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Herd immunity without vaccines? (corona question)
Obviously there is herd immunity against many viruses such as measles because of vaccines.
Can we say that there is herd immunity against any particular virus even though people are not getting vaccinated, and what virus would that be?
Do you typically get herd immunity without vaccines against viruses without vaccines or do the viruses just linger around and infect fewer people because many have already become immune after catching the virus and developing anti-bodies?
What is "normal" virus behaviour?

Can you please not substancially edit a question after it has been answered to bascially add another question to it? Please open a new question instead.

This is not just a corona related question, this is true for each disease which is can be transmitted easily and which builds up a lasting immunity.
Herd immunity per se means that a large proportion of a given population is immune to a given disease, either because of vaccination or because the population went through the disease, survived it and built up lasting immunity. This means that even when this disease comes around again, it will only infect few people who have no immunity, but will not spread through the population. This can be seen in the figure below (from here), which implies vaccination, but works as well with getting the disease.

The first case is what happens right now with SARS-CoV-2, it is a new disease to which no one has immunity, so everybody who gets in contact will get the disease (either more or less severe).
If no vaccine would be available, this infection would go on, until a big enough proportion of the population has gone through the infection, developed immunity and thus stops the spread (go to the third part of the figure). At this point a big pandemie would stop.
However, this strategy has one problem: People who are coming into the population (newborns for example) who have no immunity are susceptible for the disease. This ensures low level infection rates and will make sure that the disease will stay in the population, but mostly not noticable. Over time the number of not immune people will rise until there are enough of them to feed another big breakout.
As @bryankrause pointed out, in the past getting to the point to reach herd immunity (at least partly) for diseases like smallpox or measles and to maintain it, cost a lot of lifes.
This is exactly what can be seen in the number of measles cases before the introduction of the vaccine in 1967. Before vaccination every 18 - 24 months enough people without immunity where present, causing another wave of cases. After introducing the vaccination this pattern changes and case numbers went down drastically. See the figure (from reference 1) for illustration. This figure uses data from the US, but you see similar pattern in the rest of the world.

For some more information have a look at reference 2.
Reference:

Evolution of measles elimination strategies in the United States.
Vaccination and herd immunity: what more do we know?

Might be worth pointing out that for previous diseases in which herd immunity was present in parts of the human population, like smallpox and measles, there was a substantial cost in deaths to get to and maintain that point.

@BryanKrause Good point, I will add it.

"this infection would go on, until a big enough proportion of the population has gone through the infection, developed immunity and thus stops the spread" This assumes the vaccine, or rather the immune system, gives immunity. Influenza for example, develops unrecognisable antigens faster than our population can develop immunity, hence an individual can get the flu many times. How does that fit in with this model of herd immunity?

@James It still fits. After the mutation of the flu you don't have the same virus anymore that run through it before. There is immunity against the old virus (either from vaccination or the infection itself) but there is none to the new one. Thus we get a lot of infections until we cross the threshold in the population and reach herd immunity. Luckily we only see real pandemic flu viruses rarely, with the last one 2009 being an exceptionally mild one.

Herd immunity is not a steady state. There are always new babies born, adding susceptible persons to the population. So even in the case that there is neither immunity waning nor antigen drift in pathogen, herd immunity goes away over time, and a new wave of infections becomes eventually possible and happens sooner or later.
In order to keep herd immunity (as in the case of measles) you will have to vaccinate the children.


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network with all the interactions of the alpha-synuclein protein
I would like to make a network with all the interactions of the alpha-synuclein protein (in homo sapiens), that is, I would like to visualize the pathways where this protein participates, I would also want to include in the network the genes that encode this protein.
I would like to make this network in cytoscape. Could someone tell me where I can find a guide to do this.
thanks in advance

What have you tried and where are you stuck?

I just started using cytoscape. What I don't know is how to obtain the pathways in which the alpha synuclein participates from cytoscape (or if there is a way to download them and then import them into cytoscape). I would like to create a node with the name snca (which is the alpha synuclein), then, from that node, get the pathways where the alpha synuclein participates, but I don't know how to achieve this

In other words, I would like to build an Enrichment Map, which would show the different pathways in which the alpha synuclein involved is found (both in diseases and physiologically), that is, each node would be a pathway, but each node, too, would be a subnetwork, I should be able to view each of these subnetworks. Excuse me for the question but I am just starting in this field

source: Stack Exchange

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

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Why do meristematic cells have prominent nuclei and dense cytoplasm?
I've been reading about meristematic cells having prominent nuclei and dense cytoplasm. However, I could not understand why it is that way. Could somebody please explain?

Welcome to the site!  "I've been reading..."  would it be possible to elaborate a bit?  Context as to what you have been reading would help us understand the question.  Direct quotes is best with links for reference if possible.  Thanks!

It's from a textbook from school. The book points out the basic characteristics of meristematic cells. "As the cells of this tissue are very active, they have dense cytoplasm, thin cellulose walls and prominent nuclei." I understand that the cells are active but I do not understand as to why that would lead to having prominent nuclei and dense cytoplasm. @rotaredom

Because meristamatic cells are the ones who are undergoing mitosis to increase the height of the plant, and diameter of the plant . They undergo continuous division. So y hey don't mature. They only form the primary cell wall.
I wrote another a answer.  Perhaps this will answer the question

Welcome to Biology.SE! This looks like it could become a good answer, but to do so you need to connect "continuous division" and lack of maturation with the described "prominent nuclei and dense cytoplasm". I would expect it to also mention vacuoles. In addition, answers are much more likely to receive a favorable response if they include supporting references (primary literature is best, but a textbook would work for this). Without that support, your answer is indistinguishable from opinion. ...

... The is a good example of how to format references. ——— You may also want to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!

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Why do antibody tests target different antibodies?
I've noticed in various COVID-19 lateral flow assays, they seem to target different antibodies (S1, S2, NP). What are the benefits or downsides of choosing different antibodies? I know that some have a higher chance of cross-reactivity, but why wouldn't all tests just use the ones with the lowest cross-reactivity?

I think you're confused by polyclonal tests https://www.nature.com/articles/d41587-020-00010-2

I've used multiple assays. Some only respond positive to N Mab others respond positive to S1 Mab.


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What happens to a virus SARS-CoV-2 on an object?
Many articles say that "the coronavirus" — they probably speak of the SARS-CoV-2 — can "remain alive" for so many hours on some surfaces, so many days on some other surfaces. For example, "the virus lives 5 days on glass".
I think that this is a bad choice of word. All these articles speak about the virus SARS-CoV-2 as if it were a living being. But I think it is not a living being. The virus SARS-CoV-2 does not "live" on a glass surface. It just is there.
When a virus SARS-CoV-2 is on an object, what happens to it? If it is not there anymore after 5 days, why? What does time do to a virus?

This is almost a duplicate of Why does the SARS-CoV2 virus not remain infectious forever? Or does it?. Check out that question to see if the answers there answer your question

@Charles - This other question is interesting. But on its page there is no answer to my question. Especially, on flat glass or steel surfaces, what happens?

Edit: What does time do to a virus?

The linked duplicate asks the same question: "All these articles speak about the virus SARS-CoV-2 as if it were a living being. But I think it is not a living being." and the answer there is "Rubber bands (for example) aren’t alive either, but there are several ways they can be destroyed, including physically pulling them apart or just by having them exposed to air enough. Viruses are the same, conceptually." If you want to ask a different question I'd strongly recommend removing the trivial bits about viruses not being "alive" that implies that this should somehow make them invulnerable.

Those articles simply refer to the viability of the virus, i.e. whether it can still infect a host thereafter. (Sometimes this is referred to as "survival" of the virus.)
A unviable virion is not quite the same as it being "not there" at all, although it is so from the perspective of a host that doesn't get infected.
Those viability [in the environment] studies use a quantitative measure of how much of the virus (i.e. how many virions) are still viable after some time on some surface (or even in "the air"), e.g.

SARS-CoV-2 remained viable in aerosols throughout the duration of our experiment (3 hours), with a reduction in infectious titer from 103.5 to 102.7 TCID50 per liter of air. [...]
SARS-CoV-2 was more stable on plastic and stainless steel than on copper and cardboard, and viable virus was detected up to 72 hours after application to these surfaces [...], although the virus titer was greatly reduced (from 103.7 to 100.6 TCID50 per milliliter of medium after 72 hours on plastic and from 103.7 to 100.6 TCID50 per milliliter after 48 hours on stainless steel).

So they are measuring the time to some [chosen] statistical threshold of viability. For reference as to their particular method:

The TCID50 (Median Tissue Culture Infectious Dose) is one of the methods used when verifying viral titer.
TCID50 signifies the concentration at which 50% of the cells are infected when a test tube or well plate upon which cells have been cultured is inoculated with a diluted solution of viral fluid.

Which part of the virus machinery breaks first might depend on the environment. On copper, for example, it has been found that for "common cold" coronaviruses (e.g. HuCoV-229E):

Exposure to copper destroyed the viral genomes and irreversibly affected virus morphology, including disintegration of envelope and dispersal of surface spikes. Cu(I) and Cu(II) moieties were responsible for the inactivation, which was enhanced by reactive oxygen species generation on alloy surfaces, resulting in even faster inactivation than was seen with nonenveloped viruses on copper.
[...]
Coronavirus was exposed to metal surfaces and recovered, and the positive-stranded viral RNA genome was extracted and purified. A one-step reverse transcriptase real-time quantitative PCR (RTqPCR) was performed to detect a 139-bp region of ORF1 within nonstructural protein 4 (nsp4). Virus that had been exposed to copper and brass surfaces demonstrated reduced copy numbers of this fragment with increasing contact times. [...] . Comparison of the entire viral genome by agarose gel electrophoresis confirmed that nonspecific fragmentation occurred on copper and brass, with fragments becoming smaller with increasing contact time.

See also related q here on virus survival in small droplets, where a different inactivation mechanism is suspected.
In general, all viruses start to degrade outside their hosts at temperatures above -20C, even in the absence of some more specific environmental stressors (like unfavorable humidity, reactive surfaces like Cu, etc.) In suitable hosts, this temperature-based degradation is more than offset by the virus' multiplication.

Thank you. I have added to my question: What does time do to a virus?

@NicolasBarbulesco: Time does nothing unless the temperature is high enough or there are some other "nasty" environmental factors. Influenza viruses have been preserved for over 50 years in cryogenic conditions (once unfrozen they are viable), some viable viruses have been recovered from 30,000 years-old permafrost;.see end of my answer and the med SE q linked from there for details. Are you asking for details about temperature-related degradation (as it's the most general mechanism)?

From What happens to viruses that causes them to die?:
TL;DR: Factors such as UV light and heat causes the mix of RNA, fatty membrane, and protein making up the viruses to steadily break down.

More details:
https://www.sciencefocus.com/nature/do-viruses-die/:

Strictly speaking, viruses can’t die, for the simple reason that they aren’t alive in the first place. Although they contain genetic instructions in the form of DNA (or the related molecule, RNA), viruses can’t thrive independently. Instead, they must invade a host organism and hijack its genetic instructions.

https://www.sciencealert.com/how-long-does-coronavirus-last-on-surfaces:

Just hanging about in the atmosphere, the effect of factors such as UV light and heat causes the mix of RNA, fatty membrane, and protein making up the [viruses] to steadily break down in a few hours [or less/more].

https://www.statnews.com/2020/03/19/coronavirus-survives-on-surfaces-how-to-protect-yourself/ (mirror):

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.


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Human somatic cells have 22 pairs of homologous chromosomes?
I am studying for my Bio class and I am stuck with questions that I came up with during this chapter of Meiosis. I understand that human somatic cell is made up of 22 pairs of autosomes and 1 pair of sex chromosome. I am confused about what made up each pair of autosomes? is that 1 chromosome from the father and 1 chromosome from mother made up 1 pair of autosomes in somatic cells? and therefore, since each pair of autosomes consisted of 1 chromosome from dad and 1 from mom, we can say human somatic cells consisted of 22 pairs of homologous chromosomes (not to mention the sex of the human), right?

@PolypipeWrangler 22.5?!  You can't have half a homologous pair.  But I get what you're trying to say and it's true... There are 22 homologous pairs and half the time there is a homologous XX pair.  The other half the time there's a heterologous XY pair, though even portions of those chromosomes are homologous...

Got it! thank you so much for the clarification!

Answer: *Yes  , human somatic cells have 22 pairs of homologous chromosomes
The human genome consists of 46 (2n*(22+1) ) chromosomes.
Most of our cells are somatic and diploid (2n), they have two homolgous chromosoms (called homologs, one "father" & "mother") these cells multiply by mitosis.
Reproductiv cells or gonosomal cells, (gametes; Sperm and eggcell(ovum)) are the product of meiosis ( a part of gametogenesis ) . These cells are haploid (1n), they only have one set of chromosomes (1n * (22+1)) which is a combination of "fater&mother". When 2 gametes  combine a diploid zygote is formed.
In both cases (Mei- and Mitosis) chromosome (pair (2n)oder single(1n)) number 1 -22 are called autosome , while
Chormosome number 23 is an allosome (sex chromosome), either Y (male) or X (female).
Since the gametes are haploid (1n) they have only 1 single allosome, egg cell always X , and  sperm cell either X or Y.
If the allosome (the 23 chormosome pair) of an human is hemizygot ( X–Y ), he is genetically male. Is the allosome pair X-X
,homozygot the person is genetically female.
Somatic cells can have therefore 22  pairs of homologous chromosomes the 22 autosomes. The allosome pair of chromosomes is not considert homologous but either "homozygot / homogametic"[XX] or "hemizygot/ hemigametic"[XY].


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How do we know that the "original animal exposure event" of a human to the Covid-19 virus occurred between October and December 2019?
In a Yale med page (interview) on Covid-19 from January it is said that

The molecular dating of the virus genomes indicates that the original animal exposure event happened sometime between late October and early December of last year, very near the times that the first cases were detected. This is unlike Zika virus, for example, where transmission occurred for many months before the virus was detected.

To someone unschooled in molecular dating, how do you explain that we (seem to) know with such precision when the "original animal exposure event" occurred in that October-December timeframe?

@reuns: I'd accept that as frame challenge answer (there are some papers which say it that way, IIRC). I think for SARS it's still disputed in some corners exactly how it was transmitted to us.

From what I read in cell cultures it seems that when changing the species/cell-line the virus usually gets between 2 and 10 AA mutations in days or weeks. I think this idea deserves to be investigated a little more because if we find this mutation process usually lasts for months it would indicate that the species jump occurred a few months earlier.

Sorry, I linked to the wrong paper (in the same journal) in my previous comment. The one disputing more intensely the route of SARS to us is https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6356540/ (section 2.1)


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How do researchers know that a species is at risk of extinction?

Recently researchers present evidence that the platypus is at risk of extinction.

Source
How do researchers know that a species is at risk of extinction?  I mean Earth is so large, said species could be deep in the Pacific ocean or somewhere else that has been thoroughly explored.

Habitat. (most) species can't live under your bed.

I can give some leads to those who can write a good answer: https://www.researchgate.net/publication/23311481_Quantification_of_Extinction_Risk_IUCN's_System_for_Classifying_Threatened_Species and https://www.iucnredlist.org/about/barometer-of-life and https://www.google.com/search?q=measurement+of+extinction+risk&oq=measurement+of+extinction+risk&aqs=chrome..69i57j33l4.3520j0j4&sourceid=chrome&ie=UTF-8

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, questions need to be narrowly focuses so that they are answerable on this site. This would need a book to answer in a non-trivial manner since different species have different requirements. ——— 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!

The to assess the extinction risk of a species, Researchers first study the ecology and global populations of the species.
Then mathematical models are applied to  simulate the population dynamics and estimate extinction risk.
The results are collected in the IUCNs Red list.
https://www.iucnredlist.org/


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What kind of worm/bug is this?
Recently, I found a few worms in my bathroom and I am wondering what kind of worms are they. They move slowly and they are about 6-9 millimetres long. It seems that they are not sensitive to water. Are they harmful parasites or harmless creatures? For your information, I live in Turkey.
Here are photos of a selected worm.

Thank you for your help.

Welcome to Biology.SE! For identification questions please [edit] your post to include the location (e.g. country and region — the more specific the better) where you observed this creature. The location can be an essential clue for identifications. ——— If possible clear, closeup photos of the creature from multiple angles (e.g. from the side and below) could also be helpful. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

This is almost certainly a fly larvae of some kind. My initial guess was Psychodidae due to the bathroom location and siphon-like structure, but the body shape (wide and tapering vs long and narrow) and lack of distinct head leave me guessing this is not correct.

Possibly Fannia? (See here, here, here, and here). Can you provide any additional (BETTER QUALITY) photos or more context (where in the bathroom? do you have cigarettes in the bathroom?, any dead bodies?, anything else to note?)?

These worms were crawling on the floor. Also there was an almost full trash can in my bathroom and were no cigarettes. ResearchGate reference photos resembles these worms and your explanation of a fly larvae of some kind is pretty convincing. Because I don't own a pet or any other animal at my home. Maybe they went out from the trash can to the floor. I cannot provide better photos since I cleaned all my bathroom and fortunately there are no signs of them anymore. If you provide your answer below, I can accept it.


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blast search against UNIPROT
I would like to ask how i can search in blast against UNIPROT (TREMBL PLUS SWISSPROT) for a selected organism. In the BLAST site there is no option about UNIPROT(only Swissprot), and in the uniprot site i cannot limit the results only in one organism(E.COLI).
THANKS A LOT!!!

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

thank you and i am sorry!!

You can blast for E.coli proteins only using Uniprot. Firstly, you restrict the search to the "target database" UniprotKB...Bacteria. After performing the blast search, you can further restrict your search results to include only hits for one "Popular organism", e.g. "Escherichia".

thank you so much!!

@marilu Can you please mark my answer as correct?

is it ok?i think i did it

@marilu Yep, thank you!


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Which is more efficient as a germicide: UVC, Ozone or combination and why?
I've read many contradictory info about ozone vs UVC light irradiation and cannot come to a conclusion, I am totally confused.
As it commonly known UV germicidal irradiation is very effective against bacteria, virus, molds, but in the disadvantages chapter one can read

Another potential danger is the UV production of ozone, which can be harmful to one's health. The US Environmental Protection Agency designated 0.05 parts per million (ppm) of ozone to be a safe level. Lamps designed to release UVC and higher frequencies are doped so that any UV light below 254 nm wavelengths will not be released, to minimize ozone production. A full-spectrum lamp will release all UV wavelengths and produce ozone when UVC hits oxygen (O2) molecules.

OK, ozone is a bad guy which can cause mutations, cardiovascular diseases and other bad things.
But then I read about ozone magic germicide abilities, that it can destroy all types of bacteria, water treatment, air purification and even cleaning of contaminated soils, and maybe even COVID-19.
So why they often advise against ozone?
I've found not so much science researches about comparative efficiency of zone and UVC, for example this which seems very dated (2003), and it says that UV is less costly but not as much universal and effective for water purification as ozone.
This one, more recent, clearly states the idea I also came to:

Vacuum-UV lamps with ozone production were found to be effective for inactivating various human pathogens.

Also I've found many comparative tables like this that confirms better ozone efficiency in all circumstances

We know that UV-lamps with wavelength below 254 nm produces ozone so why not to combine their strengths together?
So where is the truth in all these contradictory sources? How to filter out all those marketing fluff that ozone and UV-lamp sellers put into our ears?
P.S. I saw this question and it covers only part of mine.

Your question contains the word "efficient". The most efficient method is the one with achieves the goal with the minimum of effort or disadvantages. And that totally depends on what you want to do exactly.

If you have a surface like a lab bench, you use ethanol or iso-propanol because its cheap, quick, relatively safe to use for that purpose and dries up quickly without remaining substance.
If you have a cabinet to work with, you use UV irradiation because you can leave it on at night where it does not hurt your eyes/skin and it can pervade the small corners in the cabinet.
If you have a pool, you use ozone or chlorine because you have liquid water here so ethanol does not reach the desired concentration. However UV is also an option, for example for sewage treatment
If you have a small volume of liquid, you can use a microfilter because it's faster than using UV and does not split chemical bonds.
If yo have a living organism, you use antibiotics which are weaker (in comparison to the measures above) and more expensive but you cannot use the other measures because they would kill the organism

So both efficiency and efficacy of desinfection have to be chosen based on the concrete situation. There is not "the most efficient" way of disinfecting.

Yes, efficient for me is the ability to disinfect living quarters with lesser harm for humans

@Suncatcher still depends on the organism. Do you have rodents, parasites, fungus, bacteria, virus?

where? in my body or in the environment? of course they reside in my house. Let's assume the organism is weak


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What changes would allow cutting mRNA-based vaccine safety testing to 18 Months
I see a lot of skepticism among my fellow citizens following an interview that Bill Gates gave the BBC on the topic of Corona vaccines. The Gates foundation is funding several study ventures on Corona vaccines, conventional vaccines as well as experimental mRNA vaccines. In the interview he said:

"We'll need to fund the ten most promising constructs because we don't know in advance which on will prove to be safe and effective [...] so we gonna have to take something that usually takes five or six years and get it done in 18 months (6:09)
  [...]
  There is an approach called RNA Vaccine [...]
  that looks quite promising but we can't count on that, so we'll back 4 or 5 of that and 4 or 5 using a conventional approach, which unfortunately, the schedule on that would probably not so quick. (6:45)

There are people on the internet that criticize that Gates would want to trade security for speed in getting the vaccine out and cite this comparison (18 months instead of five years) to make a point how unsafe that would be. I interpret the interview insofar that Gates believes that the new technology itself would provide for some speed gains (longer time needed with conventional approaches). Similarly, this review (Section "Good manufacturing practice production") mentions that mRNA vaccines are easier to produce than their conventional counterparts, for example because life viruses and toxic inactivation chemicals are not involved in the process and thus do not need to be removed reliably.
However, I lack the knowledge to judge how big the speed gains due to the mRNA platform could be. Also, the same review as above mentions in the section "Safety" that there are more problems in clinical trials than there were in preclinical ones, so there still seems to be considerable need for basic research left. Similarly, I do not know how long the phase of vaccine clinical trials normally is and how much it could be reduced by logistics without loss of information. Finally I don't know what studies could be left out for an emergency approval of the vaccine to cut the approval time if the benefit would outweigh the risk.
I would be grateful if you could help me on the questions in bold.


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How common are the "common" human coronaviruses?
I was listening to a virology expert on the Swedish radio yesterday. He said that there already were several corona viruses among humans that only affected children because basically all the adults were already immune. He said that he believed that SARS-CoV-2 will be added to this category in the future, which seemed logical to me. Basically SARS-CoV-2 will at some future time only affect children and give very little symptoms because all the adults will be immune.
By googling I found four viruses listed as "common corona viruses" that affects humans:
229E (alpha coronavirus)
NL63 (alpha coronavirus)
OC43 (beta coronavirus)
HKU1 (beta coronavirus)
1.Can something be said about how "common" these viruses are?
2.I mean if an adult for some reason has no immunity to one of these viruses how long will it take on average before he gets infected?
The reason I am asking is because if we know the answer to question 2 above for the four common coronaviruses one maybe can produce an educated guess for the likelihood for a person escaping the "first wave" of SARS-CoV-2 getting infected within a given time period after we have "herd immunity" against SARS-CoV-2.

I'd question pretty much anything else that "virology expert" says, since they seem to be well outside the mainstream understanding of these viruses.

It was this guy: https://liu.se/en/employee/lensv66 Maybe people invited to public radio fell that their role is to calm the public rather than to be totally accurate.

The common [cold] coronaviruses are pretty common:

Four HCoVs (HCoV 229E, NL63, OC43, and HKU1) are endemic globally and account for 10% to 30% of upper respiratory tract infections in adults.

To pick a more detailed study in Ghana:

This study sought to determine whether human coronaviruses (HCoVs) are associated with upper respiratory tract infections among older children and adults in Ghana. We conducted a case control study among older children and adults in three rural areas of Ghana using asymptomatic subjects as controls. [...]
Out of 1,213 subjects recruited, 150 (12.4%) were positive for one or more viruses. Of these, single virus detections occurred in 146 subjects (12.0%) and multiple detections occurred in 4 (0.3%). Compared with control subjects, infections with HCoV-229E (OR = 5.15, 95%CI = 2.24–11.78), HCoV-OC43 (OR = 6.16, 95%CI = 1.77–21.65) and combine HCoVs (OR = 2.36, 95%CI = 1.5 = 3.72) were associated with upper respiratory tract infections. HCoVs were found to be seasonally dependent with significant detections in the harmattan season (mainly HCoV-229E) and wet season (mainly HCoV-NL63).

Occasionally there are substantial outbreaks of common cold, e.g. as observed in Japan:

we conducted a longitudinal survey
between 2010 and 2013 in Yamagata, Japan, to clarify
the epidemiology of HCoVs using RT-PCR methods
[...]. In 2011, we
found that the monthly detection frequencies of HCoVNL63 were higher than 20% in January and February
(28.5% and 25.3%, respectively), whereas those of the
other HCoVs (HCoV-229E, -OC43, -HKU1) did not exceed 20%. In light of these findings, we continued
the HCoV surveillance and, thus, captured data from
the largest outbreak of HCoV-OC43 reported in the last
6 years. During the 2014–2015 influenza season in
Yamagata, Japan, the monthly detection frequencies
were approximately 30–40%.

Those percentages are from people reporting symptoms (and then swabbed.) The graph below (from the same paper) nicely shows the seasonality.

Monthly distribution of clinical specimens (A) and HCoVs (B) detected from patients with acute respiratory
infections between January 2014 and March 2015, in Yamagata, Japan.

Question 2 is rather meaningless because immunity to common coronaviruses is short lived. See (also) this answer (esp. the 2nd table) to a related question putting the common coronaviruses immunity duration in perspective; reproducing just the table below (the relevant line for common coronavirus is the 1st below the break, i.e. 1st in the 2nd section of the table).

And I've managed to track down one of the primary studies on 229E long-term immunity (or rather lack thereof)

Although after 1 year concentrations of specific serum IgG and nasal IgA were
still significantly raised in the infected group, they were much lower than at the
maximum. [...] When challenged after 1 year all of the original uninfected group were infected and 6/9 of the infected group were reinfected. [...] In the infected group there were considerable individual differences. Some lost their antibody, particularly serum antibody, completely by 1 year, some did not.

And it's basically impossible not be exposed to a strain of the common cold coronaviruses at one point; one study on newborns found that interval to be 3.5 years, but that's probably an overestimation for adults.

all of the children had maternal anti-NL63 and anti-229E antibodies at birth that disappeared within 3 months [...] on average, HCoV-NL63 and HCoV-229E seroconversion occurs before children reach the age of 3.5 years.

The real question is whether Covid-19 will behave like the common coronaviruses or more like SARS and MERS for which it is suspected (from the detection of antibodies), but not certain that immunity lasts longer.

For the SARS and MERS coronaviruses, antibodies appear to persist for several years, but no studies have intentionally attempted to re-infect people, since these are deadly diseases.

Persistence of antibody isn't a direct measure of immunity; Memory B cells remain and can mount an immune response after circulating antibodies are gone.


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How does DNA shape a living organism?
I'm haven't studied biology so excuse me if I'm getting something wrong.
I'm trying to understand how the DNA from a sperm and egg cause the egg too multiply and form a perticular shape (shape of a fetus). Or in case of plants how does dna in a seed cause the sapling to grow into a plant of perticular shape and size?
I mean how does DNA cause the cell to multiply and grow into hands and legs and heads of a certain shape and size in animals. Or to stems, branches and leaves in plants? How does DNA shape a living organism?

Answer to this question can fill (and has filled) multiple textbooks. Entire branch of biology - developmental genetics - studies exactly this. If you are interested I recomend starting with some introductory book about genetics. If you don't significantly narrow your question I doubt someone will be able to answer you here.


text:
Could someone explain the join in the SARS-cov-2 genome at location 13468?
I am having trouble understanding the reference sequence for sars-cov-2, NC_045512.2
Three nucleotides equals one amino acid, right? But the nucleotide at position 13468 seems to be used twice, so the sequence starting at 13463 reads:
tta aac ggg ttt ... which translates to LNGF
However, according to the reference, the translation is LNRV, so it's read as tta aac cgg gtt etc - like the c is repeated.
The reference says "join(266..13468,13468..21555)" but how does this work and why?

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

And if you think that's wierd, the transcriptional phase can get even more so because of the  error-prone RdRP: "For some nsNSV, like those of the Paramyxovirinae subfamily (e.g., measles, mumps, and Sendai virus) and Ebola filovirus, there is also a form of programmed transcriptional frameshifting (PTF). The most egregious example of this is parainfluenza virus type 3 (PIV3), where a stretch of 300-odd nucleotides in the middle of the P gene is translated in all 3 frames." https://rnajournal.cshlp.org/content/21/4/667.full

In the reference genome browser, it seems you are looking at the first Coding Sequence (CDS) line, YP_009724389.1, which shows the translation to LNRV...:

If you look lower down, you'll see a line for CDS YP_009725295.1, which shows translation to LNGF... as you expected.
So, these are two different interpretations of possible translations for this area of the genome.  Why does the first have the weird peptide sequence?  If you hover over the CDS line, the browser will pop up more information about it.  For the top CDS, that includes this comment: "pp1ab; translated by -1 ribosomal frameshift".  This suggests that someone believes that sometimes the ribosome translating the RNA glitches at that point and advances only 2 nucleotides instead of 3 after the "N" codon.  This shifts the interpretation frame as if there were another C present.
If you search for "pp1ab", you'll see it's mentioned in the Feb. Nature article on the sequence.

it seems there is one wiki article per coronavirus secondary structure  https://en.wikipedia.org/wiki/Coronavirus_frameshifting_stimulation_element


text:
Biophysically, how to change from a tonically firing neuron to an occasionally firing one?
In terms of membrane properties, size and neuronal biophysics (assuming no change in incoming excitation), how can a tonically firing neuron become (say during development) an occasionally bursting neuron?
Any references would be appreciated.


text:
Why would a mammalian vector plasmid require an antibacterial resistance gene?
I have been trying to understand the composition of plasmids used in recombinant DNA cloning, such as this: https://www.genecopoeia.com/wp-content/uploads/2020/02/pReceiver-M35-051818.pdf
and I am wondering what purpose the ampicillin resistance gene has when transfected into a mammalian cell host (as it says it is for).
I understand that ampicillin resistance is used for selection in bacterial cells so that only transformed bacteria are grown as well as ampicillin being needed to prevent bacterial contamination among a mammalian cell culture, but I don't see why mammalian cells require a resistance gene to an antibiotic.
Thanks

It may help for you to look into how such plasmids are generally constructed, to understand why there is ampR. https://www.ncbi.nlm.nih.gov/books/NBK21498/

I think the assumption you are making is that the ampicillin resistance gene would save a purpose in the mammalian cells.
It does not.
As you said, it is only use during the cloning process to select the bacteria to replicate and produce more of it.
There is a resistance gene on the vector you posted which affect mammalian cells: neomycin. In this case, once transfected into mammalian cells, you could select only the cells with the plasmid by adding neomycin the cell culture medium.
Note: neomycin selection can take some time (4-5 days) and higher dose than for example puromycin. Hope this helps!


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Did my wildlife camera take a picture of a lynx?
A wildlife camera took a photograph of an animal. Unfortunately this is the only picture my camera collected. This picture was taken in the central interior of British Columbia, Canada. The distance from the camera to the subject is a few meters, and the height of the camera off the ground was probably about 40 - 50 cm.

Is this animal a lynx? It looks like it might have those fine tufts on its ears and a reduced tail.

While I generally try to avoid cross-posting, I have started pooling my observations into iNaturalist. This photo can be found as Observation 110929888.

Any chance of examining the area for tracks?

No, unfortunately the snow was quite icy and compacted; found no tracks.

How about markings on the tree trunk? IIRC lynx will sometimes scratch the bark as part of marking their territory ...

I didn't notice, but I wasn't looking for that. Interesting ethology fact though. I'll take a look at the trees in the area when I return to the location.

I thought that those cameras take a photo every second when something starts moving. It's facing towards the light as well so with the snow, it's too bright. The silhouette is definitely that of a lynx though, small tail, strong hind quarters, it looks like 90% probability it's a lynx

I have not played with the settings on this camera, but I recall from the manual that I can control the rate. I don't recall what it is currently set to, but I have a feeling it isn't as a frequent as every second; something I should correct.

As with your other trail camera question about coyote, some (fairly accurate) size estimate of the tree or other foliage in the picture may help. Lynx are typically larger than bobcats.

It is either a Canada lynx or a bobcat.
From wikipedia:

The lynx is between 73 and 107 cm (29 and 42 in) in head-and-body length and stands 48–56 cm (19–22 in) tall at the shoulder; females weigh around 5–12 kg (11–26 lb) while males weigh around 6–17 kg (13–37 lb).

The adult bobcat is 47.5 to 125 cm (18.7 to 49.2 in) long from the head to the base of its distinctive stubby tail, averaging 82.7 cm (32.6 in); the tail is 9 to 20 cm (3.5 to 7.9 in) long. Its "bobbed" appearance gives the species its name. An adult stands about 30 to 60 cm (12 to 24 in) at the shoulders.

Without a clearer image or a better sense of scale I cannot say which. Their silhouette is just too similar.


text:
Did my wildlife camera take pictures of coyotes?
A wildlife camera took these photographs of these animals. These are the only pictures my camera collected of them. This picture was taken in the central interior of British Columbia, Canada. The distance from the camera to the subject is a few meters, and the height of the camera off the ground was probably about 50 cm.
I think they're too small to be wolves, and they don't appear to be any of the dogs I've seen in the area. My intuition strongly points to them being coyotes based on pictures, videos, and occassionally seeing them in the light of day. However, I'm hoping that someone can explain why my intuition is right, if it is right.

The small coniferous tree beside the road (left of center) is about 50 cm tall.

While I generally try to avoid cross-posting, I have started pooling my observations into iNaturalist. These photos can be found as Observation 110928801.

They look like coyotes to me.

Could you see if there are any footprints in that path?
It maybe would be clarifying.

That would definitely be useful information, but unfortunately I don't have it

just based on location and probability coyote is a good bet. some way to determine scale would help, such as the height of the short plant on the left side of the picture.

@John I can go back and measure that plant. I'll update the post and tag you when I have that info'.

@John I'd say about 50 cm is the height of that plant.

That makes them barely over 2ft probably less with perspective, that is pretty solidly in coyote size range.

Fantastic! Thanks for your perspective, @John !

 Short Answer
Yes, these are likely coyotes.
 Long Answer
Your options of dog-like carnivores (i.e., Canidae) in BC include the following:

Coyote (Canis latrans)
Grey wolf

British Columbia Wolf (C. lupus columbianus)1,2
Northwestern wolf (C. lupus occidentalis)1,2

Domestic dog (C. lupus familiaris)

Siberian husky
Utonagan
Tamaskan
Alaskan malamute
Northern Inuit dog
Saarloos wolfdog
Shikoku
others...

Red fox (Vulpes vulpes)

Let's start ruling out the unlikely options:
[I'm not trying to be comprehensive, but rather just pointing out the easiest evidence we can see]

Dogs: Many of these might look wolf or coyote like, but it is very unlikely that any of these domestic breeds would be forming wild packs (as is indicated by your image containing multiple specimens). (In fact, it's unlikely you'll even see half of those breeds in BC to begin with!). I'll leave it to you to peruse the links I provided if you insist on examining and comparing their anatomies/morphologies to your specimens.
Fox: Although the largest of the true foxes, this is still a relatively small canine; they typically are less than 20 inches high and 35 inches long [source]. Without some measure of scale, we can't be sure, but your specimens certainly look larger than that relative to the tree in the background. More definitely, however, is that V. vulpes has a tail that is typically half or more of its own body length. The tail also rests nearly to the ground. The length of tail on your specimens do not match either of these length characteristics. Further, the very bushy, white-tipped tail of the fox is not represented by your specimens' only-somewhat bushy, dark-tipped tails. Red fox are also typically solitary hunters (source; unlike your shot of multiple specimens).

I know what you're thinking: "duh, get to the wolves vs coyotes already!!"
See here for a guide to differentiating wolves, coyotes, and dogs

British Columbia Wolf (C. lupus columbianus): According to Goldman (1941)3 and here, this subspecies of wolf is large with a dark (black with some cinnamon brown color) coat. No mention of a light ventral region is mentioned, which is apparent even in your night-camera shots!
Northwestern wolf (C. lupus occidentalis):

Their color does not rule them out -- This wolf subspecies is quite variable in color and can range from all dark, to mottled grey to all white. (see here for visual comparison of some wolf colorations).
This is potentially the largest of wolf subspecies (27-36+ inches tall at shoulder [source] and 4.5 - 7 feet long (nose to tail tip)! [source:i, ii). Your specimen's do not look this large, but they could be juveniles. It would be great to get a height estimate of that plant in your picture or diameter estimate of that tree...
This site suggests that the average pack size is 6-12 wolves, which is significantly more than showed up on your camera (though, obviously this could be coincidence and not a definitive way to rule out this wolf).

This leaves the coyote:

Size: Between the size of the fox and grey wolf: 21-24 inches at shoulder; 3.5 - 4.5 feet long (nose to tail tip) [source].
Color: Gray (or reddish brown), often grizzled, often with whitish/paler throat, chest, and/or belly. Black patches may be seen on the tips of tails on on feet. [[sources: Bekoff (1977)4 and CDFW].
Anatomy/morphology: Bekoff (1977)4 and CDFW compare coyotes to wolves. The snouts are thinner with smaller nose pad on coyote vs wolf, and a coyote's ears are taller and more pointed. Your images, unfortunately, don't really allow us to differentiate adequately.
Behavior: typically less social than wolves and will rarely travel in groups larger than their immediate family. Even still, they often keep their distance and practice more asynchronous activity. However, coyotes are most often observed as lone individuals or in pairs (especially during breeding season)4. This matches your camera's image.
Coyotes are most active in the early evening, but their activity can be variable. Many coyote have become quite nocturnal (especially near humans), but they are known to also be sporadically active throughout the day and showing peaks of activity at dawn and dusk. [sources: Bekoff (1977)4 and Wikipedia. Wolves, though, are also active during evening and night...

Summary
So, based on the the few number of individuals, coloration, and perceived relative size of your specimens, it seems most likely that these are coyote. If you can get us estimates of height and diameter of the foliage in the background, this could be stated more definitively.
You could always go back to the site and photograph and compare the tracks, too (try starting here and here to compare)....
...
Though of course, it could always be a "coywolf" (also see here) :p.

 Citations
 1. Nowak, R. M. (1995). Another look at wolf taxonomy. In Carbyn, L. N.; Fritts, S. H.; D. R. Seip (eds.). Ecology and conservation of wolves in a changing world: proceedings of the second North American symposium on wolves. Edmonton, Canada: Canadian Circumpolar Institute, University of Alberta. pp. 375–397. [see map on p 376 here]
 2. Goldman, E. A. (1941). Three new Wolves from North America. Proceedings of the Biological Society of Washington. 54: 109–113. [See HERE for a map]

 3. Goldman, E.A. (1941). Three new wolves from North America. Proc. Biol. Soc. Wash, 54: 109-13. [available here]
 4. Bekoff, M. (1977). The coyote Canis latrans. Mammal. Spec, 79:1-9.[see here]


text:
What external signals do tell catadromous fish to go from the sea to the rivers?
What signals do tell catadromous fish to go from the sea to the rivers? Is it photoperiodicity? Are there any other signals?


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Identify this large, beige or pine cone-colored squareish beetle and/or the pine cone it's on?
I saw this large beige beetle on a large pine cone on the ground in February in Hsinchu county Taiwan.
It was about 4 cm long and 2 cm wide and the color was similar to the pine cone it was standing on. Though it was sunny it was cool (15 C) and the beetle didn't really respond when I picked up the cone.
I remember seeing a sign about (apparently) this species in November when hiking so I've attached it as well. I think the sign warns that this is a pest but I can't read it; I assume it is in Chinese.
Unfortunately I didn't remember the poster (from November) until later.
Any idea what it is and/or what the kind of cone that it's on, and what problems it can cause?

click images for full size

It is not a beetle, but a true bug. Tessaratoma papillosa, to be exact. It is relatively common in Taiwan. It can cause problems if you have a lychee tree, as it is a destructive pest to lychee trees.
Here is an image of this animal:

The nymphs look like this:

https://www.inaturalist.org/observations?place_id=7887&taxon_id=47743&view=species
https://en.wikipedia.org/wiki/Tessaratomidae#As_agricultural_pests

This is great, thank you very much! I really appreciate the extra links. I can see that February was well before the peak observation count in April. Do you know what time of year that those colorful nymphs are most likely to be seen? The Wikipedia article doesn't give any information on the seasonal behavior. I also found it interesting that this Lychee Stink Bug Lyramorpha rosea is often confused with Tessaratoma papillosa.

@uhoh Discerning what time of the year the nymphs are most likely seen is difficult because many people on iNaturalist do not specify the life stage, but it appears to be from April to May. The wikipedia article is actually for the group of insects that it belongs to as the article for that particular species doesn't provide much useful information.

This is Tessaratoma papillosa, also known as the lychee giant stink bug. It is a pest for lychee trees, this is probably the reason for this warning sign. See the image for comparision:

See also this page for more information.

This is great reading, I'm starting to see why there is such a stink being raised about them. I'm also glad that I didn't mess with this one; the defensive chemicals of tessaratomids (particularly that of Tessaratoma papillosa and Musgraveia sulciventris) are notable for being one of the most debilitating to vertebrates, probably a defense specifically aimed against birds. They can cause damage to human skin and even cause temporary blindness if sprayed unto the eyes!

See also this answer for information on the poster. I guess the pine cone is a red herring.

Can you use your mod powers to check if there was another answer here before? I don't have enough reputation to see deleted answers, but I think there was and that there was some helpful links in it, but I could be misremembering. Thanks!

@uhoh Damn, you are right. I meant to clean a flag but it seems I accidentally deleted the answer. It is mainly a repeat of the earlier answer, though.

Thanks! It seems that I was after this link in the other answer.


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Eukaryotic DNA polymerase in Leading and Lagging Strand
Different books say a different specifications on which eukaryotic DNA polymerase work in leading strand and which DNA polymerase work in lagging strand.
TL,DR: Which one is reality? and if there are multiple possibility, then which one is applicable for which organism (such as human mammal, yeast fungus, Arabidopsis plant etc.)?
Information greatly varying Such as,
According to book The Cell by G.M. Cooper (NCBI), in mammalian eukaryotic system, DNA polymerase δ works in both leading and lagging strand.

According to book Molecular biology by R. F. Weaver, ed-5; DNA pol- δ works in lagging strand and pol ε works in lagging strand and DNA pol ε work in leading strand.

Fundamentals of molecular biology, Lizabeth Allison (Semantic Scholar) says another thing, it says pol ε works on lagging strand.

The paper by Stillman B. , DNA polymerases at the replication fork in eukaryotes. (NCBI) (NCBI-PMC) (FIGURE) says in SV40 viral model the δ polymerase works in both strand but in cell chromosome, δ works on lagging and &epsilon works in leading strand.

Now which one is true? if all are true then does they applicable on different organism?

You have the seeds of the answer in the sources you quote. Some are books — which will be up-to-date perhaps a year before publication — and one is a paper. Check the publication dates, and check the paper to see if more recent related works are flagged. In fact, a review from 2018 is cited. I know nothing about the topic, but it is evident from the summaries that views have changed over the past 20 years. Read the recent review to find out the evidence for the (almost) current view, and perhaps why previous ideas have been superseded. NCBI Bookshelf is very useful, but only has old editions.


text:
Is breathing a reflex action or is it an intrinsic process?
The process of breathing is controlled by respiratory centers in the brain stem. Do these centers have an innate activity, i.e., just send out signals to breathing muscles intrinsically, and have the rate and manner in which they do so modified by various regulatory factors?
Or are they driven by imbalances (in levels of oxygen, carbon dioxide, hydrogen ions) like a reflex? Let's say that hypothetically these levels remain static in an acceptable state such that this reflex is no longer needed, would breathing stop since there's no longer a driving motive or would it continue because the respiratory centers have an intrinsic activity?

While the ultimate purpose of breathing could be considered to be the maintainance of a balance of the substances you are referring to (such as blood oxygen, carbon dioxide, and hydrogen ions), the blood levels of these substances do not directly control the production of action potentials within the motor neurons that promote the contraction of the diaphragm and intercostal muscles.
The propagation of these action potentials is initiated by signals from the medullary respiratory center, specifically the neurons in the dorsal respiratory group (DRG) and the ventral respiratory group (VRG). In the VRG, a complex of neurons known pre-Bötzinger complex is responsible for generating the signals that cause the rhythmic muscle contractions involved in breathing:

The respiratory rhythm generator is located in the pre-Bötzinger complex of neurons in the upper part of the VRG. This rhythm generator appears to be composed of pacemaker cells and a complex neural network that, acting together, set the basal respiratory rate.

Vanders Physiology, p473, 15th ed.
So breathing is indeed, as you mention, a process that is controlled by innate neuronal activity but regulated by the concentrations of PO2, PCO2, and H+ concentrations. I recommend you read pages 473 to 477 of Vanders Physiology, which explains these controls in detail, some of which do involve reflexes, say, if O2 concentration in the blood strays too low.
Interestingly, expiration, which is typically a result of actions potentials ceasing and respiratory muscles relaxing, can be controlled by a reflex, known as the Hering-Breuer reflex, during strenuous exercise when the lung is inflated by a large tidal volume. Stretch receptors in the airway in this case are activated, causing the inhibition of inspiratory neurons in the DRG.
Source: Vanders Physiology, 15th ed, section 13.9: "Control of Respiration"

That makes much more sense than the whole reflex response. The lecture our college had was using three different sources, each with a different explanation for the driving motive of respiration. Two of those were behind the innate activity idea, but for different origins interestingly enough: one source (Tortora’s Principles of Anatomy and Physiology) said the activity originates in the pre-Botzinger complex like you said, and the other one (Guyton and Hall) said it originated in the DRG, so I suppose Guyton and Hall is the odd one out here (wouldn’t be the first time it is tbh)


text:
Muller's ratchet and viruses
Do viruses suffer from Muller's ratchet?  Can it significantly influence the current coronavirus pandemic?

As with most things in the natural world, there isn't really a single straightforward answer to this question! It depends largely on the ecological contect and the population dynamics.
Basically, in organisms with high mutations rates (such as RNA viruses), Muller's Ratchet suggests that the mean fitness in a population will always decrease. In small populations, mutation-free individuals are rare, and they will be lost through genetic drift. In 1990, Chao showed that deleterious mutations are generated at a sufficiently high rate to advance Muller's ratchet in an RNA virus.
However, in general, Muller's ratchet can be argued to be ineffective in viral populations because populations are never 'small', and drift is usually very weak (or selection is strong, in other words). Chao also notes that the effective population size in nature, 8x10^9 is often irrelevant to whether or not Muller's Ratchet is active, because Viruses often pass through the bottleneck of a single individual. Additionally, frequently recombining viruses such as HIV can also be subject to Muller's Ratchet Yuste et al (1999). The results of Chao have been generalised to many other viruses.
However, these studies are lab-based and don't pertain to your question about what might happen to SARS-CoV-2 'in the wild'. RNA viruses show the highest mutations rates in nature (Sanjuan et al 2010). This can lead to Muller's Ratchet in small populations where selection is weak and drift is prominent, but can lead to high levels of adaptation in large populations. It is not just the census population size which is important, but the effective population size, which can be thought of as a proxy for the amount of genetic diversity within a population. If a population rapidly expands from a single origin, as is expected to have happened with the SARS-CoV-2 outbreak, then the census population size would be larger than the expected diversity. Novella (1995/1996) showed that there is an interplay with the size of the bottleneck and the fitness of the surviving clones; when a more fit viruses passes through the bottleneck, they are more likely to avoid Muller's Ratchet. So in the case of SARS-CoV-2, whether or not the virus would be subject to Muller's Ratchet would depend on both the variation and fitness of mutation of the viruses who jumped from the intermediate animal to humans.
At the risk of overcomplicating things, population/deme structure also plays a role. If the virus evolves in different demes within a structure population, viruses within a deme can evolve population specific mutations. If there is then gene-flow between the demes, there can exist selection between the different mutations, driving up the average fitness across demes (Mirales et al 2009) and avoiding the Ratchet.

Muller's ratchet is more relevant/more important in organisms with small effective population sizes. While the effective population size of the worldwide SARS-COV-2 population is smaller than (billions of copies per person [a typical detection threshold is 10^4 copies/milliliter of blood]) x (millions of infected people), it's very likely to be so large that Muller's ratchet is irrelevant.

Other answers cover well Muller's ratchet of the worldwide virus population.
However, drug-induced Muller's ratchet (aka mutational meltdown) might be considered on the level of the viral population that infected one patient. A recent publication Considering mutational meltdown as a potential SARS-CoV-2 treatment strategy talks about potentially inducing mutational meltdown on the within-patient viral population.
Note it's not research but a comment paper! Authors review the theory and empirical evidence that makes them think that mutational meltdown has the potential to become a coronavirus treatment.


text:
Aging: Only humans have grey hair?
I am not sure if I ever saw a monkey or a bird age and lose hair pigment as it grows. It maybe due to my lack of information. But it appears to be a general presumption that only humans age and lose hair pigment (hence developing grey hair).
If this is true, then I am curious why only humans?

I don't think it is restricted to humans. Dogs lose hair pigment as well, usually around the muzzle.
This work used graying of hair to discriminate senior dogs.
I don't know which other mammals lose hair pigment, though, nor why.

We also see this in big apes.


text:
What's the role of bromelain in pineapple?
Bromelain refers to one of two proteases found in pineapple and its relatives. Like other proteases, many believe it has therapeutic uses and it's the subject of a lot of research. But what role does it play in the pineapple itself? Why does pineapple (or papaya, for that matter) generate large quantities of protease when other plants do not?

Antifungal properties? as tested in below article.
López‐García, B., Hernández, M. and Segundo, B.S., 2012. Bromelain, a cysteine protease from pineapple (Ananas comosus) stem, is an inhibitor of fungal plant pathogens. Letters in applied microbiology, 55(1), pp.62-67. Available here

Please cite scientific papers fully using a formal citation guide. (Google Scholar does all the work for you if you want): see here

Citing is absolutely necessary here, so thank you for pointing toward a reputable study (though see my comment above and my edits). However, posts citing other's work need to summarize, quote, or otherwise explain the rationale for including the citation (especially if no further explanation is provided as part of the answer). Answers on SE need to be complete in and of themselves -- as in someone 5 years from now should be able to view your answer and feel like they had the question adequately answered without needing to leave the site. External links and citations can be for further reading

I thought the name of the paper was a good answer already, didn't want to waste peoples time reading long answers.

@PolypipeWrangler Please reread theforestecologist's comment, this is site policy not one person's opinion. Link only answers are frowned upon and decrease the quality of StackExchange. An answer doesn't need to become "long" to include more than just a link.


text:
“The rhesus macaque is pretty much the closest thing we have to humans” — why?
Vincent Munster (researcher at Oxford) states (in the context of testing vaccines for COVID-19):

The rhesus macaque is pretty much the closest thing we have to humans

I thought chimpanzees and bonobos were the two living species most closely related to humans? Why don't we try the vaccines on them instead? Why is the rhesus macaque a better candidate?

Short answer:
Chimpanzees are indeed closer, but perhaps...too close. Almost all invasive research on non-human great apes has halted for some time over ethical concerns.
Rhesus macaques are the main non-human primate still used in research (some others are also used, like marmosets). "Pretty much the closest" is in reference to which species are available to scientists as a model organism; I assume the researcher quoted included "pretty much" as a bit of a hedge, acknowledging that chimpanzees are closest while not being available for vaccine research. Even then, many countries have limited research using all primates and do not use macaques anymore, either.

Longer answer:
The primates include great apes like gorillas, orangutans, and our closest non-human relatives: chimpanzees. They also include more distant relatives, like Old-world and New-world monkeys, and even more distant lemurs.
Many humans (including influential organizations) have decided that chimpanzees and other apes are too closely related to humans to be eligible for certain types of research for ethical reasons. It has been deemed more ethical to use human subjects, who can consent to participation in studies, or to use other model animals. Apes are also difficult as model organisms: they develop slowly, grow large, and have long life spans with few offspring; all these factors make them expensive research subjects. There is no one biological fact for this distinction between apes and other monkeys, besides their closer relationship to us and the perception that they have more advanced intellectual faculties. Further discussion is outside the scope of this answer.
Old-world monkeys, including rhesus macaques, are the next-closest grouping of primates to the human lineage. Macaque monkeys live and breed fairly well in captivity, and are used in research when other model organisms like mice and rats are unsuitable (like when an aspect of their biology is not sufficiently similar to humans).
Rodents can also be models for vaccine research, but their distance from humans and differing response to certain pathogens may make them less useful for measuring efficacy. Therefore, close relatives like rhesus macaques have been used in past vaccine research.
There is no perfect model organism; even humans aren't always great models for other humans, when they vary by age, sex, pre-existing conditions, etc. There is a balance in risk and ethics in choosing model organisms for research: simpler animals like mice and rats are typically used at earlier stages of research. Primates are used when rodent models don't correlate well enough with humans or when there is a large risk to human trials.

Some references:
https://en.wikipedia.org/wiki/Animal_testing_on_non-human_primates
https://www.nih.gov/about-nih/who-we-are/nih-director/statements/nih-will-no-longer-support-biomedical-research-chimpanzees
https://www.nature.com/subjects/rhesus-macaque
https://www.sciencemag.org/news/2018/11/record-number-monkeys-being-used-us-research
Nath, B. M., Schumann, K. E., & Boyer, J. D. (2000). The chimpanzee and other non-human-primate models in HIV-1 vaccine research. Trends in microbiology, 8(9), 426-431.

As a non-specialist, this answer doesn't tell me anything. What's the difference between macaques and chimpanzees that make studying chimps too queasy for us? if macaques are farther away, why are they still useful?

@AzorAhai "Doesn't tell you anything" seems a bit strong as a criticism, unless you already knew chimp research is banned almost everywhere and macaques are commonly available research organisms - OP didn't seem to know this and I assume a majority of non-biologists don't :) However, I've expanded a bit - does this edit help?

Fair enough, I was familiar with macaques being common, although I didn't know chimps were completely banned. Thank you for expanding :)

Another aspect to this is just sheer size. A gorilla would eat more, need a bigger cage, and be harder to control than a rhesus macaque. So the exclusion of great ape species isn't all on ethical concerns. A basic concern is that the bigger the test animal the more it will cost per animal.

@MaxW From the answer: "Apes are also difficult as model organisms: they develop slowly and have long life spans with few offspring" - I can add cost to that explicitly but those are all issues that make animals difficult models. A more immediate issue, though, since (as far as I know) every country in the world except one has banned such research on chimps..well, cost isn't much the major factor at this point, even though it was in the past.

@BryanKrause Cost probably helped make the decision to ban it easier.  Since dealing with apes is already so difficult and costly compared to some alternatives, there was probably less incentive to push back against the bans.


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Chromosomal structures in S phase and Prophase
Of S Phase:

Existing DNA molecule acts as a template to synthesize new DNA molecule. The cell doubles it's DNA, yet the number of chromosomes remain the same

Of Prophase:

The chromatin condenses and during condensation, DNA strands untangle to form compact mitotic chromosomes

So in the S Phase, we're talking about chromosomes which contain double the number of initial DNA molecules, while the chromosomal number still being the same.
And in Prophase, there's condensation of chromosomes! But the chromosomes are already formed in the S Phase as per the sentence I have quoted from the textbook.
That doesn't make sense to me. I'm very confused.

This is actually an interesting question

For mitosis What happens, in G1 phase the DNA content is 2C (for diploid organism). The DNA content indeed gets 4C after S phase that is why you get 2 chromatids per chromosome before next metaphase. So after S phase is completed, the DNA content is actually 4C although the chromosome number is said to be 2n. after metaphase the chromosomes are split and then daughter cells get one of each sister chromatid, then each daughter cell gets DNA content of 2C.

Possible duplicate of https://biology.stackexchange.com/questions/52409/genotypes-in-diploid-haploid-cells-under-mitotic-meotic-cell-divisions

@AlwaysConfused first of, your explanations back there and here were quite wonderful. Thank you. Secondly, I have one more question. By chromosomes in the S phase, do we mean actual "rod-shaped" structures that are formed from chromatin condensation or it's just the chromatin threads taking the shape of chromosomes (I'm sorry if that sounds a bit naive). Also, can you elaborate on "two chromatids per chromosomes?" Does it have anything relating with visibility in the microscope: that chromosomes with sister chromatids are formed in the S phase itself and they're visible that way in Prophase?

Welcome to SE Biology. When you post a question with a query about a textbook it's always useful to give details of the textbook so if one has access to it one can check for mistakes in transcription or see the context. Is there a graphic to go with this explanation?

@AlwaysConfused Please use comments for clarification or for checking the OP's thinking; if you have an answer to post, use the answer box.

@BryanKrause I thought an answer already exists so I didn't went for a duplicate answer. but since the question is not totally a duplicate one as Maximillian said, I'll make the comment into an answer and then will delete the comments.

@BryanKrause also the OP replied why their question is not an exact duplicate but has more to ask.

A comment by user AlwaysConfused has answered one part of the question, but I think that the OP's confusion is related to a point of language or teaching. The number of chromosomes doubles during S phase (C number), but the ploidy of the cell does not change (N number). That's what your textbook is trying to tell you, it's just stating it fairly confusingly.
When we say that there are the same number of chromosomes before and after S phase, that's just a lie that we tell ourselves to keep from getting confused. We have invented the C vs. N terminology that AlwaysConfused mentions to try to handle this: we say that the 2N of a diploid cell remains constant across the cell cycle, while the C number alternates between 2C (before S phase) and 4C (after S phase).
For you, this confusion seems to be worse because how we represent chromosomes is not what chromosomes actually look like, and this has gotten mixed up with the definitions of chromosomes.
When we draw pictures of chromosomes we draw them neatly like they are in mitosis, but that is not at all what they look like in interphase. They are still chromosomes during that time, they just aren't pretty and neat ("condensed").
To sum it up more, here is a diagram of chromosomes in interphase (most of the time) vs. during mitosis:
It is only during a very specific part of the cell cycle (mitosis) that the chromosomes are packaged up ("condensed") in such a way that we can readily see them as discrete entities. The rest of the time they're all glommed together and are organized instead according to transcriptional activity etc. rather than according to which molecule they're part of. Remember: chromosomes are very big molecules and if they are "loose" they have a total length that is many orders of magnitude larger than the diameter of the nucleus; so the nucleus is like a big bowl of noodles in interphase.
In S phase it will just be a bowl with twice as many noodles in it as before, because there are twice as many DNA molecules ("chromosomes"; "chromatid" is a term that only applies to the condensed form in mitosis).

Noodles. Great analogy! Thanks a lot!

@yenashah Glad it helps- I think that using familiar objects to get a physical intuition is one of the best ways to understand biology, which is at best a pretty confusing field.

For mitosis What happens, in G1 phase the DNA content is 2C (for diploid organism). The DNA content indeed gets 4C after S phase that is why you get 2 chromatids per chromosome before next metaphase. So after S phase is completed, the DNA content is actually 4C although the chromosome number is said to be 2n. after metaphase the chromosomes are split and then daughter cells get one of each sister chromatid, then each daughter cell gets DNA content of 2C.
Further reading:
Genotypes in diploid/haploid cells under mitotic/meotic cell divisions
here is a diagram from there (highly diagrammatic) about what happens with chromosome numbers during cell cycle

"By chromosomes in the S phase, do we mean actual "rod-shaped"
  structures that are formed from chromatin condensation or it's just
  the chromatin threads taking the shape of chromosomes?"

it is just the Chromatin threads (DNA + some proteins) loosely spread in nucleoplasm (karyolymph) in an entangled, noodle like manner.
Yes, there is a visibility issue, during interphase (G1 S, G2) the euchromatin regions of the chromatin fibres stays in a decondensed form of 30 nm or somewhat more condensed 60 or 130 nm  (The Cell, G.M. Cooper, ed-4) whereas maximum resolution (d) achieved by light microscope is somewhere about 200 nm

two chromatids per chromosomes

Each chromatid stands for 1 linear DNA molecule; regardless of condensed or decondensed. It is mostly decondensed in interphase, and mostly condensed in M phase (P-M-A-T).
Here is an image of 2 chromatids in 1 chromosome :

This image from shutterstock well explained the configuration of chromosome just after telophase (1 chromatid per chromosome) and after replication to metaphase (2 chromatids per chromosome)

In the following sketch; the changes through chromosome number and form is shown diagrammatically. The terms A and B here are just for labelling purpose, they aren't any technical terms.

image A (1-5) shows what happens wth DNA; and
Image B (1-5) shows somewhat realistic appearance of chromosomes (and chromatids);
during cell cycle.
see also: Interpretation of picture of human chromosomes

Thank you so so much for such an amazing explanation. This made me love the topic even more.


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Is it possible to accelerate active transport in plant vascular system using some electronic method?
I am from electronics background and got an understanding that electrical current affect plant growth. Based on this phenomenon, I got an idea but before I formulate my hypothesis and start experimentation around it, I am looking for some expert opinion on this.
Can we accelerate mineral transport like water movement from root to leaf by some external influences?

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text:
Induce plasmid acquisition in bacteria to make them susceptible to antibiotics
Is it possible to use plasmids as a way of creating antibiotic susceptibility in bacteria.
For example; in Microbiology, an introduction 13th edition by Pearson , Page 230 "the researchers traced the drug-resistance plasmid to a plasmid found in E.coli that resided in the volunteers before the study".
I was wondering if it is possible to induce plasmids that make those bacteria susceptible.
They have to be in a first instance good for the bacteria, for example an enzyme that allows the bacteria to use a compound. But  through an antibiotic it would make that enzyme catalyze useful compounds of the bacteria, working the antibiotic as a cofactor of such enzyme.
Is it possible?
I was thinking on it as a "trojan plasmid".
Thanks.
Edit: Linking to this question: Could plasmids and conjugation mechanisms be used against antibiotic-resistant bacteria? , it talks about those "trojan horse" plasmids referring them in a way that seems to be linked to a bactericidal function, if instead the  plasmids are linked to a good survival rate in one situation (example, 36°C) but to a bacteriostatic situation ( temperature goes up to 39°) or such a way like hemoglobin works with CO, it's fundamental for us but selection hasn't worked to get through this problem and still binds to the molecule.
This type of coevolution in Wolbachia https://en.m.wikipedia.org/wiki/Wolbachia makes the host insect susceptible to needing the bacteria for reproduction despite being good in some environmental conditions it induces infertility in others.
Or inducing variants of genes that are still with functionality but trunked under certain conditions, if those conditions aren't present in the environment, the gene variant could spread without causing problems competing with the original variant until those environmental conditions are met reaching an equilibrium in which a % of the population could be used as a target of that antibiotic.

Check out this question and its answers.

@canadianer Thanks! It has solved some of my questions, but I still feel I am in a slightly different situation, focusing more in the plasmid genetic equilibrium than in the complete widespread throughout the population.


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What does a hornet nest foundress feed on?
After wintering, hornet queens will build a new nest from scratch. Once the new workers have hatched, they will fly out and collect carbohydrates to feed themselves and the queen and will also hunt for protein to feed the larvae.
I’m interested in knowing how food collection for both larvae and queen are taking place before the role is taken over by the workers (as none have hatched yet).

Does the queen collect both carbohydrates and protein?
Does the queen leave the nest to collect food when there’s already larvae (as opposed to having stored enough food before starting to breed)?
How long (in terms of weeks) after the queen started building a new nest until she can fully rely on her workers for food supply?

While I assume the answers to the first two questions to be ‘yes’, I have failed to find a source confirming this. My questions primarily refer to the Vespa Velutina (invasive in Europe), but I’m also interested to hear about differences in other wasps/hornets present in Europe.

I used the below articles to get the information.
1. the queen does collect both carbohydrates (nectar mostly) and protein (often bee flight muscles).

Only found one case study of one nest for this, so not sure. The queen did leave the nest during the period when it would be expected to have larvae. The articles I read did not mention food storage in the nest.
Same case study, the queen left the nest probably for longer than four weeks.

The developmental period was about 4I-42 days (egg 6 days, larva about 15 days, pupa about 20-21 days.
 from "Taxonomy, distribution and nesting biology of the Vespa bicolor group" (Hym., Vespinae) (1994) by Michael E Archer. found at https://www.academia.edu/4236740/Taxonomy_distribution_and_nesting_biology_of_the_Vespa_bicolor_group_Hym._Vespinae_1994_
This review article has a good overview. "Vespa velutina: a new invasive predator of honeybees in Europe" by Karine Monceau, Olivier Bonnard, and Denis Thiery.  DOI 10.1007/s10340-013-0537-3. accessed at https://www.doc-developpement-durable.org/file/Elevages/apiculture/maladies&parasites/Vespa%20velutina_frelon%20asiatique/Vespa%20velutina%20a%20new%20invasive%20predator%20of%20honeybees%20in%20Europe.pdf
A case study of a captured nest (one queen, four workers) found that the queen stayed inside the nest permanently after 27 more days.
From "Observations on the colony activity of the Asian hornet Vespa velutina
Lepeletier 1836 (Hymenoptera: Vespidae: Vespinae) in France" Article in Annales- Societe Entomologique de France · January 2009 DOI: 10.1080/00379271.2009.10697595 downloaded from ResearchGate
There are also other articles that may have the answer, but in languages that I could not read.


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How large a part of the corona-virus is coding?
If you find an example of a sequenced string of coronavirus it is about 30.000 long. Looking for example here https://nextstrain.org/ncov/europe you'll see that by far the largest part of this is actually coding. But is that because that is the entire strain or is it because they are only showing the ORF-part? If the latter is the case how large is the non-coding part then compared to the coding part?

30Kb is the total length of the genome, including non-coding regions.

And I think the reason why it's not easy to find a % of non-coding region(s) stated for almost any virus is that it's not very certain how much is actually non-coding given all the "tricks" (non-canonical translation) viruses use https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.042499-0

Viral genomes are, in general, mostly coding - often in multiple ORFs.

It is about 92% of the RNA that is protein-coding. ORF10 is not coding according to newer results, see e.g. Jungreis, Sealfon, and Kellis (2021). The article is about identifying protein-coding ORFs and distinguishing them from non-coding ones.


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Different BLOSUM matrices
What is the difference between different variants of BLOSUM matrices?
e.g What is the difference between BLOSUM 30 and BLOSUM 62?

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Thanks @David. I didn't see that. And could you please tell me are there specific instances I would use BLOSUM30 or BLOSUM62 ? Why should not I always choose BLOSUM90?

Thanks @mgkrebbs. I didn't see that. And could you please tell me are there specific instances I would use BLOSUM30 or BLOSUM62 ? Why should not I always choose BLOSUM90?

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BLOSUM is a substitution matrix employee for protein sequence alignments, which are based on maximum identity percentage  of the aligned protein sequences used in calculating them. For example, BLOSUM30 would correspond to alignments with a maximum of 30% of identity, BLOSUM62, for a 62% of identity.
The type of matrix depends on the study your are doing. BLOSUM62 is the most widely used matrix for phylogenetic analysis. BLOSUM90 would return sequences with 90% of identity.
The percentage of identity is related to the phylogenetic distance, and this to the variations in the protein sequences,therefore BLOSUM90 cannot always be used. That is why you must take into account the type of analysis you are going to perform. (https://en.m.wikipedia.org/wiki/BLOSUM)

Thanks @Armand Could you please tell me are there specific instances I would use BLOSUM30 or BLOSUM62? Why should not I always choose BLOSUM90?


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Stem and Branch of plants
What is the difference between the stem of a plant and the branch of a plant. Is the branch part of the stem?

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

To answer this question, first, we must define the terms. Major primary plant organs can be characterized as either roots, stems, or leaves. A stem is a structure that contains nodes and internodes (as a previous answer explains), and axillary buds. These buds mean that stems can give rise to more stems, roots, or leaves.
Branches can be defined as stems arising from an axillary bud of another stem. In this way, all branches are stems, but not all stems are branches. Beware of confusing the botanical definition of branches (arising from axillary buds) from the colloquial definition of a branch (a tree branch) because... all tree branches arise from axillary buds, but not all botanical branches are found on trees!
Hope this helps!

The term "Branch" used in school textbooks generally mean stem branch and the stem branches are stem in morphological identity because they have nodes, internodes, leaves, and exogenous development.

I am trying to reach Fahn and Esau but in lockdown I wont be able to acces library :(


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How antibodies are produced in our body against intracellular proteins of infectious bacteria?
When an infectious agent invades our body, then surface antigens of the infectious agent are detected by our immune system and B-cells get activated. However, we do have antibodies in our blood against intracellular proteins of the infectious bacteria. What is the mechanism which produces antibodies to intracellular proteins, which are never exposed to our immune system.

"When an infectious agent invades our body, then surface antigens of the infectious agent are detected by our immune system and B-cells get activated." Can you mention a source for this premise? (Specifically, the assertion that only surface antigens of the infectious agent are detected by the immune system.)

@AdhishSethi https://microbiologyonline.org/index.php/about-microbiology/microbes-and-the-human-body/antibody-antigen-complex
I am little confused here. Please help me to understand the intracellular part better.

Hmm, this article talks of B cell responses rather than the immune system in general. As far as I know, antibodies to bacteria are formed against toxins and cell surface molecules only. Can you also cite a source that mentions antibodies against bacterial intracellular components? (I hope you are not tired of adding sources :P) Preferably, add all your sources to the body of the question so that users don't need to look through the comments. Thanks.


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What does (deaths / (resolved + deaths)) describe in an emerging epidemic?
It would seem in a emerging epidemic, where the time to resolve a disease is long, an evaluation might be used such as:
(predictive mortality rate) =  (deaths) / (deaths + resolved)
Is this a standard metric?  And if so what is it called?
It would seem that this kind of metric would be a predictor as to the ultimate mortality rate, unadjusted for treatment advances. The intent is to describe the demonstrated mortality of those who have acquired the disease, without influencing of the number of people who have acquired the disease.  This would be helpful where R0 is large and/or Specific Interval is small. However I cannot find references to a metric similar to this.  Pointers appreciated.

The problems with the measure you've proposed have been addressed on MedicalSciences.SE:
https://medicalsciences.stackexchange.com/q/20970/8728
The short version is that this measure isn't very informative while there are unresolved cases, because it ignores what is known or expected about those unresolved cases, and it is not a standard measure.
In the long run (when almost all cases are either recovered or dead) it approaches the case fatality rate because the denominator of (resolved + deaths) becomes equal to the total number of cases. Until then, it doesn't tell you much at all.
You could track the case fatality rate over time based on time of initial diagnosis to look at effects of new treatments.


text:
How does imbibition and turgor pressure generate much force?
Both imbibition and turgor pressure together create a large force in plants such as force required to burst the seed coat open?

Please answer this question

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What are the reasons for using oligo-dT instead of oligo-U to isolate mRNAs?
dTTP oligonucleotides are used to isolate mRNAs because mRNAs (in eukaryotes) have a poly A tail which binds to the complementary oligo-dT. However, why do we not use oligo-U instead (uracil)? I would guess it is because ribonucleotides have the additional 2' OH which is reactive, so less desirable, but is there any other reason?

Note - This answer only covers the comparison of rA-dT (RNA:DNA) and rA-rU (RNA:RNA) duplexes, and not more exotic options involving deoxyuridine (dU) and ribothymidine (m5U).
I can think of three possible reasons why oligo-dT may be preferred over oligo-rU for poly(A) hybridization and mRNA capture:

The rA-dT duplex is more stable than the rA-rU duplex, thus affording a more efficient pulldown.
dT oligonucleotides are easier to synthesize or more stable than rU oligonucleotides (and therefore cheaper to manufacture).
There are methodological considerations beyond the hybridization step that make oligo-dT a better choice.

Let's address each of these...

Hypothesis #1 $\rightarrow$ The rA-dT duplex more stable than the rA-rU duplex.
Conclusion #1 $\rightarrow$ probably not
Using NMR to observe the exchange rates of imino protons, Huang and Russu compared the stabilities of homologous duplexes containing tracts of  rA-dT, dA-rU, rA-rU, and dA-dT base pairs.1 Overall, they found the rA-dT and rA-rU duplexes to be similar in terms of base-to-base stability:

(i) Among the four nucleic acid structures investigated, the highest base-pair stabilities are observed for the dA-dT tract of the DNA duplex; the lowest base-pair stabilities are observed for the dA-rU tract of the dA-rU RNA-DNA hybrid.
(ii) The stabilities of individual base pairs in the rA-dT tract of the rA-dT hybrid are the same as those of rA-rU base pairs in the RNA duplex and are intermediate between the stabilities of DNA dA-dT and hybrid dA-rU base pairs.
(iii) The stabilities of base pairs in the rA-dT tract of the rAdT hybrid and in the rA-rU tract of the RNA duplex do not vary very much with the location of the base pair in the tract. In contrast, in the DNA duplex and the dA-rU hybrid, the highest and lowest stabilities are observed for the central base pairs in the tract.

This opposes an argument that oligo-dT is preferred due to enhanced stability of the resulting RNA:DNA duplex. An important note here is that the study cited above only tested tracts between 4 and 10 base pairs long, whereas most mRNA capture protocols utilize dT oligos in the 12-25 nt range.2

Hypothesis #2 $\rightarrow$ dT oligonucleotides are easier to synthesize or more stable than rU oligonucleotides.
Conclusion #2 $\rightarrow$ yes
As stated in the question, RNA is generally considered less stable than DNA due to the reactivity of the 2′-hydroxyl group. During solid-phase RNA synthesis, iterative protection and deprotection of the 2′-OH is required for addition of each new nucleoside, meaning that there are many more steps in RNA synthesis than solid-phase DNA sythesis when comparing equal-length oligos.3 Practically, this means rU oligonucleotides are much more expensive to order that dT oligonucleotides. As of 12 July 2021, IDT quotes me \$8.55 for 100 nmol oligo(dT)19, whereas the same amount of oligo(rU)19 costs \$142.50.
Beyond the cost, the reactivity of RNA and the ubiquity of RNases means one must take special precautions when handling and storing of RNA oligos, as explained by IDT:

The inherent chemical structure of RNA makes it less stable than DNA because the additional hydroxyl group attached to the 2’ position of the pentose ring in RNA nucleotides makes RNA more liable to alkaline hydrolysis. In addition, RNases are pervasive, making RNA more susceptible than DNA to degradation. Thus, RNA oligonucleotides should be stored as an ethanol precipitate at –80°C for greater stability. For short-term storage, we recommend resuspending RNA oligos in a nuclease-free neutral to slightly acidic buffer containing a chelating agent, such as IDTE. However, it is always important to avoid RNases and alkaline hydrolysis when RNA oligos are stored.

Hypothesis #3 $\rightarrow$ There are methodological considerations beyond the hybridization step that make oligo-dT a better choice.
Conclusion #3 $\rightarrow$ yes
In state-of-the-art mRNA library preparation kits such as those available from New England Biolabs and ThermoFisher Scientific, the bead-bound dT oligos serve both as the baits for poly(A) hybridization and as the primers for first-strand cDNA synthesis. These kits use RNA-directed DNA polymerase (e.g. MMLV Reverse Transcriptase) for cDNA synthesis, which requires a DNA primer from which to polymerize new DNA. Thus, any protocol utilizing an RNA:RNA hybridization at the pulldown step would have to dissociate the strands and introduce DNA primers before reverse transcription.

References

Huang Y, Russu IM. Dynamic and Energetic Signatures of Adenine Tracts in a rA-dT RNA-DNA Hybrid and in Homologous RNA-DNA, RNA-RNA, and DNA-DNA Double Helices. Biochemistry. 2017 May 16;56(19):2446-2454.
Anderson AJ , Culver HR , Prieto TR , Martinez PJ , Sinha J , Bryant SJ , Bowman CN . Messenger RNA enrichment using synthetic oligo(T) click nucleic acids. Chem Commun (Camb). 2020 Nov 21;56(90):13987-13990.
RNA Oligonucleotide Synthesis. ATDBio.