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Would we know about a virus that causes no symptoms?
I've heard that there are a number of viral illnesses that humans can get from animals, which cause no symptoms in the animals. If there was such a virus in humans, which was very widespread but caused no symptoms, would we know about it?
As far as I know most pathogens have only been discovered when people were specifically looking for the cause of some disease. With bacteria, I think we know / can discover any that can be found in a human body, though we don't necessarily know what each type does. But viruses are much smaller.

With the modern rise of meta-genomics, symptom-less viruses can be identified by the presence of their genomes. Certainly, there is more interest in pathogenic viruses than in harmless passengers, but today it's not necessary to have symptoms to identify viruses.  For example:

Investigators can now go beyond pathogenic viruses and have access to the thousands of viruses that inhabit our bodies without causing clinical symptoms. By studying their interactions with each other, with other microbes, and with host genetics and immune systems, we can learn how they affect health and disease. This article reviews current knowledge of the composition and diversity of the human virome in physiologically healthy individuals. It focuses on recent results from metagenomics studies and discusses the contribution of bacteriophages and eukaryotic viruses to human health.

--Metagenomics and the Human Virome in Asymptomatic Individuals.
Even prior to metagenomics, some "silent viruses" were identified:

Viruses are the most abundant obligate intracellular entities in our body. Until recently, they were only considered to be pathogens that caused a broad array of pathologies, ranging from mild disease to deaths in the most severe cases. However, recent advances in unbiased mass sequencing techniques as well as increasing epidemiological evidence have indicated that the human body is home to diverse viral species under non-pathological conditions.

--Describing the Silent Human Virome with an Emphasis on Giant Viruses

So it's not just true that we could discover such a virus, but we already have discovered many of them in humans. That's fascinating!

It's still a very new field, and many of the newly-discovered silent viruses are bacteriophages that infect the normal gut bacteria, but there are a handful of apparently non-pathogenic viruses that infect humans.

I would add that the silent virome might not have been silent upon the infection of the first animal acquiring it.

Sure, but in some cases that first acquisition may have been millions or hundreds of millions of years ago (consider spumaviruses of primates) -- so it becomes questionable if it's even the same virus, or host, as in the first acquisition.

@iayork - That's exactly my point.

Theoretically, I think we can. We are able to identify viruses in humans that are asymptomatic or have yet to produce symptoms (e.g. HIV, Zika Virus). However, unless this virus causes an impact on humans, like causing death in cattle, I don't see why people in our society would invest in finding out about it. Most organisations award grants for research that they could profit off in some way.


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Where does the number 67 in the nuclear protein/antigen Ki-67 come from? Why not 66 or 68?
I have read in in the original paper that in the year 1983 a research group in Kiel, Germany (that's where the Ki- in the name comes from) developed monoclonal mouse antibodies against Hodgkin lymphoma cells in multiple 24-well plates. If I understand correctly they were able to isolate antibodies from 63 wells and divided them into 493 microtiters into several 96-well microtitre plates. Of these 493 titres, 164 cell batches were chosen for further investigation and expanded. Somehow Ki-67 emerged from there, but why this number? Who gave it that name and why?
A teacher once told us in med school, the cells producing the antibodies were found in well 67, but I cannot find any source to back up that claim.

There's this article, but who knows where these authors got the idea from...

From Wikipedia: "The name is derived from the city of origin (Kiel, Germany) and the number of the original clone in the 96-well plate".

That statement in the wikipedia article is unsourced ...

Yes that's the legend, but I want details...

source: Stack Exchange

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

sort: votes


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Tryptophan Operon Working Mechanism
The Trp operon has 2 methods to check for presence of tryptophan, one indicating the absence of free Trp and the other the absence of charged Trp tRNA. If both methods showed absence of Trp there is tryptophan synthesis. However, the synthesis of tryptophan involves 5 enzymes to be synthesized, and usually we find all the amino acids in a protein such as an enzyme. Therefore, there is high probability that Trp is found in these 5 enzymes. Where does that Trp come from if there is neither free tryptophan nor charged tRNA for Trp?

You're right that if there was really a complete lack of Trp, then the cell wouldn't be able to make the enzymes. But the cell doesn't have to wait until [Trp] drops all the way to zero -- it can induce expression of the operon when the concentration gets sufficiently low (in practice there's some continous relationship between [Trp] and expression). Note that there's always going to be a little bit of Trp around as there are constantly proteins being degraded (and resynthesized).
But you're on to something -- in fact there is some bias towards lower usage of a particular amino acid in enzymes that are responsible for synthesizing that amino acid. Here's the paper: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1839009/ although the effect isn't that high for Tryptophan.

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What's the difference between mRNA and inactive virus vaccine?
If the techniques used in both vaccines are similar and if both use the spike protein approach, then how is the mRNA vaccine more effective than the other ones and more importantly how come it is also effective towards the new variations of the virus such as the Delta variant whereas the others are not? The same protein should be built with the same mRNA, right? I am a little confused here.

The techniques used in mRNA vaccines and inactivated virus vaccines are not similar. Here's some info on inactivated virus vaccines at ScienceDirect: https://www.sciencedirect.com/topics/medicine-and-dentistry/inactivated-virus-vaccine and here is info on the Covid mRNA vaccines at the CDC: https://www.cdc.gov/coronavirus/2019-ncov/vaccines/different-vaccines/mrna.html

Re: "more importantly how come ..." is a different question and your premise is not quite correct. Here's a paper from a decade ago about SARS that discusses why the spike protein makes a good vaccine target in these viruses: Du, L., He, Y., Zhou, Y. et al. The spike protein of SARS-CoV — a target for vaccine and therapeutic development. Nat Rev Microbiol 7, 226–236 (2009). https://doi.org/10.1038/nrmicro2090

I will definitely look more into those. Thank you!

In molecular biology, a ribonucleic acid vaccine or messenger RNA vaccine is a type of vaccine that uses a copy of a natural molecule called messenger RNA to produce an immune response. The vaccine transfects molecules of synthetic RNA into immunity cells.
An inactivated vaccine is a vaccine consisting of virus particles, bacteria, or other pathogens that have been grown in culture and then lose disease-producing capacity. In contrast, live vaccines use pathogens that are still alive. Pathogens for inactivated vaccines are grown under controlled conditions and are killed as a means to reduce infectivity and thus prevent infection from the vaccine. The virus is killed using a method such as heat or formaldehyde.
mRNA vaccines are a new type of vaccine to protect against infectious diseases. COVID-19 mRNA vaccines are given in the upper arm muscle.  the cell displays the protein piece on its surface. Our immune systems recognize that the protein doesn’t belong there and begin building an immune response and making antibodies, like what happens in natural infection against COVID-19.
They do not affect or interact with our DNA in any way.
mRNA never enters the nucleus of the cell, which is where our DNA (genetic material) is kept.
For more info - mRNA and Inactivated (Killed Vaccine)

The mRNA vaccine doesn't transfect (much) into the immune cells directly, most is apparently into the muscle and vascular and lymphatic cells at the site of injection, then some transported around the body, ending up in the liver largely. Your later description is closer. You also have the links for mRNA and inactivated swapped.

Your description of inactivated vaccines is partially confused with a description of live attenuated vaccines. Both of the vaccine type descriptions are missing key elements such as how they generate an immune response, and advantages and disadvantages of each.

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Question about phylogenies and DNA sequencing
I'm reading this web page which talks about phylogenies and DNA sequencing:
https://bioinf.comav.upv.es/courses/biotech3/theory/phylogeny.html
A certain sentence says, "If we consider dolphins and sharks to be closely related because they share a similar shape we would be mistaken."
If we were to take the DNA sequence of the dolphins and sharks and compare the genes encoding for shape, wouldn't they be very similar? Wouldn't we then be able to conclude that dolphins and sharks are similar?
Or is the workaround that we would examine the entire genome, i.e. the entire DNA sequence, to see if that's the only similarity they have?

Genes reflect a phylogeny of their own. So no, the genes for "shape" (if they existed) would be very different between dolphins and sharks. Every single gene in a dolphin is more similar to its homologous counterpart in a cow than to any gene in a shark. Gene by gene, or with the entire genome, it would not matter. The similarities between sharks and dolphins are due to convergence. Convergence make sense in that there is selective pressure to have streamlines bodies to swim through the water. It is possible for genes to converge as well, but the nucleotides would differ, just as the fins on sharks and dolphins differ.

There really aren't "genes encoding for shape".  If you looked at genes encoding important metabolic pathways, it would be clear that dolphins are mammals, and sharks are not.

Ok, I see. But for example if we took really related organisms, let's say marsupial wolves and placental wolves, which are two completely different species that are unrelated. Couldn't we mistakenly conclude that they're extremely closely related even if we were to sequence their genomes? For example, we'd see that they have perhaps similar teeth, or fur, etc.

If you looked at all the coding genes, and the patterns of synteny, you would see that marsupial wolves and placental wolves looked like they belongs to different subclasses.  External similarities mask differences present at the DNA level.

There are no unrelated organisms. Wolves are related to ferns, which are related to bacteria, because life is monophyletic. Marsupial wolves and placental wolves look alike because of convergence on an efficient phenotype. However every single gene in a marsupial wolf is closer to those of Koalas than it is to a placental wolf.

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How would homologous recombination and mutations affect speciation?
I'm wondering how homologous recombination and mutations can affect how speciation can occur from one species (so that 2 will be created).
I'm doing research and I found that different mutations and genetic combinations occur in two geographically separated populations which can lead to speciation.
I know recombination can result in different genetic combinations, but how does that factor into a phylogenetic tree? Wouldn't recombination technically play no role in leading to evolution?
My (sort of) guess is that say recombination creates a population with a lot of AA genes and the other population, say by chance (genetic drift), has a population with a lot of aa genes.
We know A and a differ by perhaps a few SNPs, so on average, the two populations would become slightly different from one another due to genetic drift and geographic separation.
Do I have the right idea here? I'm not 100% sure how recombination during prophase I would affect recombination. Hoping someone can clarify this for me or provide some new insights.
Thank you!

Recombination occurs when homologous DNA sequences pair with each other and cross over, essentially swapping genetic material. Now, say that this crossover junction is in the middle of a gene, and we have some genetic differences in the top half and some in the bottom that distinguish the two alleles. If recombination occurs in the middle of the gene, then a new combination of alleles is created that didn't exist before. This new version of the chromosome can now be passed on as a single unit via sexual reproduction.
I left out a lot of details obviously, but this is the basic idea. The reason why recombination adds to genetic diversity and can lead to speciation is because it is essentially mixing and matching existing combinations to create new alleles.


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Don't understand how multiple replication bubbles work
I'm not exactly sure how multiple replication bubbles work, assuming were working with a linear, eukaryotic chromosome.
This is a diagram for reference:

It appears that the DNA is being synthesized "towards" the centre. What I mean is that in one replication bubble, the top strand is being replicated from left to right, whereas for the other replication bubble, the top strand is being replicated from right to left.
I don't understand why this is. Aren't the directions reversed? Isn't synthesis always supposed to be from 5' to 3'?
Thanks!

Take into consideration the helices.

You mistake replication direction with polymerase synthesis direction. Indeed, the polymerase synthesizes new strands 5' -> 3' but if the replication of each strand was continuous, there would be  no such structure as a replication bubble whatsoever. Take a good look at the drawings:

The thing is the direction of replication is consistent with the direction of leading strand synthesis, so the bubbles will "spread" outwards. Lagging strand is synthesized in the form of fragments 5' -> 3'. If you look closely fragments that are closest to the center of the replication bubble are synthesized first, then polymerase detaches and works on the next fragment which is actually closer to the 3' end of the lagging strand.
Here's an article on Wikipedia about those fragments: https://en.wikipedia.org/wiki/Okazaki_fragments
Hope this makes things clear.
Cheers and happy learning,
Krzysztof

That's a great explanation and also a great diagram. Thank you very much for your help.

Glad I could help ;)


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How would our circadian rhythm change over time if we had no sunlight whatsoever?
Of course, over the span of a couple days, our circadian rhythms would lengthen a few hours. But what would happen to the circadian rhythms of humans overall if we had no daylight ever? Say we can live for 10,000 years, how would our circadian rhythm be different 10,000 years from now after zero exposure to sunlight? Would it still be slightly more than 24 hours?

Your question made me curious so I found this study of fossorial species like naked mole rats. With little to no light input from the environment their societies seem to maintain a circadian rhythm: https://www.ncbi.nlm.nih.gov/m/pubmed/11134679/

Say we can live for 10,000 years, how would our circadian rhythm be different 10,000 years from now after zero exposure to sunlight?

Probably almost the same.
A circadian rhythm has - by definition - a free running period of more or less 24h. Of course this might change over time, but 10,000 years are not very much on an evolutionary time scale.
As an example there are some studies about the circadian clocks of fish that have lived in underground caves for over 1 million years: They still have a circadian rhythm (even though its doesn't react to light anymore), but even after 1million years the free running rhythm only changed from 24h to 47h. Interestingly it can also still be 'entrained' (synchronised) to other regular cues like feeding time (this is also the case for normal circadian rhythms).


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How is single nucleotide polymorphism denoted?
Currently I'm studying an article on TERT promoter mutations in human melanoma and find myself unfamiliar with included denotations,I would appreciate it if someone could explain to me what C228T in the sentence below means.

Two tumors with a C228T transition also contained an adjacent C>T transition (at position chr5,
  1,295,229), which is indicative of a dinucleotide CC>TT transition

C228T is a mutation from Citosin to Thymin at the 228th basepair.
Maybe this website helps? Nomenclature for the description of mutations and other sequence variations
I see they write the mutation different (following their format it would be 228C>T), but the general idea is the same.


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Is this lizard protected or endangered?
We think that it's a type of alligator lizard. It was found in the open space area near my home in Moss Beach California (about 10 miles south of San Francisco). Thank you!

It appears to be a California Alligator Lizard - Elgaria multicarinata (subspecies multicarinata), although another photo from the side would be helpful for a positive ID. This species seems to fit the range for the observation as well.
According to CaliforniaHerps.com, there are no associated conservation concerns for this particular species.
Elgaria multicarinata multicarinata conservation status


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What does the presence of 6 molecules of water in this equation indicates to?
so I was studying biology today and I went over this weird question that says:

The presence of 6 molecules of water in this equation:
C6 H12 O6 + 6O2 --> 6CO2 + 6H20, Indicates that the:
a) Complete Glycolysis of a glucose molecule (Obviously not correct)
b) Occurrence of Krebs cycle Twice
c) Complete occurrence of oxidative phosphorylation process
d) Storage of energy in NADH and FADH2 molecules

Alright so this is the oxidation of one mole of glucose equation (Without the ATPs) but till now I don't exactly know the correct answer for this question, but to not create any confusion this question is related to the Aerobic respiration (Glycolysis, Krebs Cycle and Electron transport chain).
Here's how I approached this question:
(a) is obviously not correct because the products of glycloysis are 2 pyruvate molecules and 2 ATP molecules so I checked off this choice.
(b) However seems correct because the products of 2 Krebs cycle is 4 CO2 and there is already 2CO2 when the pyruvate acid formed the 2 acetyl CoA molecules so in total that's 6CO2, but still what about the 6 Water molecules?
(c) is a very debating choice because when there is a "Complete occurrence of oxidative phosphorylation process" so that means 2 Krebs cycles had already occurred and formed the 6CO2, and during the oxidative phosphorylation process Water molecules are formed. and ATPs too? I don't exactly know about the ATPs, but aren't they supposed to be in the equation's products in order for this choice to be correct?
(d) This choice indicates to Krebs cycle but the water molecules only are formed during oxidative phosphorylation only.
So basically all the choices seems very debating and confusing and if I were to choose then I'll go with (C) because it's the only choice that makes sense for the water molecules (and the question asks for water), but I want someone to please answer this question with a brief explanation to why he chose this answer,
Thanks :)

You have my sympathy. Even for an MCQ this is a really stupid question. Nobody cares about water molecules in biochemical pathways, nor is it generally practical (or at least the practice) to count their production. The purpose is presumably to have you look at the pathways and see where the water is generated. Forget about everything else (i.e. the important stuff). PS You could improve your writing style by not imitating informal speech patterns. "So" is not required to start a sentence, is bad style, and removing superfluous material improves readability.

This reaction only means complete oxidation of glucose to 6 molecules of carbon dioxide and 6 molecules of water.
Reaction presented in question is very generalized, but the presence of six water molecules only means complete cellular respiration. Check out the actual biochemical pathways which take place to oxidize one glucose molecule.
And other options do not represent the complete cellular respiration, so there will not be formation of six water molecules, only option C means complete oxidation of glucose.

Via: https://en.wikipedia.org/wiki/Cellular_respiration
Water molecules shown by solid blue arrows.
During glycolysis, One glucose molecule releases two water molecules. This is the 9th step  of glycolytic pathway controlled by Enolase. Two water molecules are produced because two reactions are taking place.

(Image source:  https://johncarlosbaez.wordpress.com/2016/01/08/glycolysis/)
During Citric acid cycle, 2 water molecules are used in two enzymatic reactions performed by  Fumarase and Citrate Synthase. And Aconitase performs the  isomerisation of citrate to isocitrate so it has no net effect on water molecules. So, 4 water molecules are used here.

(Image Source: http://www.biosciencenotes.com/citric-acid-cycle/)
During Electron transport chain, 12 water molecules are produced due to oxidation of NADH (FADH2).
As electrons in this chain are passed, they move from higher to lower energy state, and release energy. Some of the energy is used to transport hydrogen ions across the membrane. This creates electrochemical gradient. And electrons are transferred to molecular oxygen to form water.
This makes net total of 10 water molecules. But 4 water molecules during cellular respiration are used in substrate level phosphorylation. Check out its explanation here   (Via : https://onlinelibrary.wiley.com/doi/pdf/10.1016/0307-4412%2895%2900140-9)

(Image Source: https://www.khanacademy.org/science/biology/cellular-respiration-and-fermentation/oxidative-phosphorylation/a/oxidative-phosphorylation-etc)

Couldn't agree more, thank you for sharing your knowledge! But don't you know anything about wither they should add the ATPs to the equation or not?

The reaction catalyzed by aconitase doesn’t have any net usage or production of water (it’s an isomerization), which is actually shown in the diagram you used. Ignoring the water produced by ATP synthase, 10 molecules of water are produced by the biological oxidation of glucose, not 6.

yes..you are right, then why don't we show 10 water molecules in this reaction.

@canadianer I tried to improve my answer. Kindly explain me why we only show six water molecules. Thankyou

Good question. Check out this answer, the paper linked to therein, and Roland’s comment underneath.

Thanks a lot for making it clear

Although I tend to agree with David on the validity of the OP example as a good MCQ question, I think that the 'required' answer is (c) Complete occurrence of oxidative phosphorylation process.
However, I think that this answer is potentially flawed (see below) and a more acceptable alternative might be something like

(c) Complete oxidation of glucose via cytochrome oxidase of the respiratory redox chain.

Glucose makes 12 pairs of electrons (all 'held' in C-C and C-H bonds) available to cellular respiration. (See, for example, the letter on TCA cycle confusion by D.E. Atkinson published in TIBS and kindly made available by David).
It takes four electrons to produce 1 water molecule in the cytochrome oxidase reaction.  Therefore, if six water molecules are produced, all of 24 electrons 'supplied' by glucose have been passed to water: glucose has been 'completely' oxidized.
The reduction of oxygen to water is a four-electron transfer.  A two-electron reduction produces H2O2, and a one-electron reduction produces superoxide.  If either of these compounds were produced, or if electrons from glucose were 'diverted' elsewhere (thus never 'arriving' at cytochrome oxidase) the stoichiometry of water production would be less.
However, possibility (c) specifically states "Complete occurrence of oxidative phosphorylation process. This, to me, is confusing and is arguably false. There is no requirement that oxidation and phosphorylation be coupled in order for six water molecules to be produced in the respiratory redox chain. In the presence of (excess) of an uncoupler such as dinitrophenol, no ATP is produced (oxidation and phosphorylation are completely uncoupled) but this in no way precludes all 24 electrons from glucose being passed to oxygen resulting in the formation of 6 water molecules.
For example, if possibility (a) were to state 'complete oxidation of a glucose molecule', then IMO that is by far the best answer (and all others are false or ambiguous).

Yes exactly, this question is very inaccurate, but I guess I'll just go with (C) as it's the most suitable answer for this question, Thanks for your answer.


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How to drop a grid of points in DICOM images of a CT scan (imageJ? Horos?)
I have a series of DICOM images from a CT scan of a bucket of rocks. I want to systematically measure the size of the interstitial spaces. The reason I'm doing this is to compare it to a simulation I've made to check that my simulation is giving accurate data.
In order for the measurements to be comparable to data from my simulation, I want the method for measuring the gaps to be as follows: define a 3D grid of points within the rocks (say, every 5 mm). At each point that falls within a gap (not in the centre of a rock), measure the gap width from that point in the X, Y, and Z directions.
I've tried messing around with both Horos and ImageJ but I can't work out how to define points (ROIs?) in a systematic way, or to have them show up in all three directional slices of the scan (I'll need to measure two dimensions from one 2D image e.g. X,Y and then switch to the X,Z image to get the third measurement, but use the same defined point).
Ideally once I know how to drop points and understand how they work, I could program the software to automatically do these measurements. Can anyone point me in the right direction?
Thanks!


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What tool can I use to align multiple protein sequences to one reference sequence?
I have a protein of interest which is ~300 amino acids in length. I also have around 40 short sequences (all 9 amino acids in length); these are all very different from each other. I would like to perform multiple pairwise alignments to see if these sequences match up with (or have high sequence identity similarity) any areas in the protein of interest.
Since the short 9-a.a. sequences are very heterogeneous, they will have similarities in different regions of the protein of interest. I would like to know if it is possible to perform the alignments for all 40 sequences in one step, rather than using COBALT 40 times (and checking each of the short sequences against the reference sequence individually).
Please let me know if the description of my problem is not clear enough, I would appreciate any help in identifying a way to do this.

Hi and welcome to Bio.SE! It sounds like you are reinventing BLAST. I'd be careful about aligning those short regions. I don't see a problem with running 40 pairwise alignments if you can run the pairwise alignment programmatically.

Possible duplicate of Do all multiple sequence alignments employ global alignment algorithms?

This appears to be a bioinformatics question rather than one about biology. —— Please take the time to take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

What you want to perform is commonly called a multiple sequence alignment.  As @Wayne_Yux said, the first step is to put all of your protein sequences in a single fasta file.  You can then use one of several online tools to apply different alignment algorithms to your protein sequence set.
A popular sequence alignment algorithm is Clustal, which progressively builds a multiple sequence alignment from all of the pairwise alignments.  genome.jp hosts a web-based alignment tool that allows you to choose from Clustal and other alignment types (1).  For alignment of many small sequences to a single larger sequence, you should use the "SLOW/ACCURATE" option (2).  After you upload your fasta (3) and execute multiple alignment (4), an aln file will be generated which you can download (5).

You can then take this aln file and upload it to a different tool that allows you to visualize alignments.  Personally, I like ESPript, which gives color-coded alignments in pdf or image formats.  Because you want to compare many sequences, it will probably be necessary to change the "Alignments output layout" parameters, e.g. change "Gap between blocks" to a smaller number to fit all of your sequences in one frame.

In a multiple sequence alignment, the algorithms will attempt to align the sequences along their length (global alignment). What you need is a local alignment approach with a high penalty for base mismatch.
The E-INS-i algorithm in MAFFT might provide the desired functionality. Select the Advanced Settings and there:

Strategy -> E-INS-i algorithm
Align unrelated segments -> Leave gappy regions

Depending on how heterogeneous your sequences are, you might need to fine-tune other settings as well. Without the data, it is impossible to provide a more detailed guide.

You can store the 40 sequences in a fasta file and then use blastp to align them all at once to your reference sequence.
After that, you can inspect the alignment hits and see wether they fit your quality expectations


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Why are HeLa tumors purple?
I remember hearing that the tumor where HeLa cells originated from was purple and jelly like, and I've seen pictures from studies with rats and HeLa tumors, and their tumors appear to also be purple. So what makes these tumors purple?

HeLa cells themselves are not pigmented, and usually appear translucent/gray under light microscopy. The growth medium may however be colored, and a common color is magenta.
The tumors themselves will appear purple, as most tumors do, due to the broken vascularization. Tumors commonly secrete growth factors leading to angiogenesis, but the resulting vessel networks are convoluted and not well organized, commonly full of anastomoses. The resulting poor vascularization leads to significant hypoxia, which results in a bluish coloring of the blood.

It would be nice if you could add some references to back up your answer.


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Why there is no ELISA for SARS-CoV-2?
As far as I know, SARS-CoV-2 tests currently used worldwide are real-time RT-PCR. Why there is no ELISA for SARS-CoV-2?
Compared to PCRs, ELISA is:

Way cheaper;
Way faster;
Does not require trained technicians or complex equipment.

Because the virus is spreading for only a short time?

Yeah, @Chris has a point. While the test itself is easier to perform, the production and purification and labeling of antibodies for tests such as the ELISA does take some time.

Marion Koopmans and Florian Krammer both have preview papers describing SARS-CoV-2 ELISAs. There simply hasn't been enough time to prepare antigens, validate ELISAs, publish papers, and manufacture tests. I think this question will be out of date in a few days or weeks, so maybe isn't a good match for SE, where answers are expected to be useful to other people in the future

Another preprint (posted yesterday): Evaluation of antibody testing for SARS-Cov-2 using ELISA and lateral flow immunoassays

@iayork The fundamental question is good for future use and probably reapplicable, and it is good to have a record of why this wasn't possible at a moment in time, and indeed this is a timely question. I would say that this argument requires a bit of editing to the question semantically and a lab-techniques label.

once you are comparing ELISA with RT-PCR i will assume we are speaking about antigen tests for SARS-CoV-2. In that sense, we can note that whichever type of ELISA chosen, all of them will depend on the Ig specificity for the virus antigen.

therefore, the main reason has to do with the fact that

mutation regions in the virus appear mainly in the spike protein, we do not know whether the antibodies produced against the original spike protein can recognize the new variant spike proteins. article

I agree with @mpprogram6771 and @iayork. Development of ELISA kits consumes more time to develop and validate - the first on the market last year were not recommendable.
Now a variety of immunoglobuin SARS-CoV-2 ELISA kits are available. Mainly using IgG or IgM - IgM to detect early signs of infection, IgG for long term response.
Eg: here

This does not provide an answer to the question. Once you have sufficient reputation you will be able to comment on any post; instead, provide answers that don't require clarification from the asker. - From Review


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Fresh Water Fish Identification
A couple of days ago I just adopted a group of 7 fishes, 2 inches long each, orange-pinkish color, a black dot before the tail, very fast, active and peacefull. Looks like a kind of tetra fish. Anyone?

Some kind of barb.

Could well be the Rosy Barb, which is a common beginner fish (I believe, not being an owner of a tank at all).
They have a distinctive reddish colouration which is brightest when in the mating season, but otherwise much paler. Their scales seem to be slightly iridescent and they have a black dot at the base of the tail. The males have black tips to the fins, but the females do not have the black tips.


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question about stem cells
I was reading this paper:
https://www.ncbi.nlm.nih.gov/pubmed/26119455
and became confused after this sentence:
"The  ICM-derived mouse embryonic  stem  (ES)  cells and epiblast-derived
human  embryonic  stem  cells have  the  full  potential  to
differentiate  to  ectoderm, mesoderm,  endoderm, and trophoblast."
As far as I know, the trophoblast is originated from morula cells that are totipotent, and ICM cells are pluripotent...
Moreover, are ESCs derived from the ICM of the blastocyst? Because if yes, does it mean that they can also become primitive endoderm and give rise to some extraembryonic tissues? Because as I know only epiblast (primitive ectoderm) gives rise to 3 germ layers... does it mean that ESC are derived from epiblast only or not?
Thanks


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Can you vaccinate against bacterial diseases? Are there existing vaccines for such diseases?
I have the (maybe wrong?) preconception that we only vaccinate against viral diseases, and that there can only exist vaccines against viruses. I think the idea comes from the idea that only for viral diseases are you becoming immune after contracting the disease, not for bacterial. The question Is there a vaccine against the plague (Yersinia pestis)? made me think that I don't really have a justification for that, seeing that the mechanisms for combatting viral diseases and bacterial diseases should be the same (is that right?).
So, is it possible to vaccinate against bacterial diseases? Do we have existing vaccines for any bacterial disease?

Of course we can - and do - vaccinate against bacterial diseases, as these are some of the dangerous infectious diseases.
Among these are:

Tetanus (although here the vaccination is targeted against the toxin, not the bacterium itself)
Tuberculosis
Diphtheria
Pertussis
Haemophilus influenzae type B
Cholera
Typhoid
Streptococcus pneumoniae
Meningococcus: against the strains ACWY, B

A list of the vaccines against bacterial diseases can be found here.

Vaccine works by instructing our immune system to recognize and fight against infectious agent (pathogen), so it can be virus, bacteria or any other microorganism.
Particles from particular pathogen are introduced into the body which stimulates immune system and thus works to fight against it.
Bacterial vaccines can be  of different types: toxoids, subunit vaccines, killed vaccines, and live attenuated vaccines. (Via: https://www.sciencedirect.com/topics/medicine-and-dentistry/bacterial-vaccine)
List of bacterial vaccines can be checked in this wiki link


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Apical dominance in plants
Could someone help me understand a few concepts related to apical dominance
1) why auxin is a dominant over other hormones?
2) how exactly the mechanism of apical dominance works?

Which link did your research produce, and what concept from that link is it that you don't understand?


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Re-establishment of Hardy Weinberg Equilibrium After Selection
I have been given this question:

In a population of 2500 mice, light-colored fur is dominant to dark-colored fur. 2400 mice originally have light-colored fur. However, an owl species moves into their environment, preying mainly upon the light-colored mice as they are easier to spot when hunting at night. When the owls finally leave, 80% of the dark-colored mice are left, and only 10% of the light-colored mice. After many generations, Hardy-Weinberg equilibrium is re-established. Approximately what percentage of mice now have dark-colored fur?

Answer choices are:

A) 10%
B) 15%
C) 20%
D) 25%
E) 30%
F) 35%

My thought process goes as such:
When the owls leave, the groups are 240 light mice and 80 dark mice.
$q^2 + 2pq + p^2 = 1$
q is recessive allele, p is dominant allele.
$0.5^2 + 2*0.5*0.5 + 0.5^2 = 1$
Apply fitness:
$0.8*(0.5^2) + 0.1*(2*0.5*0.5) + 0.1*(0.5^2) = 0.275$
(0.8 and 0.1 correlate to the fitness of dark and light mice, respectively)
Now divide everything by 0.275 to figure out new allele frequencies:
$0.727 + 0.182 + 0.091 = 1$
This means that 0.727 = 73% is the new frequency for homozygous recessive (dark) mice.
However, the correct answer is B) 15%
Any idea what I did wrong/how the correct answer is achieved?

After many generations, Hardy-Weinberg equilibrium is re-established. This is a pretty awful sentence (not your fault). HW equilibrium is reached after in a single generation.

I agree it's not written well. But as long as it doesn't alter the meaning of the question... :)

Revised to add complete solution
Before the owls arrive, 100 out of the 2500 mice are dark-colored. This ratio provides the frequency of the recessive allele
$$q^2 = \frac{100}{2500}$$
So $q$ is 10/50 or 0.2. This means that the frequency of the dominant allele $p$ is 1 - 0.2 or 0.8.
Knowing these frequencies, it is possible to calculate the number of each allele
$$AA = (0.8)^2 \times 2500 = 1600$$
$$Aa = 2 (0.8) (0.2) \times 2500 = 800$$
$$aa = (0.2)^2 \times 2500 = 100$$
Of the light-colored mice, 2/3 are AA and 1/3 are Aa. The same proportions hold after the owls leave, but the total humber has been reduced. The dark-colored mice are all aa.
$$AA = \frac{2}{3} \times 240 = 160$$
$$Aa = \frac{1}{3} \times 240 = 80$$
$$aa = 80$$
From these values, the total number of each allele may be calculated
$$A = 2 \times 160 + 80 = 400$$
$$a = 80 + 2 \times 80 = 240$$
These numbers provide the frequency of each allele post-selection
$$p = \frac{400}{640} \approx 0.63$$
$$q = \frac{240}{640} \approx 0.37$$
Applying Hardy Weinberg for the new equilibrium
$$aa \approx (0.37)^2 \approx 0.14 $$
which is, "approximately" 15%.

0.8*(0.2^2) + 0.1*(20.20.8) + 0.1*(0.8^2) = 0.128. Dividing homozygous recessive (0.8*0.2^2 = 0.32) by 0.128 leads to a frequency after selection of 0.25 = 25%. That's still not the correct answer... unless the answer key is incorrect.

I'm sorry, but I don't understand what that calculation is supposed to be saying. I updated my answer with the complete solution.


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Hamilton's Rule in practice
I came across this question in USABO 2013 open exam:

A mother antelope and its child are galloping along the plains, when they encounter a group of hungry lions. If the two antelopes try to escape the lions together, there is a 75% chance that both will be consumed and eaten, and a 25% chance that both will escape alive. If, however, the mother sacrifices herself to the lions, she may be able to buy her baby additional time to escape.
What is the minimum chance that the baby can have to escape from the lions following such a sacrifice such that the mother’s action will be evolutionarily favored?
You may assume that the baby antelope, once escaped, will be guaranteed to survive into a reproducing adult, and that the mother antelope is at the beginning of reproductive age.

I suppose one should use Hamilton's Rule ($r \cdot B > C$) to solve this issue. I'm not familiar with the working of this rule to put it into the question's context. To my understanding $r=0.5$ but this is pretty much how far I managed to go.

I'm voting to close this question because this style of homework question doesn't lend itself to the format of SE. It's unclear exactly what about the topic you don't know. This question may involve someone answering correctly, but only after long commentary about the topic. Other users might disagree and with a few edits this might be a very decent question.

http://meta.biology.stackexchange.com/questions/3393/this-is-the-title-of-the-meta-post-i-just-wrote @LittleDragon please use a more informative title.

I'm new to Bio SE, so sorry for the formatting. What can I do to improve my question?

I disagree with the close votes that say the question is "unclear" or "too broad". I agree it is a homework question but it is hard to suggest what kind of efforts the OP might do to make the question perfectly on-topic. I edited the post hoping to slightly improve it.

@James I agree that this question is a homework question, but what's the problem in answering it. It's quite visibile that  this question is a good one. Iwould not vote for closing the question.

It doesn't have to be that complicated.
The evolutionary value of the offspring to the mother is half that of herself (0.5). Then the relative value of both mother and offspring is 1 + 0.5 = 1.5. So the value of preserving both lives is about 3 times the value of preserving the offspring alone, given the simplistic assumptions from the question. Therefore, to choose to make this sacrifice, the probability of survival of the offspring alone must be at least 3 times the probability of both surviving otherwise. 3 times 25% = 75%.
Edit:

In terms of B and C as requested (though I think it's simpler to step away from this):
B is the benefit to the relative. This is not the probability of survival given the action of sacrifice, but the increased probability of survival. The baby already had a 25% chance of survival, but this action will increase that chance to some p, which we are looking for. B is the improvement in the situation:
B = p - 0.25
C is the cost to only the individual (the mother). This is not 1 (loss of survival), but the difference between the situation without making the sacrifice and the situation when she makes the sacrifice. She's only giving up a 25% chance of survival. So:

C = 0.25.
r is the relation between mother and offspring.

r = 0.5.
So the equation is:
0.5(p - 0.25) = 0.25
0.5 p - 0.125 = 0.25
0.5 p         = 0.375
p = 0.75
Someone feel free to format if you want...

That's be great if you could put that in the $rB>C$ equation! I will then discretely delete my answer as if I never wrote it :)

Hmm, this is an interesting way to view the question!

@Remi.b If I'm reading your math correctly, you made two mistakes. First, it seems that you are looking for the minimum probability of survival of the baby after the incident, independent of the mother's choice at this moment, given an assumption that immediate survival is guaranteed by the sacrifice. This is a much harder question, and not what was asked. I believe the correct answer to that harder question though, would have been 0.67, because in your scenario B=p(1-0.25) => p = C/(r*(1-0.25)) = 0.25/0.375. Does it make sense why B is p(1-0.25) in that scenario?

@Remi.b I suspect you also forgot the parent's contribution to fitness, which is assumed to be 1. This is added to the offspring's fitness, giving a total of 1.5 fitness if they escape the lions, and 0 fitness if they do not.

Of course, I can't help but point out the place where the math ceases to support the reality around us, thus begging a greater explanation: The mother has another choice, which, in higher mammals, is almost impossible to even consider. She could sacrifice the baby, probably as easily as simply outrunning him. All else being equal (and it's not - she has a better chance of survival alone than he does), this choice would have double the value - the obvious choice. So there's your take-away ponderable...

@MarkBailey The converse can be seen frequently in other species (eg rodents) which eat their children in times of severe stress. Perhaps it might be due to the difficulty in raising another child for K-specialists as opposed to the r-specialists.

There is another way to look at this question, which I suspect is even quicker (it is certainly more intuitive for me). Mathematically, it is identical to Mark's answer.
If the parent chooses to not sacrifice herself to save the child, they have a net fitness of 1.5 (1 parent + 0.5 child) if they escape, and 0 fitness if they do not. Therefore, their average fitness is 1.5*0.25 = 0.375.
If the parent sacrifices herself to save the child, they have a net fitness of 0.5 if the child escapes, and 0 if the child does not. Therefore, in order to have an average fitness >= 0.375, the probability of the child escaping must be >= 75%.


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Evolution of diversity and extinction resistance
I saw a comment on an answer to another question that touched on an interesting topic:

keeping diversity is useful for parameter exploration or to adapt to future environmental change

My initial thought was that evolution doesn't "know" about the future, so natural selection might decrease genetic diversity even if it meant dooming the species in the long term.
On the other hand, species that have low genetic diversity may be more likely to go extinct eventually.  So perhaps over time the surviving taxa are those that have evolved mechanims to "hedge their bets" against future environmental changes.
It's clear that some of the parameters that affect genetic diversity within a species (e.g. mate selection, mutation rate) are heritable, but it's unclear to me how the short-term processes of natural selection relate to the extremely long-term processes of speciation and extinction.  This gets into some of the same issues as group selection — how can natural selection, acting on individuals, lead to traits that benefit entire populations or clades?  (Perhaps this simply cannot happen.)
Has any work been done on the topic of extinction resistance or the evolution of mechanisms to create and preserve diversity within populations or taxa?
This is a big question so I don't expect a full answer here.  I'm just looking for some references as a starting point to learn more about this topic.

This is a big question, that one of the evolutionary biologists here can probably give a fuller answer to, but you might check out this article by Jablonski

The topic you describe is very interesting and known as "species selection." Some traits exist that not only affect the reproductive success of individuals, but also affect the diversification rate of the entire species, either through affecting the extinction rate, the speciation rate, or both.
To give you an example, I'll summarize this paper by Goldberg et al 2010. Self-incompatibility (SI) in plants is the ability of a plant to reject its own pollen to prevent inbreeding. This mechanism is expected to increase the genetic diversity of the plant's offspring. Self-incompatibility has been lost many times in the history of flowering plants, yielding self-compatibility (SC), which allows a plant to breed with itself. A plant that can breed with itself has an advantage in that even if the population size is low and it can't 'find' another individual to breed with, it can still breed with itself to produce offspring. However, this trait is expected to result in decreased genetic diversity in the offspring due to inbreeding.
The transition from SI to SC is a common transition that cannot easily be reversed. One might expect, then, that SI would be very uncommon as lineages would lose it to SC. However, it turns out that SC lineages have a lower diversification rate than SI plants in the Solanaceae due to the fact that SC lineages have a higher extinction rate than speciation rate. This difference in diversification allows SI to persist. This is an example of trait-dependent net diversification rate. It is not known exactly why SI lineages have a higher net diversification rate, but it could be related to the higher effective population size which results in "increased polymorphism,
lower linkage disequilibrium, more
efficient response to purifying selection, more
extensive geographic distribution of genetic diversity,
and lower rates of extinction".
If you want to read more, I can suggest a few more papers:
The Units of Selection by R.C. Lewontin
Darwainism and the Expansion of Evolutionary Theory by S.J. Gould
Species Selection: Theory and Data by D. Jablonski


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Effect of light spectrum on photosynthesis
It is said that the blue and red fraction of VIBGYOR is mainly used for photosynthesis. Can somebody explain why this is so?

The there are two main types of chlorophyll involved in photosynthesis, chlorophyll a and chlorophyll b. Each one is effective at absorbing energy in the form of light at a different frequency - one absorbs red light best, the other absorbs blue light best. The two are also used in two different photosystems, I and II, which have different functions, but the end result for both is that the chlorophyll gains energy for the plant to use.
The rest of the spectrum isn't used because plants haven't evolved proteins that utilize the rest of the spectrum; what they have is apparently sufficient for their needs.
This is a good resource to get a better understanding of the details of photosynthesis, and honestly Wikipedia doesn't do a bad job of explaining it.


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DNA synthesis in nucleus
I read somewhere that according to a research, I don't remember what the date was, that our cells stop synthesising DNA around noon and restart it around the sunset. The research told that it was actually a survival benefit for cells when ozone was not formed so that the DNA does not get damaged. Would somebody like to guess how our cells know when to do so and if it is a protection against present ozone depletion due to CFCs?


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DNA of cellular organelle
Why do some cellular organelles like mitochondria and plastids have their own DNA. And what is the basic difference between the DNA of the nucleus and these organelles?

Mitochondria and plastids are the result of two ancient mergers. A kind of symbiotic relationship where one cell phogocytized another. Rather than being digested, the phagocytized cell, complete with its own DNA cooperated with the cell that "ate" it. This was part of the evolution of eukaryotes. This idea is called endosymbiosis, and was championed by Lynn Margulis in the late 1960s. Mitochondria and plastids come from Bacteria, and carry the traces of their original DNA. However, a complete genome was no longer required for the new function, so mitochondria lost many redundant genes. Mitochondrial genomes are much smaller. Plastid genomes are larger than mitochondrial genomes, but smaller than the genomes from which they originated.


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What is the incentive for plants to add rich nutrients to food?
As we know fruits are good sources of vitamins and minerals. What is the incentive for plants to add so much of vitamins and minerals to fruit pulp. My thought is that  seeds would need is some protection, and why waste rich nutrients and vitamins by adding it into pulp?

What research have you done before asking it here? I think you should start with "what is the use of fruits?"

I think i found answer. It is for reproduction, so that when animals and birds eat fruit, seeds will be transported and it'll help plants to go to new regions and of course  for protection of seeds.....

Yes. And the point here is that when an animal will get more nutrients from a fruit, it will prefer that fruit over others, which will increase the chances of the fruit's seed's dispersal. Now, you should close/delete this question as it is likely to be closed as off-topic.

Not sure why it's off-topic. At any rate, OP, first separate minerals from vitamins - minerals are absorbed from the ground (see here and note p. 784) while vitamins are usually synthesized by the plant's cells (see this as an example). Also keep in mind that plants have no "incentive" to do anything - all reactions happen according to energetic considerations. Seek and you shall find.

Thank you. I'm kind of newbie for biology.  I was asking from evolution point of view, wondering why would they put so much effort in producing fruits..


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What is the scientific name of this leaf?

Has anyone seen this before? I got it from India as a gift but I have no idea what it is called or how to take care of it. Thanks

If you use an Android device there're several plant identification apps available such as Pl@ntNet and there're some websites too which can help you.

Looks very similar to Naringi crenulata which is found in India.  More information can be found on this Encyclopedia of Life page.

Image source: https://commons.wikimedia.org/wiki/File:Naringi_crenulata_leaves_and_flowers.jpg

Following on from Kurt's response, there is a similar irregular margin version called
Hesperethusa crenulata which is perhaps apparently used as a beauty cream, Thanaka, unverifiably promoted as "skin whitening" i.e. bleaching by some sellers, antioxidant, antibacterial and moisturizing, mostly famous in Burma, and which can be bought around the world. So it's also a cultivated tree and you'll find a lot of common and cultivar names for it. the sources of information for it are confused, there seems to be Limonia Acidissima and Limonia crenulata which are closely related. Perhaps both are used medicinally.
Thanaka also appears as Thanaka tree with reference to Hesperethusa so it seems that it has some Natural remedy / Ayurveda properties from the same plant in Burma and India.
In depth page for it here: http://idtools.org/id/citrus/citrusid/factsheet.php?name=Hesperethusa+crenulata
one with bark havested


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Why EtBr migrate toward the opposite direction？
We known that DNA would run toward the positive electrode, because of they have negative electricity. then why EtBr migrate toward the opposite direction to DNA?
is because they have positive electricity?

EtBr runs the same direction as DNA. If it runs the wrong way, you probably have your red wires on top (mixed up)

Ethidium bromide itself is neutral in charge, however in aqueous environment it's a positive ion and it travels towards the negative electrode, opposite to DNA, as DNA is negatively charged and travels towards the positive electrode.
The thing is, it doesn't matter all that much. Whether you prepare a gel with EtBr added or you add EtBr to the electrophoresis buffer, it will instantly start intercalating the moment you insert your sample or start running the gel. The moment the electric current is applied, EtBr will indeed start migrating towards the negative electrode but some finite amount would have already intercalated into the DNA and it's going to be visible under UV only when bound to DNA. Keep that in mind that EtBr is a much smaller molecule and penetrates the gel easily, but will get trapped in between DNA base pairs if it happens to find some.
With that said, as one of the commenters pointed out, if your samples seem to have travelled the other way around, you have probably swapped the cables. The charge of the electrode depends on the charge applied by the source of electric current and if you mistake the cables, you will actually make the samples travel towards the opposite direction.

Negatively charged anions migrate towards the anode electrode during electrophoresis.  Likewise, positively charged cations migrate towards the cathode electrode in electrophoresis.  Neutral molecules, lacking any net charge whatsoever will remain immobilized in the loading wells.  The net charge on a molecule in an aqueous buffer depends on the both the molecular structure, and the pH of the buffer.  If you agree with all of these facts, then you have answered your own question.


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Is an animal's body height dependent on its environment?
Imagine the follwing situation: a newly born animal is brought into a small room. This room has no windows, but artifical light to imitate the sunlight. Furthermore, this light behaves like the sun, so that there are artificial nights and days in the room. The animal will be provided with food and water, too, so that it has enough nutrients to develop in a normal way. What will happen with the animal, when the room is so small, that it would limit the body height of the animal?
(One extreme example: an elephant, living in a normal sized room)
Would the growth of the animal be limited by some biological/biochemical mechanism? Or would the animal grow in a more or less normal way?
In summary, my question is: does the body height of an animal depent on its environment? If yes: how strong is this dependence?

The animal would grow normally to its natural height, but if limited, would continue to grow but become deformed. Do you have a specific reason for asking this?

@anongoodnurse Do you have any sources to read more about this? No special reason, I have just been curious about it. So no reason to panic: this is (of course) just a hypothetical situation!

Have you ever heard of the binding of feet in Chinese women? Hormones , and nutrition, etc.control growth, not space. Growth hormones + limited space = deformity. Sources, no. Any such experiment would be unethical, not to mention unhelpful.

@FlashTek do you think examples from anongoodnurse answers your question? If not, please explain why.

@anongoodnurse I did not really think about big experiments but rather observations about situations in which something like this has happend. Initially I thought, that the an animal in such a situation might release hormones which hamper growth hormones, so that the animal's growth will be limited.

Nature is red in tooth and claw. I can't see your situation occurring in nature. Likely the animal would die from starvation if confined to a small space unless in a lab for this particular, unethical, experiment. Even joey's outgrow their space...


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What is this unusual structure inside this banana?
I was eating a banana, and I found this strange biological structure inside of it.

It was a bit tougher than the banana, and ran inside of the body through most of the length. To be clear, I peeled back banana with my fingers to reveal it; it was enveloped inside. It was accompanied by a small void.
No idea what this is, never seen anything like it. It didn't taste good. I'm thinking it might be a mutation. Anyone know what this is?

"didn't taste good"? Are you insane?

@A.I.Breveleri thought it might give me powers.

@A.I.Breveleri I would assume that's how OP found out something was wrong with their banana. :-)

@John yep :√)

It looks like some species of Nigrospora genus took over the inside of that banana. According to Wikipedia, N. sphaerica was first isolated from bananas. The other species that you will find referenced online is N. oryzae. In the articles I
cite below the colonies are grown in potato dextrose, though.
Here is a picture of the red fungus inside a banana (from the Canadian Food Inspection Agency):

Googling 'Nigrosporia banana' also returns lots of similar pictures.
To get a better answer, a sample could be taken from the banana and then cross-check what you see under the microscope with the oryzae morphology images seen in the researchgate article.

Well I won’t be eating bananas again.

That's freaky, I don't like that.

@Phoenix Just get revenge on their (distant) family, by consuming copious amounts of mushrooms.  It's just like the mafia... only eating food.

Wikipedia says it has antiviral properties. Maybe you should eat it?

@CJDennis It has some side-effects too, so I wouldn't recommend it. Although apparently they've successfully used it against MRSA cultures, so perhaps it has potential in derivative form. But I suspect this is one of those cases where the cure is worse than the original ailment.


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Induction of disease
In the paper they are infection WT and IL-22-/- mice with C rodentium on some occasions they use oral infection, on others they use IV and on some they use a bacteremia model. Can anyone please clarify why they may have done this?

Please provide a link to the paper you are referring to. Have you any ideas why they have done this? Any suggestions? You may be right or wrong and that way we can explain it, rather than provide answers without a context for you. Typically this may be done out of experimental limitations (time of onset, stage of disease, strength of induction, or age of animal, etc.), or to show that a treatment efficacy holds independent of the method of induction, since the methods are not created equal, i.e. multiple lines of evidence are stronger than a single kind of attempt.

Welcome to Biology.SE! In addition to following the suggestions from @SPr, please also 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, your title should give a better sense of what you are asking. In addition, please improve your posts clarity — the grammar and lack of punctuation make parsing your first sentence difficult (e.g. I'm guessing infection should have been infecting). Finally it is best to spell out the bacterial genus and define abbreviations like IV. Thanks!


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What evolutionary advantages does a longer muzzle have against a shorter muzzle and vice versa
Basically I'm curious as to why when it comes to mammalian predators that some like say bears and canines tend to have longer muzzles than those like big cats.
aside from their ancestors/evolutionary line and such, what advantages or disadvantages do short muzzles and long muzzles have against each other and which is better?

Welcome to Biology.SE! We 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). Note particularly that "which is better" is probably the wrong question — I suggest starting with the assumption that varying traits (e.g. different muzzle shapes) have costs and benefits with optima that depend on the circumstances.  ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and edit your question accordingly. Thanks!

This paper, The biomechanics of foraging determines face length among kangaroos and their relatives might provide some insight, but very likely misses a lot of factors that would apply, e.g., to wolves vs cougars.  In the case of carnivores or omnivores, hunting strategies, prey capture methods, and even tearing & chewing techniques are likely to interact synergistically with muzzle length via the Baldwin effect (Wikipedia). Another paper The Baldwin Effect and Genetic Assimilation compares the Baldwin Effect to the Waddington effect, which can have similar results.
Edit:
In response to the suggestion by @Willk and @tyersome, I've added the following explanation:
The Baldwin Effect is widely accepted among evolutionary biologists.  The Waddington Effect is not as widely accepted and is sometimes (incorrectly) interpreted as a form of Lamarckism.
In essence, the Baldwin Effect works like this:

a population is subjected to a new environmental challenge or opportunity
a few individuals learn a new strategy that overcomes the challenge or exploits the opportunity
natural genetic variation makes some individuals in the population more capable of learning the new strategy
Individuals whose genetic makeup makes them more capable of learning the new strategy have a fitness advantage and produce more descendants, so over time the proportion of individuals in the population who can are genetically equipped to learn and use the new strategy, increases.
Individuals whose genetic makeup gives them a physiological advantage in regard to using the new strategy will have a further fitness advantage, and will consequently produce more descendants than others in the population.

Let's say the environmental challenge for two different kinds of carnivore (let's call them Bogs and Dats) is to catch Mophers.  Both Bogs and Dats initially have the same medium-to-short muzzles.  Some Bog individuals figure out that they can dig  Mophers out of their burrows, and some Dat individuals figure out that they can catch Mophers at night when the Mophers leave their burrows.  Both strategies are successful.  Some Bogs happen to have longer muzzles than their cousins, and find it turns out that longer muzzles work synergistically with the digging strategy, allowing Bogs to stick their noses into the Mopher burrows to grab escaping Mophers.  The resulting fitness advantage results in an increase of the long-muzzle trait in further generations of Bogs.  Note that in this scenario it is the adaptive behavioral strategy that creates selective pressure that favors a particular genetic adaptation.
Dats on the other hand, because of their nocturnal hunting strategy, benefit from improved night vision; and long muzzles don't provide any fitness advantage to Dats because Dats don't dig Mophers from their burrows.  As long as Bogs and Dats don't hybridize, they will most likely end up with long and short muzzles respectively.
The Waddington effect, also called “Genetic Assimilation”, is somewhat more direct:

An environmental stress causes a proportion of a population to develop one or more abnormal traits, by interfering with embryological development.
If there is a selective pressure in the environment that favors some subset of those traits, individuals whose genetic makeup makes them more likely to develop that subset of traits, those individuals are likely to produce more descendants than other members of the population.
If being “more likely to develop” that subset of traits results from a weakening of genetically determined development controls that would otherwise prevent development of that subset of traits, then the subset of traits can eventually become the normal phenotype.

An explanation of how the Waddington effect might influence muzzle length requires a bit more hand-waving, largely because there is no evident environmental factor that would cause perturbations in the embryological development of, e.g., dogs.  However,  I'd assert that an abrupt release of a strong selective pressure can have a closely analogous result.  Wolves really have to look and act a lot like wolves in order to survive in the wild (partly because of their survival strategies), so they are subject to strong selective pressure.  Domestic dogs, on the other hand, are subject to much weaker selective pressure.  Moreover, when a variant shows up (a pug, for instance which has a very short muzzle), it is often considered “cute” and is bred separately to fix the trait in a subpopulation.  Although the "release of selective pressure" mechanism isn't quite what Waddington contemplated, the process is closely analogous.
Note that the Waddington effect and the Baldwin effect are not mutually exclusive.  Relaxation of selective pressure that reduces fitness of variants, and environmental factors that cause disturbances in embryonic development (a la Waddington) both produce a rich source of variants upon which the Baldwin effect depends.
However, It is very difficult to prove that any specific phenotypic trait in an existing species was caused by a particular selective pressure. At best we can only make plausibility arguments supported by models and rather sparse environmental & ecological data from the geological record, from analyzing genotypes, etc. In the case of canines vs felines (which split off from a common ancestor perhaps 42 million years ago), we can really only guess what the environmental challenges & opportunities might have been, and what behavioral strategies may have been adopted by different individuals and populations.

Curious to know why this was downvoted.

Because that is what happens on the Biology Stack.  Fleshing out the Baldwin effect so save me the wikipedia click would be nice.  Upvote from me, though.

I think your answer deserves better than anonymous downvoting, but I would guess that the down voters felt like that this wasn't a good answer. I don't have time right now to read the links you've given, but a superficial scan of the Wikipedia article on the Baldwin effect left me unconvinced of its appropriateness in an answer to this question. If you elaborate on the Baldwin effect and its relevance, I would expect you to get a more favorable response.

Thanks for that advice.  I'm not looking for favorable responses per se; just want to be helpful to the OP.  I will elaborate on how the Baldwin effect and Waddington Effect might be relevant.

The problem you have is it does not answer the question, which is what functional aspects of muzzle length favor different relative lengths. I get that you are saying it is difficult to answer but you need to say that explicitly, basically you need to say your not answering becasue it can't be answered (which is wrong but hey its your answer)

Its mostly due to different forms of predation.
Longer jaws are deeper and can reach farther around a prey item, it also increases the chances of catching a moving target in the jaws becasue the area the jaw covers is larger, all things being equal it should always be favored but things are rarely equal, everything has a cost. It is common to see longer snouts in animals that hunt primarily with the jaws. There two ways to do this which depends on how big the pery to are after is, for predators going after relatively small prey they favor long thin snouts, is really noticable in aquatic predators like gharials, it makes for a very fast bite with a wide attack range. Alternatively if they are going after large prey they need to balance strength with speed so you see long, but not as long, more robust snouts. Think alligators, hyena, wolves. Whereas cats who attack with their forepaws can use a smaller head and jaw and favor a more precise bite, becasue they are moving with the prey becasue they have grabbed it, the arms are absorbing most of the stresses. Cats favor grabbing and strangulation for which a small short jaws works fine. Energy and material saved here can be used elsewhere. A longer snout would be weaker unless they add a lot more muscle to stabilize it. In terms of resources it is a lot of cost for little gain, whereas in wolves it is worth the cost becasue they need that strength anyway, becasue they jaw is where all the stress of the struggling prey is being transmitted.
You see the same thing in dinosaurs, predators that can attack with the claws have weaker bites/smaller heads. In the case of dinosaurs however snout length varies less because the small heads favor slashing bites, which favors a longer snout (thus a longer cutting row of teeth) there heads get narrower and weaker more than shorter.  Mammals can't use this strategy because they don't get replacement teeth, and they would quickly not have a tooth in their head, so instead you see strangulation favored instead.
Of course an animal can try to balance a range of strategies and there are all kinds of specialized forms like saber teeth, venoms, ect. Of course this is also simplified a lot of other things effect snout length as well, things like climate (long snouts cause less heat/water loss through breathing), sense of smell, or even vision.
https://www.cambridge.org/core/journals/paleobiology/article/dinosaurian-and-mammalian-predators-compared/BE3492DA7E0A103C6F6E77B9611D86A9
https://link.springer.com/chapter/10.1007/978-1-4615-0161-9_14
https://www.cambridge.org/core/journals/paleobiology/article/constraint-and-adaptation-in-the-evolution-of-carnivoran-skull-shape/77B1591461066F9D0E30F309F6C495C6
https://www.sciencedirect.com/science/article/pii/0034568770900757


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will a plant grow faster if it is exposed to concentrated sunlight?
I know that plant grow faster depending on the hours of sunlight it has, but what happens if i put a giant mirror focusing light to the plant?.
Will the growth rate be limited by the damage the sunlight produces, or will it be limited by the speed of the photosythesis?

The Wikipedia page on photoinhibition has a good explanation of the relationship between light intensity, photosystem damage, and photosynthetic potential.

Welcome to Biology.SE! We 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). In addition, this is an unanswerable question without knowing the type of plant and the light levels before and after concentration (different species tolerate different level of light).  ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Thanks!

In nature, there is often ample sunlight available to plants. From this NIH page:

However, even at the maximum light intensity encountered by photosynthetic organisms (tropical noontime sun, ≈1.2 × 1020 photons/m2/s), each reaction-center chlorophyll a absorbs about one photon per second, which is not enough to support photosynthesis sufficient for the needs of the plant. To increase the efficiency of photosynthesis, especially at more typical light intensities, organisms utilize additional light-absorbing pigments.

In other words, plants are not entirely photosynthetically efficient and do not typically use all of the light available to them. From Wikipedia:

Photosynthesis increases linearly with light intensity at low intensity, but at higher intensity this is no longer the case (see Photosynthesis-irradiance curve). Above about 10,000 lux or ~100 watts/square meter the rate no longer increases. Thus, most plants can only utilize ~10% of full mid-day sunlight intensity.

Up until a point more light will accelerate plant growth. Beyond that it will stop helping and then become damaging. The optimal level of light to give commercially valuable plants has been studied extensively, and varies substantially between plants.
This concept is formalized in the daily light integral, the number of moles of photons per square meter per day a plant optimally needs, and the photoperiod which is the number of hours per day that light should be distributed over. You can look up values for different plants.


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Source for an upper bound in the number of genes based on mutation rates
So I've found myself referring in an answer once again to the idea that complexity (insofar as it's a quantity for which "number of genes" is a proxy) has an upper bound, limited by Muller's ratchet-related processes. The idea being that if harmful mutations happen faster than natural selection can cull them, the genome will accumulate harmful mutations and the organisms' fitness will degrade over time; and that this imposes an upper bound on the size of a functional genome, because the number of harmful mutations that can happen obviously depends on the size of the functional genome (i.e. how many bases there are where a mutation would likely be harmful).
I knew about Muller's Ratchet, and when referring to it I usually refer to the Wikipedia page for it. But I first came across the concept that this defined an upper bound on complexity (as opposed to being a huge paradox of evolution and a plausible reason for sexual reproduction) in this Less Wrong post (it might have been edited since I first read it).
I've pretty much adopted this concept as a thing that happens; it makes sense to me, and I have seen other references to such an upper bound limited by mutation rates from biologists, for example most recently in this talk by Nick Lane (at 39:15).
However whenever I talk about this in discussions or debates and look for sources I cannot find an easy-to-link source that presents this argument, as seen from within the field of biology. The Wikipedia page on Muller's ratchet only talks about it in the context of asexual reproduction and LessWrong isn't a biology source. The post claims that George Williams makes this argument in his book Adaptation and Natural Selection, and that may also be what Nick Lane is referring to in the video, but a book is hard to refer to online and I would expect such a powerful concept to have more material about it anyway.
Is this concept actually the consensus in the field of biology, or evolutionary biology failing that? Either way, where can I find good, preferably linkable, sources explaining the concept or debating it if it isn't the consensus?

Muller's ratchet is a process that depends upon the population size. What population size are you willing to consider? The question will be a bit hard to address I am afraid but you might want to search the literature for the terms '[mutational meltdown]', 'mutation load' (see this post on the maximum number of babies possible) and 'drift load'.

Btw, please realize that a proxy should be a correlated variable, not a definition. What I mean is that if you don't clearly define complexity, it sounds funny to consider having a proxy for it rather than considering that you define complexity as being the number of genes. Of course many people will not find intuitive to define complexity as the number of genes also that might make some crop botanist happy :)

@Remi.b I know what a proxy is and I used the word correctly. I didn't define "complexity" in my post at all, deliberately so, but the most exact expression of what I meant would be "there are many concepts, some well-defined others vague, associated with the word 'complexity' in biology, a subset of which can be considered a quantity correlated with gene number such that gene number can be used as a proxy for it (whether specifically and vaguely), and when I use the word "complexity" here I am referring to any member of that subset".

To clarify; you are specifically asking for sources that discuss Muller's ratchet in relation to an upper bound for complexity?

@fileunderwater Yes. I hope that is clear enough, if not I would still be happy with whatever you think I meant, if nothing else it would help me know what I need to clarify.

@RozennKeribin No, that is fine. I just wanted to make sure that you weren't asking about the mutational load-aspects of Muller's ratchet, which are more well known and discussed. Finding papers/references that cover those aspects would be easier (but less interesting). You could maybe put the man question closer to the top, since the Q is quite long.


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Covid-19 is a respiratory illness. So how could you catch it by touch?
The U.S. department of agriculture put out a statement in February 2021 in which they wished to underscore that at the time there is no epidemiologic or scientific information that COVID-19 spreads via food or food packaging.
The press release continues to state "that COVID-19 is a respiratory illness that is spread from person to person". Which stuck with me.
Why are touch surfaces even considered potentially contagious when Covid-19 is a respiratory disease contracted by breathing in virus particles?

I do think this sort of question is better posted on SE Medical Sciences than here, as it does not involve any basic biological principle. Anyone answering this sort of question here is unlikely to be a specialist and is more likely to be repeating what they have read recently in the scientific literature. There was an piece on this topic in a recent issue of Nature, which you could try searching for yourself.

https://skeptics.stackexchange.com/a/47225/29579

Transmission through inanimate objects is referred to as "fomite" transmission. It's really hard to know exactly how important fomites are for a particular illness. There is, however, strong evidence that respiratory viruses can spread via this method. Generally, the emphasis is on how contact with hands can lead to infection when someone touches their hand to their mouth, nose, or eyes.
The review by Boone & Gerba, 2007 touches on several issues of fomite transmission. In general, it is easiest to demonstrate evidence of the potential rather than the actual rate of fomite transmission, by looking at viability of viruses on surfaces and how well they transfer to other objects and the hands. However, they also write about epidemiological evidence:

Several epidemiological studies have supported laboratory studies by indicating environmental contamination as a potential vehicle for virus transmission. During an outbreak in a Honolulu nursing home, it was determined that staff hands or fomites (e.g., towels, medical cart items, etc.) spread influenza virus (51). An outbreak of coronavirus (SARS) in a Hong Kong apartment complex may have resulted from fecal-oral transmission combined with environmental contamination (62).

When natural rhinovirus colds were studied, rhinovirus was found on 39% of symptomatic individuals' hands (35). Additionally, volunteers touching contaminated objects and/or the fingers of symptomatic individuals had a higher attack rate of colds if they inoculated their own eyes or nose (35).

They also refer to studies of disinfection/hygiene intervention. The only practical way for these methods to interfere with transmission is by preventing fomite transmission, so if cleaning surfaces and washing hands reduces infections, you can infer that these are contributing routes of infection:

In addition, a review article by Barker et al. cited over 15 research studies that indicated a decrease in viral contamination and viral infection when hand washing was used regularly as an intervention (7). Subsequently, disinfection and hygiene intervention studies, which have cited a reduction in nonspecific illnesses, only support interruption of disease transmission.

I've also attached the reference from that Barker et al paper, which is a simple, informative read.
Barker, J., Stevens, D., & Bloomfield, S. F. (2001). Spread and prevention of some common viral infections in community facilities and domestic homes. Journal of Applied Microbiology, 91(1), 7-21.
Boone, S. A., & Gerba, C. P. (2007). Significance of fomites in the spread of respiratory and enteric viral disease. Applied and environmental microbiology, 73(6), 1687-1696.

In addition to the first answer that was posted, I would point out that, like many other coronaviruses, SARS-COV-2 is also an enteric pathogen, capable of primary infection in various GI tissues. To my knowledge, there's no conclusive evidence that an orally transmitted GI infection can cause severe respiratory symptoms (or even occur in the absence of respiratory infection). But it was something that was worth considering at the start of this pandemic, and is still being investigated as a potential risk for certain medical procedures (like fecal microbiota transplantation).


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Motile egg cells
According to the Wikipedia article on anisogamy, some types of this form of sexual reproduction involve motile egg cells, i.e. they're capable of movement under their own power, just like sperm cells.
Is the "egg cells can be motile" part true? If so, what examples of anisogamous species exhibit this? Because this could have tremendous implications on how to define "male" and "female"; having motile egg cells means that you could have a hypothetical species in which it's the female that "inseminates" the male with her gamete(s), with the sexes being assigned based on which gamete absorbs the other as in oogamous reproduction.

Eggs of Laminaria angustata are flagellated.

No other examples?

This article mentions that rabbit eggs can move quite far: https://academic.oup.com/biolinnean/article/120/1/1/2864987


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Correctly depicting spider anatomy
First off, my specific query: When depicting a spider - be it in a picture or in textual/verbal description - should the chelicerae be always be placed so that they project outwards from the ventral side of the cephalothorax's anteriormost part, like in this diagram? Or are there other possibilities (e.g. attached by their basal undersides to the front of the cephalothorax) that are still anatomically correct?
Second, a more general inquiry: Are there any common pitfalls in depiction of spider anatomy that I should be aware of?


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Cnidarian life cycle, a case of ontogenetic polymorphism?
Cnidarians have a complex life cycle which usually goes as follows:

Egg hatches larva.
Larva settles on sea bottom and transforms into a sessile polyps.
Polyps undergoes strobilation and asexually buds off juvenile, free-swimming medusae.
Medusae eventually mature and reproduce sexually to beget new eggs.

Given the morphological and physiological disparity between the three forms (larva, polyps, medusa), and how each form comprises a distinct stage in the cnidarian's development (i.e. ontogeny), would it be accurate to say that the cnidarian life cycle is an example of "ontogenic polymorphism"?

The question has a feel to me like an invertebrate biology class question, though I have given a brief answer below anyway.

Sure it would.  I would usually use holometabolous insects as an example of this (egg, larva, pupa, adult), but Cnidarians certainly fulfill the basic requirements encapsulated by the phrase "ontogenic polymorphism." It appears that the pressures of finding/establishing food sources and escaping predation in competitive environments has driven both Cnidaria and Insecta toward this evolutionary strategy, though that is a field of active study still (at least in insects).


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Why are plants unable to take up Phosphorus directly in their organic form like Phytic Acid?
I am researching acquisition strategies of phosphorus by decidious trees. I am reading a lot that plants take up nutrients as their inorganic form. In the case of P according to literature this is mainly $H_2PO_4^{-}$ (Schachtmann et al. (1998), Hinsinger (2001), Buchanan (2015)). So far so good...
In forest soils for instance, Phosphorus is much more concentrated in the form of phytic acids (derivates of inositol hexaphosphate), which are organic acids. Not in any paper which I have read before, it is stated why organic P is not taken up directly, only that it is enzymatically cleaved before it is taken up as inorganic P. The best, which I have found so far is that

Although organic P ($P_o$) is present in soil solution at higher concentrations than inorganic phosphate (Ron Vaz et al., 1993; Seeling and Jungk, 1996), direct uptake of ($P_o$) compounds by plants is considered unlikely. --Hayes et al. 2000

My problem - or rather limited understanding - is that I wonder, whether plants in fact do have the ability to take up nutrients directly as organic forms.  I would prefer not to take the presence of enzymes as a proof that organic P cannot be taken up directly by plants. Also phytate seems to be used in plant tissue for storage of P.
Unfortunately my understanding of biochemistry is limited, that's why I'm pretty sure that I am missing some basic facts, which could clarify the situation. My best guess so far is, that organic sources of P are simply too big to pass through the cell wall.
So my question is: are there certain structural or biochemical barriers or obstancles, which would prevent plant roots from absorbing organic P directly, or is it for some reason better to cleave phytates "outside" the cell?
I would be very happy if you could point me in the right direction. Thanks in advance
Sources:
Buchanan, Bob B.; Gruissem, Wilhelm; Jones, Russell L. (Hg.) (2015): Biochemistry & molecular biology of plants. 2. ed. Chichester, Rockville, Md.: Wiley Blackwell; American Society of Plant Biologists.
Hayes, Julie E.; Simpson, Richard J.; Richardson, Alan E. (2000): The growth and phosphorus utilisation of plants in sterile media when supplied with inositol hexaphosphate, glucose 1-phosphate or inorganic phosphate. In: Plant Soil 220 (1/2), S. 165–174. DOI: 10.1023/A:1004782324030.
Hinsinger, Philippe (2001): Bioavailability of soil inorganic P in the rhizosphere as affected by root-induced chemical changes: a review. In: Plant Soil (237), S. 173–195.
Schachtman, Daniel P.; Reid, Robert J.; Ayling, S. M. (1998): Phosphorous Uptake by Plants: From Soil to Cell. In: Plant Physiology (116), S. 447–453.
https://en.wikipedia.org/wiki/Phytic_acid

Welcome to Stack Exchange Biology, and congratulations on a very well constructed first question.

I am not a plant biochemist but would make a couple of points that may or may not be relevant or helpful.

The living organisms that preceded plants had evolved a wide repertoire of systems for transporting ions across membranes, involving variations on a few general designs. Given the importance of inorganic phosphate in living organisms, phosphate transporters would have evolved early on.
Phosphate may have been more abundant in soil before sophisticated evolution of plants led to secondary metabolites like phytic acid. If this were the case it would explain why roots developed phosphate transporters.

This is not to say that it is impossible for organisms to develop transporters for more sophisticated molecules — there are many such examples — but in this case such a development would only be expected if there was such a lack and intense competition for phosphate that it would convey an evolutionary advantage.
This sort of question is always a matter of conjecture. One imagines there is a tipping point when the difficulty of developing a new system is outweighed by the advantage it would bring. This clearly hasn’t happened, but which of these factors is most important is difficult to say (for me, at any rate).

Might be worth pointing out that this is quite the same in animals; even though we might think of the gut as "inside," developmentally and historically the gut is "outside": all the proteins and other macromolecules a human ingests are broken down into consitutent amino acids, simple sugars, etc before they ever get "inside" and much of that work is done by excreted enzymes. Bacteria do this as well.

Thank you for your answer, it did in fact turn me in the right direction. I looked for inositol transport proteins and actually some exist and are located in the plasma membrane. So far I think at least it has not been clarified whether they play a role in inositol-P uptake from the soil. http://www.jbc.org/content/early/2009/09/21/jbc.M109.030247.abstract


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Coronavirus: Why does soap inactivate the virus on skin, but not on surfaces?
In a comment on "Stability of SARS-CoV-2 in different environmental conditions", published today in The Lancet Microbe, it is stated that household soap is highly effective on the skin. Not much further down the same paragraph it is noted that soap cannot be used as a surface disinfectant for SARS-CoV-2.
So why is it so effective on hands, but so ineffective on a sink?

Are you sure that's what the comment actually says?

Can you please cite the paragraph which states that?

In the third paragraph it says, "The virucidal effects of different disinfectants on SARS-CoV-2 were investigated with a number of incubation times (eg, 5, 15, and 30 min), and no infectious virus could be detected in all cases with the exception of a 5-min incubation with hand soap."

My question is meant as "why is soap effective on the hands, but not on surfaces". Perhaps it is due to different modes of application between washing and disinfecting. One involves constant friction, the other just exposure.

Where does it say anything specifically about the effect of disinfectant on SURFACES?

The entire subject of the research, the paper and the comment is the stability of the virus on surfaces in various conditions.


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SARS-COV-2 detectability versus viability
This week (#47 of 2020) two meta-reviews were published in the Lancet.
Ct values and infectivity of SARS-CoV-2 on surfaces, a brief review published on 19 November in The Lancet Infectious Diseases, observed that culturable virus samples are correlated with Ct values of 29·3 (steel surface) or 29·5 (plastic surface), whereas Ct values of 32·5 (steel surface) or 32·7 (plastic surface) correlate with the detection of non-culturable virus.
SARS-CoV-2, SARS-CoV, and MERS-CoV viral load dynamics, duration of viral shedding, and infectiousness: a systematic review and meta-analysis, published on 19 November in The Lancet Microbe, furthers this observation and concludes that by such metrics individuals infected with SARS-CoV-2 are not infectious after day 9.
Does this suggest an upper bound of nine days for viable virus in a standard environment (22°C, 40-60% RH) or may surface conditions be more hospitable than living cells?


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Does thimerosal have some of the same mechanism of action as sodium benzoate?
I noticed that thimerosal's molecular structure is basically just sodium benzoate with an attached chain that includes a mercury atom.
Sodium Benzoate

Thimerosal

The Wikipedia article for thimerosal only mentions the oligodynamic effect (biocidal effect of the mercury).  However it doesn't explain the oligodynamic effect very thoroughly:

The metals react with thiol (-SH) or amine (-NH(1,2,3)) groups of proteins,

I read that sodium benzoate works by being absorbed into microbes and lowering their pH.  Thimerosal is also an anion - can it also be absorbed into microbes and disrupt their pH? Or is it unable to pass through the same channels as sodium benzoate?  If it is absorbed is the pH effect insignificant compared to the oligodynamic effect?


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Cell-autonomous viral defense involving oxidative burst?
I'm looking for a mechanism by which a cell detects a virus (probably a retrovirus) within itself, then triggers an oxidative burst in response. This should all happen within the cell itself, independent of any immune-specific cells outside. Ultimately interested in humans, but any pointers whatsoever would help.

Could you clarify. Do you have any reason to think such a system exists, or is this just a conjecture that such a response would seem to you an effective cellular response?

@David conjecture, based on staring at one of the holes in current theories of aging and asking what would be about the right shape to fill that hole.

Better to do some research into what is actually known, I think. Try intrinsic immunity and respiratory burst. The known examples of oxidative bursts against pathogens occur within specialized organelles in neutraphils, presumably because they would be dangerous in the general cellular environment you envisage.


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Does the harvesting time of broccoli sprouts change their glucoraphanin content and sulforaphane formation capacity?
Does anybody know if the harvesting time affects glucoraphanin content and sulforaphane formation of broccoli sprouts? Do they also get affected by light exposure or lack of it?

Welcome to SE biology. This review looks like it has information on at least the light exposure aspect of your question - it might be worth checking it out https://bit.ly/3gkoqPZ

Thank you for the article. In case, someone else is also interested in this topic, here is the link https://orgprints.org/11395/1/11395.pdf to another study in which researchers compared glucosinolate profiles of different B. oleracea sprouts. To my surprise, the researchers found that red cabbage sprouts contained about twice as must glucoraphanin as broccoli sprouts.