functions of rough and smooth ER is a separate question and should not be included here. I imagine you can find that by reading, so I have edited it out. You can roll back the edit if you wish, but it won't help you get an answer to your main concern.

The endoplasmic reticulum (ER) is one of the largest continuous membrane bound organelle of the cell.
The rough ER and smooth ER share the same membrane and some membrane proteins can diffuse between them. At the same time there are specific markers for ER sheets (rough ER) and ER tubules (smooth ER). The terminology of rough and smooth come from early electron microscopy and biochemical work where large amount of ribosomes (polyribosomes) were found on the rough endoplasmic reticulum membrane, and less on the smooth. These membranes can be biochemically separated one being more heavy (RER because of attached polyribosomes) than the other.
In general the ER has several functions: protein synthesis, calcium storage, entry of the secretory pathway and lipid synthesis. It can not only produce phospholipids but also a large array of precursors for steroids and neutral lipids.
This is a topic of research itself but it is general thought/accepted that the smooth ER is the one responsible for the synthesis of phospholipids.
In reality, there are multiple ways to produce phospholipids (from recycled membranes, from lipid droplet stores, etc) and there are multiple possible pathways for producing lipids and lipids precursors (de novo synthesis). This also implies that there are multiple enzymes involve in this process. Now these enzymes are often ER membrane proteins and they can but do not always specifically localize particularly to one part of the ER.


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Can you be immune to a coronavirus?
Can one be immune to the new coronavirus?
Another question is what is the exact definition of "being immune". Does it mean that even when the virus enters my system, it cannot multiply?

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

It is hypothesized that exposure to and recovery from SARS-CoV-2 (as with other coronaviruses in humans) would generally result in short-term immunity to this strain, but we do not yet have data on this:

However, according to Dr Stephen Gluckman, an infectious diseases physician at Penn Medicine and the medical director of Penn Global Medicine, who spoke to the outlet, it seems likely that having the disease once results in immunity in most individuals - as is seen with other coronaviruses.
“Coronaviruses aren’t new, they’ve been around for a long, long time and many species - not just humans - get them,” he explained. “So we know a fair amount about coronaviruses in general. For the most part, the feeling is once you’ve had a specific coronavirus, you are immune. We don’t have enough data to say that with this coronavirus, but it is likely.”
This means that people who initially recovered are more likely to relapse rather than get reinfected with the virus.
According to one study, people with mild infections can test positive for the virus by throat swabs “for days and even weeks after their illness”.
But, that doesn’t mean it isn’t possible to contract the disease again, especially in those who are immunocompromised.
“The immune response to Covid-19 is not yet understood,” the Centers for Disease Control and Prevention (CDC) explains. “Patients with MERS-CoV infection are unlikely to be reinfected shortly after they recover, but it is not yet known whether similar immune protection will be observed for patients with Covid-19.”

Coronavirus: Can You Get Covid-19 Twice Or Does It Cause Immunity?

It is also hypothesized (in humans) that previous exposure to coronaviruses may enable immunity to certain other highly related strains:

These data indicate that challenge immunity to coronaviruses is strong, but highly virus strain-specific.

Virus strain specificity of challenge immunity to coronavirus., Archives of Virology (1989)

But these are all examples of adaptive immunity - not innate.

No, you cannot be immune to the virus, if you haven't been in contact with it before. You are also not immune to the influenza viruses (flu), you just happened to not contract any of them.
Simply speaking, being immune means that your immune system knows the specific virus and can disarm it effectively. But the immune system has to learn to recognize and how to fight a pathogen first. That's the adaptive immune response. It is build once you encounter the virus for the first time, but can also be activated by a vaccine. Having immunity enables your body to fight off the virus, before it can harm you or spread further.
How sick you get from a pathogen the first time around depends on how fast or strong your immune system can build immunity and on your innate immune response. None of this works perfectly. Even with immunity you can still get sick.

In other words, "Yes, you can be immune to the virus, but only if you have been in contact with it, and some time has passed." Then, you are likely to develop immunity.

(..or received vaccine against it.)   If you've never had the flu, it doesn't mean you are immune to the influenza viruses (flu), you probably just happened to not contract any of them.  But throughout the tree of life, some parts of the tree, including subspecies, do not suffer from certain infectious diseases that other parts do.  -Good edits?

The question was worded differently before people edited it. It was about having some "natural" immunity without exposure, because they also never got the flu.. I just wanted to help a worried person. The reality is more complicated and some data now suggests that there is actually the possibility of a "cross-immunity" from our other coronaviruses.

The CCR5-Δ32 mutation (2 deletions) which interferes with HIV might offer "immunity" to the virus causing the pandemic. -- This was the mechanism the experimental CCR5 antagonist Leronlimab (IgG4 mAb) may have accomplished with Covid-19 for several patients.

Welcome to Biology.SE! This looks like it could be the start of a useful post, but as currently written this would seem to be more appropriate as a comment. Answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then [edit] your answer accordingly. Thanks!


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Examples of alkali metal and halogens covalently bonded in biological molecules?
Divalent and monovalent ions are often non-covalently bonded in biological molecules, they are primary building blocks of the machinery of biology. Iodine, the halogon in period 5, is covalently bonded in thyroxide. What are other examples of covalently bonded monovalent ions, alkali metals and halogens? Are there molecules that covalently bond Flourine, Chlorine, Sodium and Potassium?

Sodium and potassium are not going to be covalently bound in biological molecules. For fluorine: https://www.tcichemicals.com/en/ap/support-download/chemistry-clip/159-07_ChemistryChat.html, an example for chlorine: https://en.wikipedia.org/wiki/Epibatidine

Thanks, very good answer. The Wiki page on Epibatidine mentions an "extremely high affinity". Gilbert Ling did some work between 1950 and to his death last year, and mentions Robert W. Taft, that may relate to why Epibatidine has "extremely high affinity". It seems that halogens like chlorine polarize the molecule. I'm assuming thyroxine has similar properties since iodine is also a halogen, also, the large effort required by organisms to synthesize thyroxine suggests it should pay off for some reason, so I'm looking a bit for information about that.

Try searching for "bioinorganic chemistry".

A "covalent bond" affords close-to or full homopolarity of both bonding partners. Metals are genuinely low in electronegativity as in contrast to organic bonding partners like C,O,N, ... Thus there never can be colvalent bonds between such metal (cations) and organic moieties.


text:
Virus viability on fabrics
According to the article How long do viruses live on surfaces: Plastic, stainless steel, fabric, and more:

With fabrics, it's unclear how long viruses can last. But generally, they tend to last for a shorter amount of time on fabric compared to hard surfaces like stainless steel, according to the Mayo Clinic.

Can someone kindly explain why this is so?
What is it about fabrics that decreases virus viability?

I would like to point out here that in many cultures our ancestors had figured it out empirically.  In North India, where I hail from, many old people will eat bread, snacks etc. from a cloth (especially a woolen fabric) if their hands are dirty.  The simplistic explanation given is that this type of fabric "stays pure".

A VERY interesting question that I had to think a lot about, and frankly I couldn't come up with an answer.
Nevertheless, this article may have.
https://www.statnews.com/2020/03/19/coronavirus-survives-on-surfaces-how-to-protect-yourself/
"Viruses covered in “envelopes” have the most trouble surviving outside a living cell. On surfaces, the surrounding light, heat, and dryness break down the envelope, killing the virus. (Porous surfaces pull moisture away from viruses that land on them, accelerating the destruction of the envelope.) Most rhinoviruses have such envelopes; so do some influenza viruses. Norovirus doesn’t, enabling it to last longer in the environment."
Here are the author's relevant credentials.
Sharon Begley, senior science writer, covers genetics, cancer, neuroscience, and other fields of basic biomedical research. She was previously the senior health and science correspondent at Reuters, the science columnist at the Wall Street Journal, and the science editor at Newsweek. Among her favorite awards are an honorary doctorate from the University of North Carolina and the Public Understanding of Science Award from the Exploratorium in San Francisco.


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How to filter out the antibody light chains into kappa and lambda types on the PDB website?
The antibody light chains can either be kappa or lambda types. I am searching homologous sequences on the RCSB PDB website. Is there a way to filter out these two types?

The instructions are as follows.

Go to the RCSB PDB Webite.
Under the search bar, click Browse by Annotations.
Click the blue tab labeled SCOP.
Click the white arrow next to the folder titled All Beta Protiens.
Click the white arrow next to the folder titled Immunoglobulin-like beta-sandwich (...).
Click the white arrow next to the folder titled Immunoglobulins (Superfamily).

This is where it splits, based on your specific search.
For Light Chain, Constant Domain:

Click the white arrow next to the folder titled C1 set domains (antibody constant domain-like).
For Kappa Type, Click the folder (not the arrow) titled Immunoglobulin light chain kappa constant domain, CL-kappa.
For Lambda Type, Click the folder (not the arrow) titled Immunoglobulin light chain lambda constant domain, CL-lambda.

For Light Chain, Variable Domain:

Click the white arrow next to the folder titled V set domains (antibody variable domain-like).
For Kappa Type, Click the folder (not the arrow) titled Immunoglobulin light chain kappa variable domain, VL-kappa (...).
For Lambda Type, Click the folder (not the arrow) titled Immunoglobulin light chain lambda variable domain, VL-lambda (...).

This should get you to the list of proteins that you are looking for.

Very very helpful! Just to confirm, would it be possible that some antibody PDB are not fully annotated so not included in this search?

Yes, a lot of them are not included in the above searches. However, you can find most of the rest here -> https://www.rcsb.org/pdb/search/smartSubquery.do?smartSearchSubtype=TreeQuery&t=12&n=1933

@lanselibai Would you like me to add instructions for heavy chain types as well?

Of course, go for it!


text:
Would "Pox Parties" of the young/healthy (while isolating the vulnerable) be an effective method of combating the COVID-19 outbreak?
It is commonly said that most people, especially the healthiest would only develop mild syndromes.
Therefore, shouldn’t we, instead of confining all the population as a whole proceed as follows :

isolate the most fragile people (older people or those with known health issues) in their home or in some other safe places.
invite healthy people to join some kind of "controlled contamination" campuses for 3 to 4 weeks. During this period, these people would get the virus inoculated on purpose, will get sick, will most of the time recover since they are healthy, and will become immune to the virus.

This way the general population will, step by step increase its immunity and as a result, the more fragile people would become less exposed to the virus.

This strategy is known as a "Pox Party".

SE Biology is a question and answer site — not a discussion site or a site for floating ideas. It is concerned with the mechanisms of biological processes, not medical or social aspects of biology. I therefore think  that your question on dealing with the coronavirus outbreak is off-topic here. The question might be on-topic at SE Medical Sciences. Otherwise you are advised to consult more appropriate reputable sources for such information, some of which are listed here.

Apart from the inherent wisdom or lack thereof of this course, it assumes that "smart people" are in charge.  Observation suggests otherwise :-(

This is a proposed/tentative answer only...
Statements from official public health sources could be summarized as: older people and those with certain pre-existing health conditions including compromised immune systems are more likely to be more severely affected.
"More severely affected" means requiring hospitalization, suffering permanent lung damage, or dying. "Requiring hospitalization" may be equivalent to a death sentence if the health care system is so overwhelmed that not all who need the necessary care can receive it.
"More likely" means that younger or otherwise healthy individuals are by no means certain to recover from an infection free of any long-term consequence... they are just more likely to.
There are already reports in the media of younger, otherwise healthy individuals dying as a direct result of COVID-19 infection. There doesn't yet seem to be enough known about this disease to make any reliable predictions about the effects of an infection on any given individual; it can at best be expressed as a probability.
Regardless of age or health status, deliberately allowing people to become infected knowing that as a direct result, some fraction of the population will suffer permanent lung damage or die is not ethically sound policy. There can be no guarantee that isolation measures will be good enough, or that there will be a high enough level of public compliance to protect the safety of the vulnerable, so it will place the vulnerable at risk anyway.
The whole point of immunization vaccines is to do the same thing as you suggest, but without suffering the effects or consequences of the disease. The problem is that it takes time to develop, mass produce, and distribute a safe, effective vaccine targeting a new virus. The whole point of social distancing is to slow the spread of a disease in order to minimize the harm it will do, and if a vaccine is ultimately coming, buy the time it takes for that be accomplished. The other possible outcome from social distancing is that the virus could eventually "burn out" - when all infected individuals recover and and become non-infectious before they have an opportunity to infect anyone else.


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Are there any documented instances of coronaviruses being directly transmitted from bats to humans?
Many human coronaviruses have ancestral host origins in species of bat. However, all instances I am aware of identified other animals as intermediary vectors:

SARS-CoV: Human ← Palm Civet / Raccoon ← Bat
MERS-CoV: Human ← Dromedary Camel ← Bat
HCoV-229E: Human ← Alpaca ← Bat

Are there any known cases of direct bat to human transmission of coronavirus?

Source: Bats and Coronaviruses, Viruses (2019)

Have you ever thought of "identified other animals as intermediary vector" as a kind of necessity? An  intermediary vector is a necessary, searched for missing link for the very fact that bat virus strains just do not infect human cells (recent research in Cambodia found bat virus strains with even better affinity to target receptor ACE2 - it is not at all clear  if those species were able to infect a human cell. "I guess not!")

It is possible, but unconfirmed, that the first incidents of SARS-CoV were directly infected by bats, and that palm civits were infected parallelly:

The new study demonstrates that Chinese horseshoe bats harbor a pair of SARS like viruses that are very closely related to the strain that caused the 2003-2004 pandemic and that these strains have the capacity to directly infect human cells and civet cat cells as well as bat cells. These findings suggest that bats may have directly infected humans and that civet cats may have been incidentally infected.

More Evidence Emerges That Bats May Have Spread SARS, JAMA (2013)


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If every person between 15-60 had an immune system equal to the healthiest people, would this affect the spread of coronavirus?
Has anyone calculated the speed or breadth of the spread of something like coronavirus (or any cold, flu, airborne pathogen) based on how well the population can master the virus with their immune system? Just as a simple example, let's say you shortened the window of contagiousness by 2 days. Would that have a significant impact on the spread of the virus?

SE Biology is a question and answer site — not a discussion site or a site for floating ideas. It is concerned with the mechanisms of biological processes, not medical or social aspects of biology. For one of these reasons I think  that your question on the coronavirus outbreak is off-topic here. Question of a medical nature might be on-topic at SE Medical Sciences. Otherwise you are advised to consult more appropriate reputable sources for such information, some of which are listed here.


text:
How does the immune system distinguish between a TH1 and a TH2 response?
Hello and thanks for taking the time to read my post.
I know that naive T-Cells (T0) can be induced to become mature T-Helper cells (TH1 or TH2)
by induction with either IL2 or IL4.
IL2+  TH0 -> TH1   Humoral (antibody-mediated)
IL4+  TH0 -> TH2   Cell Mediated response
But what I would like to know is the causal chain that creates the IL2 and IL4 cytokines.
The reason I ask is because one clinician has reported that Azythromycin(an anti biotic) is useful in treating COVID-19(a virus) disease and was wondering if the immune system might become confused about whether should develop a TH1 or TH2 response.
If you can provide me with any help I would greatly appreciate it
Thanks in Advance
Michael Mckeon

From what I have read, the Stage 3 differentiation depends on the surrounding cytokine environment. IL-2 does not specifically promote T-Cell differentiation, it is a general growth factor which promotes proliferation, and is secreted by both profiles.
Differentiation of T-Cell into Th1 is controlled by Interferon Gamma, the production of which is stimulated by IL-12, which is secreted by many APCs (upon stimulation by IFN Gamma produced by cells, in a self-feeding loop). IFN Gamma also suppresses IL-4 production.
Th2 cells are promoted by IL-4. It is not exactly known which cell initially produces IL-4, but it could be basophils. IL-4 then acts in a self-promoting loop, which encourages T-Cells to produce IL-4 as well as other effector cytokines, and also stimulates IL-10 production, which suppresses production of IFN Gamma and IL-12.
Thus, each pathway is self-promoting and suppresses the other pathway, ensuring that the immune response is set in stone.


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Can a gene be split between different genomic locations several kb appart?
Can you have exons and introns of the same gene separated by hundred of kb in a genome? If so, how is the full mRNA assembled in such distance?
I'm working on plant mitochondria and I've seen an annoted gene that is cut between very distinct part of the genome.

Is the sequence of this plant mRNA in the public domain or one you have determined yourself. If it is in the public domain you should give a citation.

The isolated exon that led me to this question is nad5 in Arabidopsis thaliania mitochondrion genome (GenBank accesion NC_037304.1). I came accross this related question link and the word "trans-splicing" led me to a paper from 1991 reporting its discovery PMC453077. I still can't understand how these pieces can be put back together amongst all the other pieces available.

Well, yes, the GenBank data shows the nad5 gene to have three exons, quite a distance apart. Plant mitochondria are rather specialized, so it sounds as if you will need to read some specific reviews on introns and splicing in that system, assuming that you have read up generally on RNA splicing first.

Are you asking if transcripts with introns above length 100 KB exist? Or are you asking if a gene can be separated by a DNA-stretch that is not transcribed?

Yes you can have exons and introns of the same gene separated by hundred (even thousands!) of kilobases.
Here is an example for the human genome:
"On average, there are 8.8 exons and 7.8 introns per gene. About 80% of the exons on each chromosome are < 200 bp in length. < 0.01% of the introns are < 20 bp in length and < 10% of introns are more than 11,000 bp in length."
Source: https://www.ncbi.nlm.nih.gov/pubmed/15217358
For the splicing process, it is not really a problem for the distance. Let me reframe the questions by challenging the assumption you are making: long distances in a sequence correspond to long distance in space.
Actually, DNA/RNA molecules are can have a lot of tertiary structure for example, G quartets for DNA, hairpin structure for RNA.

Source: https://upload.wikimedia.org/wikipedia/commons/5/5d/ATPC_secondary_structure.jpg
Long sequence distances are a poor indication of the real distance in space. Thus although from an engineering point of view it is incredible what molecular splicing can achieve mechanistically speaking. As far as I remember, the length for the intron/exon is important for the efficiency/timing of the splicing process (I might be wrong here on the specifics).

The averages you quote are for human genomic DNA. The question is about plant mitochondria.

Indeed there are for human genomic DNA. I would suggest that you re-read the question: the person work with plant mitochondria, but the question is not about plant mitochondria. I interpreted it as a more general question to which I gave a general answer to help the person identify the knowledge gap. I have edited the answer to include this precision thanks for the suggestion.

Thanks for your help, it's a good reminder to keep in mind the tertiary structure. I now realise my title was unclear. My interogation wasn't about the total lenght of a gene but more about having only an exon of gene really far from the other exon (without having an intron in the middle but non-coding DNA or other genes). I came across the idea of trans-splicing, I think it's what it is? Then, how does the spliceosome knows which pieces come together in a single gene?