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Why is the GenBank entry for the genomes of RNA viruses like coronavirus written as DNA?
The reference genome in GenBank of the sars coronavirus from Wuhan is written in the following format:
attaaaggtttataccttcc

(The first 20 nucleotides)
Considering that coronaviruses are RNA viruses, the bases of which are adenine, cytosine, guanine and uracil, I was surprised to see the t symbol in the sequence, which stands for thymine, found in DNA, not in RNA. Additionally, no u symbols are present in the sequence.
So, what's going on here? Where did Thymine come from, why no Uracil?

RNA is sequenced by reverse transcribing it to cDNA, and this is the sequence that is submitted. In fact, I don't think I've ever seen a sequence in NCBI specifying uracil instead of thymine (not that I've looked).

Thanks! Some further questions persist. Is this cDNA ever present in nature or is it an artifact of the secuencing procedure? Are there any other differences between ARN and the transcripted cDNA?

Retroviruses naturally have cDNA as part of their life cycle. The mechanism of retrotransposon transposition also involves cDNA.  In this case, it’s just due to the sequencing method.

It would appear that the current policy at GenBank is to represent all genomic sequences as DNA, even though this is not made explicit in any of the easily retrievable documentation on their website or in their publications. The way in which one determines the nature of the genome is from the first (LOCUS) line in the report, which, in the case of SARS-CoV-2 is:
LOCUS       NC_045512              29903 bp ss-RNA     linear   VRL 30-MAR-2020

The ss-RNA indicates a single-stranded RNA genome.
The only indication I could find that this might be GenBank policy was a reference to the fact that a separate RNA division of GenBank used to exist, but was discontinued in 1999:

The RNA division of GenBank was removed in release 113.0 (August 1999). Sequences that were previously in the RNA division have been moved to the appropriate organismal division.

The genomes of certain RNA phages were originally sequenced as RNA (as were bacterial rRNAs and 18S rRNA) — that of phage MS2 was the first in 1976. The GenBank entries for these are currently in DNA format. Thus V00642.1 contains references to the 1976 MS2 paper by Fiers et al., but is in DNA format. As GenBank was not established until 1982 it is not clear whether the original entry in GenBank was in RNA or DNA format.

UPDATE 15.04.2020
I wrote to GenBank to ask them whether there was a specific policy and if so when it had been introduced. I had a reply from someone on their help desk to the effect that GenBank policy was that of International Nucleotide Sequence Database Collaboration, the shared rules of which includes table "7.4.1 Nucleotide base codes (IUPAC)". This states that "t" can represent thymine in DNA and  uracil in RNA. However my respondent could not find out whether this representation was used in GenBank for RNA viruses from the beginning or introduced later. As originally GenBank releases were on CD-ROM this is difficult to check.

It's not GenBank's policy, it is a long standing tradition in molecular biology to express sequences in DNA form.

@TumbiSapichu — unsubstantiated assertions are valueless on SE Biology. If you read my post you will see that RNA sequences were determined before DNA sequence methodology emerged, and that originally they were stored in databases as RNA. I was there and remember it. So much for "traditions in molecular biology"! For ribosomal RNA and tRNA it is still necessary to have databases with the actual bases because many are modified.


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Why don't we bleed interstitial fluid?
Interstitial fluid is the fluid between cells in tissues - forming the medium between cells and capillaries. From what I gather, the typical human has 5L of blood and 11L of interstitial fluid. This raises an interesting question. If I get cut, why do I not bleed interstitial fluid?
When humans are cut, generally their capillaries open and blood comes out. But this should also allow the interstitial fluid to come out - so why don't we see it?

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 particular, I'm almost certain your assumption that interstitial fluid doesn't escape is wrong — I've had (and seen) many injuries where clear fluid leaked out around the wound. ——— 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!

For fluid to flow from a wound there needs to be a significant pressure gradient between where it is now and the outside of the body. Your skin generally does not have a strong compressive effect, which is why a deep cut exposing fat will not lead to the fatty tissue being expulsed from the body any more than the interstitial fluid is.
Blood, however, flows. For it to circulate there needs to be a pressure gradient between where it is now and where it is going. Since veins (including the vena cava, which channels blood back into the heart) do not have vascular walls strong enough to create a suction effect (i.e. lower pressure than the surrounding tissue), you can conclude that the pressure of blood vessels is always higher than that of surrounding tissues, and thus higher than the pressure outside of your body. This is why all blood vessels, including veins, will bleed, whereas less pressurized systems such as interstitial fluid will not.

Or, as my biology teacher used to say: just because the bucket is missing its cover doesn't mean the water will jump out.

I'd argue that in something like a graze, you can see interstitial fluid "bleeding" (it's the clear fluid that forms on the surface. It's just that a) it's not pressurized, and b) mixed with blood, it's totally eclipsed by the heme. You'd have to be under fairly specific circumstances to see it without blood present

Besides the answer by TheChymera, there's also the "problem" that interstitial fluid can't really flow freely.
Blood runs in veins, allowing to quickly circulate through your entire body. And if you cut yourself (and cut one or more veins), there is a direct path for the blood to take.
Interstitial fluid, however, has to creep through all kinds of small openings, not having a free path. Compare driving on the highway (crowded though it might be) and crawling through houses in a crowded city. Sure, if you're an experienced parkour-athlete you can get through. But if everyone wants to get out of a city, getting out over the highway will be the fastest.
By the way, there is one situation where you may "bleed" interstitial fluid: in a blister.
Here, the waterproof (and interstitial-fluid-proof) part of your skin detaches, and the fluid can accumulate. But it will do so only slowly, creeping through some small openings.
And the fact that it comes in slowly is also what makes a blister a problem, as it also means it can't flow back quickly. So if you press on it, it feels like some trapped fluid, even though you could in principle keep on applying pressure and push it back.

This is a very good addition, as it also explains — with respect to the bigger picture — why veins will “bleed” more than capillaries, even though the pressure at that point in the vascular system is lower.

source: Stack Exchange

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How can I classify the 3 clades(S, G, V) of the coronavirus that are found on GISAID?
On GISAID they classified the corona using 4 clades(S, G, V, Other).
I would like to know exactly how these genomes were classified for my research.
So how do you classify a coronavirus genome as belonging to one of the clades.

is there something in your question that is not answered on the GISAID website? e.g. https://www.gisaid.org/references/statements-clarifications/clade-and-lineage-nomenclature-aids-in-genomic-epidemiology-of-active-hcov-19-viruses/#:~:text=Clade%20and%20lineage%20nomenclature%2C%20July%204%2C%202020&text=GISAID%20clades%20are%20augmented%20with,pandemic%20strain%20causing%20COVID%2D19.

*The question is a duplicate of this one.
There are many techniques, all encompassed in what is known as molecular phylogenetics. To get 'clades' or any other groups, you need the sequences of your organism (a virus, in this case, each sample will have its own sequence), and then you need to align these sequences (to match the regions that can be compared, remove 'blanks', 'duplicates', etc). The alignments will differ in some informative positions, and these differences will give you an estimate of how close are some sequences to others, forming groups (or 'clades' in technical terms). So, how do you actually do this? I don't think Stack Exchange is the proper forum for this if you are doing scientific research (I'd recommend you talk to your advisor or a colleague). But if your research is just for curiosity and you need some basic place to start, I'd recommend you to check out MEGA, and this paper. There they explain, step by step, how would you go about this.
And where do you get the sequences? Well, if you are looking at a specific paper they usually give you the 'accession number' of the sequence(s) they are reporting, and if you just want to find your own sequences for your own study, you can search the GeneBank.

Thanks for the answer. I already have the genomes and I already have done many alignments in the past so this is not new for me. What I need to know is how to exactly classify a coronavirus genome as belonging to one of the clades mentioned in the question. I asked a similar question before and got a very appropriate answer. This is the kind of answer i'm looking for(In the link).
https://biology.stackexchange.com/a/90896/57497

If this is for serious research I'm sure you have people who could really help you in your university/department, and not a random stranger in Stack Exchange. However, I noted that the answer you are looking for is already in the top left corner of your image. The criterion the authors of the study used is there in plain sight. Good luck!

The clades have an origin point from which they can see changes in the virus structure to define the clades themselves. The origin point, or reference is the established SARS-CoV-2 reference genome, NC_045512. The clades are mainly named after the mutations that amino acids and proteins have had.
Source: https://www.who.int/bulletin/volumes/98/7/20-253591/en/
They look for different types of mutations and what variants in the SARS-CoV-2 lead to these. Sequences are submitted from across the globe and uploaded to GISAID and analyzed. For example, the S and L variants. There's been a change in the amino acid leucine to serine. So the clade encompasses both but the change to serine (S) defines the clade.
For ORF8-L84S (as seen in picture), the ORF8 gene underwent a mutation of the amino acid L at the 84th position of the gene’s protein to the amino acid S. In other clades, such as G changes aspartic acid at position 614 to glycine. Clade V is labelled NS3-G251V, where the NS3 gene’s glycine at position 251 changed to valine.
So for the naming in general it goes like this:
Clade S - ORF8-L84S
ORF8 (gene undergoing mutation)
L84 (L indicates amino acid leucine at position 84)
S (last letter indicates what it changed into, and defines the clade)
Here's a picture of the SARS-CoV-2 encoding sequence structure and location of common mutations:
Source: https://www.biorxiv.org/content/10.1101/2020.05.03.066266v1.full
The mutations define the clades. You collect the sequences and run a maximum likelihood (ML) phylogenetic. This will show you how the sequences are clustered compared to your reference genome. You can then do a lineage classification software (Pangolin COVID-19
Lineage Assigner).
So for classifying the clades they align the struces with reference genome NC_045512. They look for changes or mutations in the virus and separate them into clades. This might also be done by functional and non-functional mutations but I am not sure if that is included into GISAID.

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Are ligand gated channels saturable?
A major difference between simple diffusion and facilitated diffusion is that facilitated diffusion has a maximum transport and velocity; the rate of diffusion is limited, whereas in simple diffusion, it isn't.
Ligand Gated channels (like any protein 'channel') transports molecules through simple diffusion, so they should not be saturable, but how does that make sense ? The channels open by the binding of a specific ligand/molecule, can't they be saturated by this ligand just like carrier proteins are saturated by the substance/molecule which will pass through ?
If they were in fact saturable, how are they considered to be part of simple diffusion?

Yes, they are saturable, because they have a finite number of 'binding sites', depending on the particular example you are looking at. Then, once they join the substrate to be transported, they need to release it at the other side of the membrane, which takes time (in very short time scales, but time nevertheless). Therefore, the saturation rate and speed of transport depends on the number of transporters on the cell's surface, the gradient differential, and the number of binding sites.
Facilitated diffusion, which needs a transporter as you point out, is a form of passive diffusion, which implies that there is no energy cost to the cell to transport the solute (as opposed to active transport). This is the key difference: energy. It does not mean that it goes as fast as osmosis or any other type of passive diffusion/transport, because, the transport that goes across the membrane (small gas molecules, and other small molecules) will clearly be faster. Also, passive diffusion does not mean that there is no upper limit to diffusion, in fact, diffusion is always limited by the concentration difference of the diffusive molecule across the membrane, no matter if this is passive or active transport.
In short, it is simple/passive diffusion because it does not need energy. Whether is saturable or not is not what matters for this classification. In fact, all diffusion has a limit.

Oh, I was thrown off by the figure in my physiology textbook (Guyton). here's a link to the image :https://imgur.com/a/TMGX9F6 Did I interpret it incorrectly ?


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what are the factors that can be used to compute the probability of getting the coronavirus?
Our team and I work on a project for the Lauzhack 2020 and to achieve this work, we need to determine some factors that can tell us what is the probability of contracting the coronavirus.  Is there any one who know what are the determining factor to compute the probability of catching the virus ? (for example some research paper about it). For example, we know that if we are old, and if we are in contact regularly with people, we are most likely to catch the disease. We would like to have some basic knowledge about the transmission of the virus. We would need data about the probability of being infected as a function of the time we had been in contact with someone who have the disease. Any help would be appreciated !

For example, we know that if we are old, and if we are in contact regularly with people, we are most likely to catch the disease. -- Yes, contact with other people is a risk factor for transmission, but is age?  Sure, older folks are more likely to succumb to the virus, but I think it's important that you parse the concepts of probability of viral transmission and likelihood of symptomatic viral infection.

I'd refer you to a couple of papers in Lancet, here and here. They, in fact, have a mathematical treatment of this very question, and in the supplementary material they list some parameters that might be useful to you. Good luck!

hello and thank you ! where can a find these lists  in the paper ?

In the supplementary information of the second reference (a PDF file you'll find at the end of the paper) you'll find a table with the parameters they used.


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Is there in vivo evidence of Amyloid beta toxicity?
Amyloid beta is thought to be toxic, however from a brief search, this is based on (1) in vitro (2) measurements of some proxies of toxicity (e.g. Ultrasensitive Measurement of Ca2+ Influx into Lipid Vesicles Induced by Protein Aggregates referenced in Wikipedia).
My impression is that we do not have any high-quality evidence that amyloid beta is toxic in vivo and that there is significant circumstantial evidence against it being toxic (links below). Is this correct?

"30% of elderly people have #Alzheimers pathology (plaques &/or tangles) but no disease"
There's an elderly woman with large amounts of amyloid plaques but no symptoms of Alzheimer's
According to Derek Lowe "all of those amyloid-antibody trials have ended in grievous, expensive failures"

From a quick search, it seems that there is plenty of solid evidence for in vivo toxic effects. A couple of papers here and here.

An answer is expected to stand for itself with references being useful for further reading. Your "answer" is basically one sentence containing three links. Please edit it to avoid its deletion. This also applies to some of the other answers you wrote recently.

You can delete them if you want! ;)

@TumbiSapichu - we'd rather not delete them, and we appreciate your efforts. However, posts as this are below our standard and not conform our guidelines. If you don't improve these posts we will have to delete them.

@TumbiSapichu The aim is not to delete postings - which the mods could easily do - but to improve the quality. If this doesn't happen, it might be the last resort.


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Do biologists use the word "solubilize" to mean "dissolve"?
I work with biologists who often use the word "solubilize" to mean "dissolve".
Is this correct usage? I keep correcting them (I'm not a biologist, but I help with writing), and we've argued about it. Not all are native English speakers, so I've been attributing it to that. But maybe they're right. I want to know.
The context here is pharmacology - taking drugs in powder form and dissolving them in a vehicle for dosing lab animals.
I thought "solubilize" means to make something more soluble by adding (for example) soap. (for example: https://www.thefreedictionary.com/solubilisation ).
But they use "solubilize" to mean "dissolve". That usage doesn't seem to be standard English, but maybe it's normal usage as a term of art in pharmacology.
Is it?
For scientific writing in pharmacology, what is the standard usage? When we mean (standard English) "dissolve", which word should we be using, in order to be clearly understood and conform with standard professional terminology?

Added: Some of the commenters seem to misunderstand what I'm trying to ask, so I'll try to clarify.
I can read dictionaries as well as you can, and Google is my friend, too; I'm not asking what the standard dictionary definitions are (I already know).
I'm asking about how working biologists, English-speakers, use these words.
Do practicing biologists/pharmacologists use these terms differently than the standard English definitions? Are these "terms of art" in those fields, with a different definition? Or not?
Some of my colleagues insist that, in their field of biology/pharmacology, the word "solubilize" is used to mean what the dictionary says "dissolve" means. Are they correct, or are they mistaken (presumably because they're not native English speakers)?
I'm not a biologist and so don't know from personal experience. The people I work with are biologists but not native English speakers, so I'm not convinced they know either.
Thus, I'm asking here.

I've been asked for a sample sentence re how it's used. I don't see how that affects the answer, but here:
"Diphtheria toxin (List Biological Laboratories, Cat #150) was solubilized in sterile water at 2 mg/mL, aliquoted, and frozen at -20 C."
Is this correct usage or would "dissolved in sterile water" be better?

I think you'd need a more concrete example than "I work with biologists" for anyone to judge this.

@David I'm not trying to be critical - I just want to know how the word is used by biologists, so I can use the word in our writing that will be understood best.

@BryanKrause This is mainly in the context of dosing drugs. We start usually with a compound in powder form, then stir/heat/sonicate/mix various other things (vehicles) to produce a dosing solution. Not being a biologist, I'd call that "dissolving". We write a report about what we did - should I call that "dissolving" the drug, or "solubulizing" it? I'm not trying to be a language Nazi; I just want to be understood clearly.

@nerdfever.com so you could say that you are making things more soluble by stirring/heating/sonicating them? Why would a chemical treatment (soap) differ from a physical one (heating)?

@MaximilianPress I don't know - the soap reference was something I found in a dictionary. I'm asking about how working biologists use these words. I'm not a biologist and I don't know; the people I work with are not native English speakers, so I don't trust what they think about it.

If you take Maximilian’s question to be rhetorical, it’s worth considering. It sounds like, in your context, both terms could be appropriate.

Sometimes 'solubilize' is a more precise description of a process, even though 'dissolve' would technically be correct. For example, I write a protocol where a user must solubilize a compound in ethanol before adding it to a growth medium. I could correctly say 'dissolve' instead of 'solubilize' here, but 'solubilize' provides a more complete description of the process by giving a context clue as to why it's dissolved in ethanol first. There are also situations where only one of those words is correct. Siderophores solubilize ferric iron, but don't dissolve it.

I think I found an answer at Science Direct where multiple definitions are provided, among one from Thomson (2012):

Solubilization is the action of certain chemical reagents on organic materials (such as animal or plant tissue) that effects a structural breakdown (or digestion) into a liquid form that can then be directly dissolved [...]

and from Lau (2011):

Solubilization is the increase in solubility of a poorly water–soluble substance with surface-active agents. The mechanism involves entrapment (adsorbed or dissolved) of molecules in micelles and the tendency of surfactants to form colloidal aggregations at critical micelle concentration levels.

From these definitions I understand that solubilization is a process to make something dissolvable. The process of dissolving thus happens after the solubilization (definition #1) or during the process of solubilization process (definition #2). Thus, solubilization and dissolving are separate processes (definition #1) or dissolving is considered a part of the process of solubilization (definition #2).
So admittedly, at this stage I am unsure to what exactly the two terms mean exactly, but they are certainly not interchangeable terms.
And regarding your comment

...that it's not unusual for experienced biologists themselves to be unsure which is the proper term here. Even native English speakers

I totally second Bryan's response

Language is messy, scientific terminology included...

This is because terminology tends to stick after having been adopted widely, even if it proves to be incorrect. Consider for instance the fact that current always flows from + to - in schematics, but that electrons definiely choose to go the other way around. Scientific terminology is messy indeed.
References
- Lau, Preformulation Studies. In: Handbook of Modern Pharmaceutical Analysis: 173-233
- Thomson, Handbook of Radioactivity Analysis (3rd ed.) 2012: 575-623

Thanks, but I can read dictionaries, too. That's why I've argued over this with my colleagues. I'm looking for answers from experienced biologists who know how the terms are, in practice, used in the field.

@nerdfever.com Pretty sure AliceD is in fact an experienced biologist. I would consider myself one as well, and this answer is probably as close as you are going to get to an "official definition". At the same time, I guarantee you this term, like many others, may not be used strictly. Language is messy, scientific terminology included. So, getting back to my old comment (which I didn't really explain), you need better context for the description you give for anyone to judge the "correctness", but I highly doubt anyone would confuse the meaning in context.

@BryanKrause Thanks. I'm interpreting that to mean that it's not unusual for experienced biologists themselves to be unsure which is the proper term here. Even native English speakers.

@nerdfever.com It's hard to even argue what the proper term is when you haven't given an example; you say your colleagues use "solubilize" to mean "dissolve" but it seems just as likely to me that they mean "solubilize" and you think they mean "dissolve". AliceD has explained they aren't quite interchangeable yet their meanings are a bit intertwined.

@BryanKrause I did try to clarify the question. It now includes "taking drugs in powder form and dissolving them in a vehicle for dosing lab animals." What other context would be helpful?

@nerdfever.com An entire sentence where the term is used would be helpful. I can't see how that would be difficult to provide, but if for some reason it is, maybe at least a specific drug and a specific vehicle, so you can construct your own sentence "we solubilize (specific drug A) in (specific vehicle X.Y mM Z in PQRS)"

@BryanKrause I don't see how the specific drug and vehicle affect the answer, but I've added an example sentence to the end of the answer. My colleagues and I have debated this - I think "dissolved in" is more appropriate here, but others disagree. Does this make things clearer?


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How likely is to develop an infection from a single virion entering a single cell?
Is there any research (including mathematical or computational modelling) regarding how likely it is to infect an organism starting from a single virion entering a single cell?
I am interested in any virus and any multicellular organism (including immunocompromised).

This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology! I'm glad we encourage such questions from curious people who want to learn more.

This is called the Independent Action Hypothesis, described here:

The Independent Action Hypothesis (IAH) states that pathogenic individuals (cells, spores, virus particles etc.) behave independently of each other, so that each has an independent probability of causing systemic infection or death.

Zwart et al. (2009) tests this theory, and their results support the hypothesis that a single virus particle can infect a cell:

The ‘independent action hypothesis’ (IAH) states that each pathogen individual has a non-zero probability of causing host death and that pathogen individuals act independently. IAH has not been rigorously tested. In this paper, we (i) develop a probabilistic framework for testing IAH and (ii) demonstrate that, in two out of the six virus–insect pathosystems tested, IAH is supported by the data.

The modeling done in this paper may be worth reviewing.

See also this paper showing that for influenza in two pigs cages with one contagious it is usually two PFU that caused the infection is the second one, where in a PFU all the virions have (almost) the same genome. The other question is once a viable virus entered the correct cell, what is the probability that it succeeds in finding the right organelles membranes and achieving its replication. The answer is mainly how to translate PFU/ml into number of viruses/ml.


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Osmosis and hydrostatic pressure
I'm confused about the role of hydrostatic pressure compared to osmotic pressure.
Q1:If I have a U-tube with a membrane permeable only to water molecules and equal volumes of water on either side but only 1 side (side B) has NaCl, the osmotic pressure would cause water to move from side A to side B,correct ?
Q2.But then hydrostatic pressure would cause water to move back to side A.
So, the water would move from side A to side B until the effect caused by the hydrostatic pressure = effect caused by osmotic pressure ?
Q3. The last statement wouldn't be correct If I said that "water moves until the hydrostatic pressure=osmotic pressure" would it ?
and lastly, My friend said the water would move until the hydrostatic pressure on both sides was equal
Q4. If water is moving from side A to side B then the we have more water molecules at side B, how would side A ever reach the hydrostatic pressure at side B ?
Do I have a misunderstanding in the concept of hydrostatic pressure ? In this context, I understand that it is the pressure exerted by the water molecules on the selectively permeable membrane.
The more I google hydrostatic pressure the more lost I get because all sources seem to explain in terms of equations and physics and I'm only taking this for an introductory course in physiology.

Do the answers at https://biology.stackexchange.com/questions/89609/osmotic-pressure help you?

I understand everything thats written in that page, I think of osmotic pressure  as a vacuum too but I might have a misunderstanding in hydrostatic pressure and what equals what at equilibrium


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Does an FAD:FADH2 ratio exist in the cytoplasm? (similar to NAD+:NADH ratio?)
I have learned about a lot of enzymes/proteins which are covalently bound to FAD, and use this as an oxidising agent. In vivo, FAD is (almost) always protein bound (very low concentrations of free FMN/FAD [source]). Would an "FAD:FADH2 ratio" make sense (if it isn't free)? I know that the NAD+:NADH ratios in the mitochondria and in the cytoplasm are important, same for NADP+:NADPH (e.g. low NADP+:NADPH ratio in cytoplasm makes the reducing environment for fatty acid synthesis). Is it the same for FAD?


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What makes the cytoplasm a reducing environment?
It is known that the cytoplasm is a "reducing" environment, where disulfide bonds cannot form (will soon be reduced to 2 cysteines) [I'm not putting a link as this is a fact in many biology textbooks].
The NAD+:NADH ratio is high in the cytoplasm (around 1000 (725 in this paper)), which should make the cytoplasm an oxidising environment. The NADP+:NADPH ratio is low, making a reducing environment. Also, there is Glutatione Reductase, which should also make the cytoplasm a reducing environment. Which one of these is the underlying cause of this reducing environment? Or is FAD also involved in this?
As an additional question, what does reduce disulfide bonds? Is it using the NADPH or the FADH2 or the glutathione reductase?

The redox buffer in the cytosol is glutathione (reduced GSH and oxidized GSSG), which is present in large amounts (López-Mirabal & Winther 2008 , doi: 10.1016/j.bbamcr.2007.10.013).
Proteins with disulfide bonds are often secreted, since the disulfide bond ensures proper structure outside of the cell. These proteins are imported into the endoplasmatic reticule (ER) that contains enzymes (e.g. PDI) and an oxidative milieu for disulfide bond formation. Thioredoxin breaks down disulfide bonds in the cytosol and is regenerated by TrxR, which in turn is regenerated by NADPH (Bulleid 2012, doi: 10.1101/cshperspect.a013219)


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What relation do glycerol-3-P DH and acyl-CoA DH have with Complex II of the ETC?
I am sorry if this may be a purely definitional/nomenclature question.
Complex II of the electron transport chain (ETC) would be succinate dehydrogenase, transporting electrons to ubiquinone (and forming ubiquinol with the addition of 2 protons).
Both glycerol-3-phosphate dehydrogenase (DH) and acyl CoA DH are integrated in the inner mitochondrial membrane, and form an ubiquinol, which can be used by Complex III of the ETC - very similarly to succinate DH. I was wondering why, then, these 2 enzymes weren't also part of "Complex II" or whether they were just not part of an "ETC complex" because they aren't part of the TCA cycle, or something? Are they in any way also related to the ETC supercomplex/respirasome?
Thank you.


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why does translation occur more frequently than transcription?
In our textbook it says that translation occurs more in a cell than transcription but I couldn't find anything that explains why it happens

Suppose you had a book that said how to make a candle mold, and you wanted some candles.  Would you make molds from the instructions as often as you would make candles from the molds?

The simple answer
Under the assumption that each mRNA molecule is translated at least once, by necessity translation will happen more often than transcription. This is because the only way to get a protein is to translate an mRNA.
In other words, as long as there are more protein molecules (translation products) than mRNA molecules in a cell, then the process of translation must have occurred more than transcription.
One estimate of the ratio of protein molecules to mRNA molecules given here is on the order of 100-1000 for E. coli. ("Under exponential growth at medium growth rate E. coli is known to contain about 3 million proteins and 3000 mRNA (BNID 100088, 100064). These constants imply that the protein to mRNA ratio is ≈1000, in line with the estimate given above. [MP note: the numbers quoted are actually closer to ~400K and ~1.4K, so this is not completely accurate; the source paper itself estimates between $10^2-10^4$ for the same ratio of protein to mRNA. Note though that the yeast cell estimates are even higher.]) So there are likely between 100 and 10,000 times as many translation as transcription events.
The speculative answer
From the perspective of "why" this is the case in terms of why cells might "choose" to have this ratio of proteins to mRNA (accepting that it must be true based on the ratio of protein to mRNA), we might say that proteins are useful and mRNA is not. Therefore, it's better to have more proteins (implied but not stated by @mgkrebbs comment). Or rather, mRNA is only useful because it gets you proteins, which are useful.
So it "makes sense" for cells to minimize the amount of energy put into generating mRNA and maximize energy put into making proteins. But that's human logic projected onto the cell, we can't know that that is the logic for why cells do what they do (or evolved to do, or whatever).

I accept that a comment is not an answer, but I would have left the poster to work things out for herself, given that she has not even finished reading the Tour.  I find your contorted additional stuff about usefulness and energy unhelpful. It’s your logic, not “ours”. And please don’t talk about logic in relation to cells. The best way to express this is “why this happens” or “why it has developed in this manner”.

@David thanks for your input.

Your answer and link is unclear. See the original article supplementary materials : a way to estimate the ratio is to synthesize DNA encoding for yellow fluorescent protein, electroporation into bacterias, synthesize many small fluorescent probes complementary to a piece of the mRNA for the YFB, add to the culture with RNase inhibitor, 9h later select some cells expressing YFP and observe to estimate how many mRNA there are and how many YFP have been synthesized.

Hi @reuns, thanks fo checking. I looked into it and edited the answer to reflect more closely what the bionumbers actually are and to add more context.

Albert Lehninger had no problem in speaking about the 'molecular logic of living organisms' or about the 'molecular logic of the living state' (Biochemistry, 2nd Edn)

@user338907 i think this kind of language is fine as long as everyone is very clear that that logic is post hoc imposed by humans onto the cell, which is what i think i was trying to do here. cells don't reason. i feel the same way about "logic circuits" and similar models for cellular behavior- it's fine as long as you know it's just our model of what's going on, it isn't literally true.

the problem with this answer is there are many forms of RNA besides mRNA. Ribozymes, tRNA, rRNA, ect, also have to be transcribed, but don't get translated.

@John- you are correct. I will have to think about addressing that, but in particular for rRNA it is an issue, as that is most RNA in the cell.

Short answer: multiple Ribosomes can stack on the same mRNA making multiple proteins on a single mRNA strand before it gets recycled. A single mRNA strand may be translated dozens of times or more.

source
source
source

It would be very wasteful (and hence evolutionary unfavorable) for cells to have the process other way round (more mRNA than protein). Remember it takes a lot of energy to synthesize mRNA, so it must be used as efficiently as possible (make many protein copies from a single mRNA).

I fail to see that your answer adds anything to that from @MaximilianPress except most dubious and unnecessary remarks about energy utilization and efficiency. If your argument is correct, eukaryotic introns in pre-mRNA are a waste of energy. Let it rest with the obvious. The comment about candle moulds should have been enough for the poster and anyone else.


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Is anything known about the speed with which viruses spread geographically in R. affinis (or at least bats in general)?
RaTG13, which is the closest known relative of SARS-CoV-2 at full genome level, was sampled (just) in a R. affinis (bat) specimen in Yunnan Province... which is about 1,500 km away from Hubei, the epicenter of the first Covid-19 cluster.
So, what if anything is known about the speed with which viruses spread geographically among bats, particularly R. affinis? Basically, do we have any idea how long it would take a virus to "travel" in (R. affinis) bat populations 1,500 km?
A paper still in draft estimates that the most recent common ancestor of SARS-CoV-2 and RaTG13 "lived" around 2009.

the inferred the time to the most recent common ancestor in the recombinant region of the clade leading to RaTG13 and SARS-CoV-2 is no later than 2009 (2003-2013, 95% HPD limit).

I'm trying to figure out if this time frame is compatible in some sense with the speed with which viruses are known to spread in bat populations.

You can make SIR model acquire the diffusion equation characteristics by adding the spatial variables. That will give you the spatial diffusion (spread) speed.

Look at the sarbecovirus phylogeny and add the precise locations and years. @Hans we don't have any model for how the different bat caves/species exchange viral strains from years to years, we need to built it directly from the sparse data..


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Can muscles remake pyruvate from lactic acid, or does it have to go to the liver in the Cori cycle?
When the muscle is exercising, and only anaerobic respiration is done, pyruvate -> lactate to regenerate NAD+. Lactate is then transported out of the muscle and into the liver, to regenerate glucose, which is then shuttled back to the muscle (the Cori cycle).
I was wondering whether once the muscle stops exercising, the muscle itself could regenerate pyruvate (using lactate dehydrogenase), or whether muscles always release their lactic acid to the liver? Or maybe there is no way of knowing this (how would this be tested experimentally...).

What would you envisage the skeletal muscle doing with the pyruvate, assuming that the liver had not cleared the lactic acid?

Once there is enough oxygen, I would think that the pyruvate could be used for oxidative phosphorylation.

But the whole point is that the muscles that are used for exercise need an energy source primarily under anaerobic conditions, and have few mitochondria. There is no way of storing pyruvate and in very light aerobic exercise other substrates for mitochondria available.

Oh okay thank you. Would it be possible for you to explain or attach a link about these myocytes with few mitochondria? I always believed muscles had a lot of mitochondria.. Also, would the other substrates for mitochondria in aerobic exercise (which you mentioned) be fatty acids? Thank you very much for clarifying.

I never was a card carrying metabolism man, but I always understood that you could tell a muscle’s metabolism by its colour: red muscle has a good blood supply for oxidative metabolism — hence it would have the requisite complement of mitochondria; white muscle would be mainly anaerobic. Muscles working continuously, like heart and the flight muscle of migratory birds, would need to be capable of aerobic metabolism. And yes, fatty acids can be used by heart muscle, sparing glucose for tissues like the brain. (All directed by the liver.)


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How does exercising/starved muscle import glucose (released by liver)?
Adrenaline releases glucose from the liver during sport or if starved. This glucose goes to the blood through GLUT2 transporter. But how does it get transported into the muscle cells? GLUT4 is the glucose transporter into muscles, but it is activated (translocation to plasma membrane) by insulin, but when exercising/starved, there is no insulin. So is the glucose transported through some other transporter?

GLUT4 is the major glucose transporter in muscle even in exercise. However, during exercise, it is translocated to the cell surface by contraction-triggered, insulin-independent mechanisms, such as AMP-activated protein kinase (AMPK) activation.
For more, you could read this review.
Note:
'No insulin' is too strong a phrase; exercise and fasting are associated with low but detectable insulin levels. The reference range for fasting insulin in healthy individuals is $<174 \ \text{pmol L}^{-1}$ (contrast this with levels upto $1917 \ \text{pmol L}^{-1}$ one hour after glucose ingestion). Exercise studies have shown levels around $60-80 \ \text{pmol L}^{-1}$.

A nice concise answer, and a most useful reference. However you might comment on the poster’s statement that “there is no insulin”. The concentration of insulin may be decreased, but surely not to zero. Do you know any figures?

@David I edited the answer.

A valuable contribution to the site. Hope to see more posts from you.


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Trees growing around objects vs pushing them away. Where is the threshold?
If a tree grows against a taut wire then the tree will grow around it, eventually enveloping the entire wire. This often scars the tree, and if the wire is thick enough, it will interrupt nutrient flow and cause more significant damage.
But if the tree grows against a larger obstacle, such as a wide board, the tree displaces the obstacle as it grows.
As a real-life example of this, I have a large pine tree on my property next to an old wooden building. The tree, as it grew, pushed hard enough against the building's eaves to bend a 2x4 piece of lumber five inches out of the way. When that 2x4 finally met the rest of the building, the tree could no longer move the board and started growing around it.
Where is this threshold? I assume it can be described as a simple pressure (force over area), and that it is dependent on the specific type of tree. Is this tabulated somewhere?
Specifically, I wish to hang a 40lb (18kg) weight, permanently, from a branch of an ~80ft (~25m) lodgepole pine. I intend to use some sort of wider material in between the cord and the branch. It would be great if I could simply run the cord through a larger-diameter pipe and position this pipe over the top of the branch. But if this wouldn't be sufficient then I'll use boards (or similar) to distribute the weight. I won't be constricting the entire circumference of the branch.
I know that mounting a bolt into the tree would be better, but that isn't an option for me in this case.
I don't want to do this: (!)
image source

I'd have checked a forestry forum for experience there.

@com.prehensible Yeah, I also considered the gardening stack. But I'm more interested in the science behind it :)

No matter what it is is it is solidly mounted to the tree or against the tree, it will try to grow around it. your best bet is to drill into the tree and use a stainless steel bolt or screw. Just don't mount it flush and don't use anything that can corrode. wire tends to cut off a large section, it is essentially partial girdling. but a screw disturbs very little of the living portion of the plant.

Thanks, @John, the bolt is a good idea. Unfortunately I can't use one in this case. I've modified my question a bit.

its not hard to imagine that every tree has its own unique behavior...

Since you asked for the science I'll try to give a scientific but simple explanation.
Trees (and plants) become wider and taller over time. This growth is due to cell division and cell elongation from meristematic cells (analog to stem cells in animals).
The stem (upper part of a plant) becomes wider because is it constantly creating new vascular tissue from the cambium. The cambium creates xylem to the center of the tree and phloem to the outer parts. The bark that peels off is the phloem and other tissues irrelevant for the explanation. Here you can find a good illustration.
Since the tree adds new xylem all the time the, cambium gets further away from the center of the tree.
When the tree pushes against a wire, the wire cuts and kills the phloem cells and after that the cambium cells. But the plant has mechanism to regenerate the cambium ring and that's why the tree continues to grow there. In the photo the wire is already in the xylem section.
When the tree pushes against a wall there is a barrier in the whole section. Either the wall collapses (or, more commonly seen, the sidewalk rises) or growth in that sections stops.
I saw graphs of cells having up to 3MPa of turgur pressure but the actual pressure you should check is that of the bark which can be higher or lower. It changes between plants species, sections of plants and plants itself so the best is to simply check.
I wouldn't hang a weight from a tall tree. Trees get diseases and many times you only see that they are rotten from the inside when it is too late.


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Why do some viruses cease being a problem even though no vaccine or cure is found?
No vaccine or cure has been found for SARS-CoV or MERS-CoV yet the world is not too concerned about them. How can it be? Did all people who had those viruses die or do viruses just randomly decide to stop being infectious at some point?

Infections spread in a population when the number of new infections caused by an infected person is greater than or equal to 1.
If each infected person spreads the virus to less than 1 person, eventually no one will be infected, without a need for any sort of cure. Of course, the longer a deadly infectious disease spreads in a population, the more people will die during this process. Ideally you want to get the number of transmissions as close to zero as possible as quickly as possible.
SARS and MERS are each a bit different, but share some similar characteristics. Compared to COVID-19 caused by SARS-CoV-2, both are more severe in a larger fraction of the people infected (note: all three viruses are closely related betacoronaviruses). This made it easier for public health officials to identify and isolate infected individuals.
The MERS virus is really not gone at all: it lives on in animal reservoirs, like camels (so it is primarily only a concern in places where those reservoirs live). Cases continue to occur sporadically. However, MERS is usually not that transmissible between people, having a natural transmission rate that is already less than 1: that means that most people who get it get it directly from an animal, and don't continue to spread it to others besides occasional infection of individuals with close-contact, like a family member. There have been exceptions where isolated incidents involved substantial human-to-human transmission. Some of these incidents were associated with "super-spreaders": particular individuals who got infected and spread the virus to way more people than the average. See https://wwwnc.cdc.gov/eid/article/26/2/19-0697_article for more.
SARS caused by the original SARS-CoV virus indeed seems to be gone, with no cases reported since 2004. The elimination of SARS from the human population occurred via controlling the human-to-human spread through isolation and contact tracing. See https://apps.who.int/iris/handle/10665/70863 for a report on the epidemic and how cases and spread in different locations were handled.
Viruses don't have any agency: they can't decide to do anything. However, humans can, and our best response to outbreaks of novel diseases is to trace the spread and try to limit transmission as much as possible.

Good answer. It at first puzzled me how a disease with R0<1 could spread in the first place, since on average, the case count won't be continuously increasing. But that's just an average, it's still possible for patient zero to spread it to several other people, some of whom will then spread it again, with the final result being an outbreak, but one that has a quickly and naturally decreasing case count. It's the super-spreader events you mention that cause sporadic (but not ongoing) problems, and those are by definition rare given the low R0 of those diseases.

@NuclearWang Yeah, it's particularly interesting that mutations don't seem to be a factor in the different rates of spread among MERS cases. Well, at least not mutations in the virus. Instead, it's particular people that just dump a lot of virus to the environment they share with other people, especially when they are sick and in a healthcare setting. The CDC report I linked has more on this.

To belabor the obvious, if you get a disease from camels, it's not going to be a problem for people who never come into contact with camels.  It's basically the same reason why many tropical diseases aren't a major problem outside the tropics: they have vectors (usually insects) that don't tolerate cold.

Are we sure that viruses have no agency?

@personjerry Yes.

@personjerry viruses have as much of an agenda as rocks, or grass. They don't live, they are the biological equivalent of snippets of computer code. Those snippets that happen to be packaged in a way that they get injected, and that also happen to cause the cell to create more replicas, those are what we call a "virus"; snippets without these properties exist but we don't even notice them, let alone give them a name.

Nice answer! I wonder about one thing: as SARS and MERS are both more severe in a larger fraction of the people infected, could SARS-CoV-2 (going through it or being vaccinated) pandemic positively impact our resistance to these two?

Bryan Krause's answer addresses the reasons pertinent to SARS and MERS. If you meant those two as examples but are interested in the title question more generally, I can note an additional mechanism. This is herd immunity, which fits the bill in that it can occur when "no vaccine or cure is found" and when it is neither the case that "all people who had those viruses die" nor "viruses just randomly decide to stop being infectious". After a significant fraction of the population has been infected and recovered, herd immunity can bring a virus with $R_0 > 1$ to an effective rate $R < 1$ if those that are recovered are immune to reinfection and this immunity lasts for long enough.

And considering the title more broadly,
We learn to live with them, manage the infections, and consider a significant death toll or other related injuries as "normal".
For example, a measles vaccine was only developed in the 1960s. Before that, it was just known as one of the diseases children would usually get when they were young, because the virus was endemic in the population. On average, 2.6 million people a year died of measles globally, and that was just expected. (For comparison, that's now down to 122,000 by the way, and most of them are in extremely poor countries who either can't afford the vaccine or can't reach clinics.)
For an alternative case, the rate of congenital disabilities or birth defects in children was simply accepted as what it was - something which just happened without any cause. It was not until 1941 that the connection was made to rubella (German measles) causing up to two-thirds of all birth defects. Before that point, we didn't know that this wasn't "normal".
And currently of course we still have no solid vaccine for flu. The vaccines we do have are relatively effective and certainly do reduce the impact, but they are not effective to the same extent as, say, the MMR vaccines. As a result, we still have thousands of people dying of flu every year, and currently that is "normal". Maybe one day we'll crack it, but until then we'll just expect people to continue catching it, doctors and hospitals to continue treating it, and some people to die from it.

One more effect: a pathogen that is both deadly and highly contagious either triggers strong response (when we talk about humans, human pets, cattle, etc) or simply wipes out the population it infects (and disappears with it).
This creates a strong selection pressure over the pathogen. In order to successfully spread, it either becomes less deadly, or less contagious, or both. The generations of the pathogens change quickly and mutation rate is usually high, so the pathogen (given time and groups of hosts to infect) will react to the selection pressure.
The groups, once survived the less-deadly version of the pathogen are at advantage - they are most probably immune also to the original. The pathogen is also at advantage - it gets less organizational reaction (quarantines, vaccines, etc) and more hosts to infect (because survived hosts reproduce and the new hosts are not immune).
p.s. a second-order of the same effect is the pathogen becoming less dangerous only to minors of the host. We all know a lot of examples.


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Why is a penis an organ?
According to Wikipedia an "An organ is a group of tissues with similar functions". I don't know anything about anatomy but it doesn't seem to me that a penis can be delimited somewhere to form a "group". Therefore  I do not understand why a penis is considered an organ.
Can you explain it to me ?

Organic = carbon based, thus teeth = organic

I though theeth were mineral

Frankly, that's a terrible definition by Wikipedia.
Merriam-Webster defines an organ as:

a differentiated structure (such as a heart, kidney, leaf, or stem) consisting of cells and tissues and performing some specific function in an organism

or

bodily parts performing a function or cooperating in an activity

The important defining feature of an organ is not that the tissues have similar functions but that, together, the tissues comprise a functional whole that achieves some end goal.
For the penis, it consists of multiple tissues with different functions:

(from https://www.ncbi.nlm.nih.gov/books/NBK525966/figure/article-20668.image.f1/ - original from Gray's Anatomy)
The different tissues pictured here: the fibrous envelope, the corpora cavernosa, the septum pectiniforme, the urethra and blood vessels, the nervous tissue in the skin: all of these tissues have different individual functions: structural, erectile, carrying urine or semen, etc.
The key that unifies them into an organ is that the functions of the penis at the organism level (principally sexual function) are not served by any of these tissues alone, but rather by their combination in a full structure: an organ.
Ultimately, organ definitions are somewhat opinion-based: people are lumpers and splitters, so you might find conflicting definitions for which groupings of tissues reflect distinct organs, but I think by most standards you would find the penis to be considered a distinct organ, affiliated with but distinct from the primary sex organs and associated glands.


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Electrical transmission vs Chemical transmission
"The advantage of electrical transmission, apart from speed, is it can favour synchrony in firing. For example, in the brain stem a nucleus called the inferior olive can generate oscillations due to gap junctions."
Can somebody explain this idea? I do not understand the meaning of oscillations in this context. Do they mean that the neuron can send impulses and receive them at the same rate ? Is that what they're trying to put across ?
Source:Lecture Handouts

Please include a reference when you quote from a source; failing to do so is plagiarism.

Its from my lecture handouts


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What is a neuronal loop?
Stanford Medicine's OCD page says that

Many investigators have contributed to the hypothesis that OCD involves dysfunction in a neuronal loop running from the orbital frontal cortex to the cingulate gyrus, striatum (cuadate nucleus and putamen), globus pallidus, thalamus and back to the frontal cortex.

What is a neuronal loop? I have looked it up on DuckDuckGo with no usable results.

The answer is right in the second half of the sentence:

running from the orbital frontal cortex to the cingulate gyrus, striatum (cuadate nucleus and putamen), globus pallidus, thalamus and back to the frontal cortex

Orbital frontal cortex, cingulate gyrus, striatum, globus pallidus, thalamus, and back to (orbital) frontal cortex: these are all different brain regions. If A connects to B, B connects to C, C connects to D, D connects to E, and E connects back to A, you've made a loop.
The page is saying that there is a hypothesis that there is dysfunction somewhere along this loop in OCD; it doesn't say where exactly, but you can infer that changing something along this path would affect all of the other regions connected in the loop in some way, because they are all causally related to one another.

@ds_secret I rejected your suggested edit because the source does not use the word "cause" with respect to this pathway. It may be implied, but I'm not going to put words in their mouth: they are likely using this language intentionally because they have mostly correlational evidence for the relationship rather than causal evidence. Causality is very difficult to show in psychology/psychiatry.

The website states "In the section below, we have outlined a more detailed description of the various theories and hypotheses involved in the biological basis of OCD."

@ds_secret "The biological basis" is not the same as "cause". They are very closely related, may sometimes be treated as "cause", and it's okay if you want to provisionally treat it as evidence for "cause", but I'm not going to use that word.


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Which is more evolved Rays or Sharks
I know the Theory of evolution explains that life transforms to become more complicated, sophisticated so that it's more equiped for survival, Just like the survival of the fittest, the fittest are the evolved and always survive
I learnt that rays evolved from sharks, but I see sharks eating rays in documentarys, Infact rays are afraid of sharks, they are nothing compared to killer sharks
I also learnt that by skeleton comparison chicken evolved from dinosaur, but dinosaur are like gods to chicken
If man evolved from animals, we've become wiser and they've become pets
What really is evolution speaking, evolved animals do they become stronger than their competitor or weaker?
From unicellular organism to complex organisms, is the pattern of evolution going forward or backward or no pattern
Thanks for your answer

"more evolved" is not a biologically justified statement. See answers here https://biology.stackexchange.com/questions/832/what-is-meant-in-biology-by-the-term-evolved.

Hi Aderinsola, welcome to Biology.SE. There is no such thing as "more evolved". It is just the diversity among organisms being shaped by their environment, their way of living, and so on over thousands of years. We might be "more evolved" than those tiny microorganisms, but come to think about it, we cannot survive inside glaciers or in volcanoes—two behaviours noted in several bacteria. There is no connection between progress and evolution.

Evolution isn't a contest between two species, it's the interaction between a species and its overall environment. The only real measure of evolutionary "success" is the ability to leave behind offspring that survive to have still more offspring.
Tyrannosaurus Rex may have been bigger, stronger, and fiercer than any chicken, but apparently something changed in the environment that interfered with its ability to leave behind offspring. Maybe it was a meteor striking the earth and changing the climate. Giant reptiles wouldn't do so well if the climate suddenly got colder. Smaller dinosaurs that had feathers might have done better. Clearly, in today's environment, chickens are able to produce billions and billions of offspring!
Sharks may eat rays, but they aren't eating all the rays! The rays are leaving lots of offspring behind, and so are the sharks. This means that both species are well adapted to the current environment.

From unicellular organism to complex organisms, is the pattern of
  evolution going forward or backward or no pattern

No pattern. Whatever adaptations allow more offspring to survive will tend to last, and traits that interfere with offspring surviving will tend to disappear.
A good web site for learning more about evolution is Evolution 101


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How does excessive acute inflammation damage tissue (eg, in sepsis or cytokine release syndrome)?
While inflammation is necessary to recruit immune cells to sites of infection in order to clear the etiological agent of disease, excessive inflammation has often been implicated in many of the poor outcomes associated with systemic infection, specifically end-stage organ failure (eg, in sepsis).
However, what is not clear to me is what the effector mechanisms of excessive inflammation are which mediate the tissue damage necessary to cause the organ damage. It's very clear to me that excessive signaling through neutrophils can, through positive feedback loops, create a large amount of systematically circulating inflammatory cytokines. But what's less clear to me is what the link is between extremely high levels of cytokines and the ultimate tissue damage associated with excessive inflammation. Presumably, it cannot be due to the direct effector functions of humoral responses or cell-based responses, as both antibodies as well as TCRs are exquisitely specific to foreign antigens. One common explanation is excessive fluid accumulation in tissue due to enhanced vascular permeability - a classic feature of the inflammatory cascade and necessary to allow leukocytes to enter the tissue space. But are there other effector mechanisms by which excessively high pro-inflammatory cytokine levels cause tissue damage?
In short then, while I understanding the pathogen --> inflammatory cytokine secretion stage, what I don't understand well is the inflammatory cytokine secretion --> ?? --> organ damage.
Sources:

https://en.wikipedia.org/wiki/Sepsis
https://en.wikipedia.org/wiki/Cytokine_release_syndrome

You can assume there are no effective antibodies. See immune response to respiratory virus: balancing virus clearance and immunopathology. This paper explains how cell suicide with in the same time call for phagocytes to clear the nearly dead cell is the normal way to eliminate infected cells and hence the virus. The inflammation enhances those processes but supposedly in a tightly controlled way.


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Does Remdesivir interfere with human transcription?
Remdesivir is metabolized into a nucleotide analogue. It is incorporated in the viral genomes causing either termination of transcription or a dysfunctional genome. Thus, the new viral particles produces within infected cells are dysfunctional.
However, how does Remdesivir intefere with human transcription, or does it? I'd imagine that a nucleotide analogue could be incorporated into a human mRNA. Can it?
edit: The mithocondria are discussed below. I would also be interested in usual, i.e. nucleic transcription. Is Remdesivir transported into the nucleus? Does human RNA polymerase accept it?

Look at ribavirin, remdesivir is supposedly much less active on human RNA polymerases than on viral RdRp, possibly due to proof-reading mechanisms.

Some liver issues were reported during ebola trials, but you might keep an eye out here: https://clinicaltrials.gov/ct2/show/NCT04292730

Quote from paper referenced by reuns: "In contrast, purified human mitochondrial RNA polymerase (h-mtRNAP) effectively discriminates against remdesivir-TP with a selectivity value of ~500-fold." So it seems that it cannot be incorporated in human mitochondrial RNA. Do you know if it can be transported through the nuclear membrane?

The question in the title asks a medical question — does a drug have side effects — which would be off-topic here, although probably on-topic on SE Medical Sciences. The body of the question asks if the drug affects a particular process in human cells, which is on-topic. Please edit your title to fit your question.

However, how does Remdesivir intefere with human transcription, or does it?
Via https://www.ncbi.nlm.nih.gov/books/NBK548938/:

Nucleoside analogues can cause liver injury by several mechanisms. Most characteristic is a mitochondrial type of hepatic injury that is probably caused by the nucleoside analogue becoming incorporated into or blocking mitochondrial DNA synthesis by the mitochondrial gamma polymerase, leading to a depletion of mitochondria or decrease in their function. Mitochondrial injury can affect multiple tissues thereby causing myopathy, neuropathy, pancreatitis, bone marrow suppression and/or hepatic injury.

Remdesivir trials for treatment of Ebola virus infections included in vitro studies of hepato- or liver toxicity. Via https://www.who.int/ebola/drc-2018/summaries-of-evidence-experimental-therapeutics.pdf?ua=1:

Remdesivir and the parent nucleoside analog GS-441524 were extensively profiled for in vitro cytotoxicity and mitochondrial toxicity in multiple relevant cell types. Both remdesivir and GS-441524 exhibited > 3.5-fold margins in most in vitro toxicity assays. Data from in vitro studies with liver cell culture systems demonstrated that human hepatocytes are susceptible to remdesivir mediated toxicity, likely due to high cellular permeability and effective intracellular metabolism of the drug. Systemic metabolites of remdesivir detected in vivo in plasma do not exhibit any in vitro hepatotoxicity at pharmacologically relevant levels.

However, treatments in vivo did not show much in the way of negative effects:

Single dose of remdesivir IV infusion from 3 to 225 mg was well tolerated with no dose limiting toxicity observed. No treatment emergent AEs were observed in more than 1 subject per arm. No evidence of renal or liver toxicity was observed. All AEs were Grade 1 or 2.
Multiple-dose IV administration of remdesivir 150 mg once-daily for 7 or 14 days was generally well tolerated. No subjects had a Grade 3 or 4 treatment- emergent laboratory abnormality during the study. Reversible Grade 1 or 2 ALT or AST elevations were observed in several subjects without abnormalities in total bilirubin, alkaline phosphatase (ALP), or albumin. There was no abnormality or clinically significant change in international normalized ratio (INR) in any subjects. Remdesivir did not show any effects on renal function in the multiple-dose study.

Stereochemistry of the active portion of remdesivir may help make it less toxic.
Human DNA polymerase selects for or preferentially incorporates right-handed or "D" nucleosides. Nucleosides that are of the left-handed ("L") enantiomeric form will still be incorporated by RNA polymerase and have clinical effect from blocking viral replication, but will less likely be used by the machinery in human cells.
Here is another paper that explores how DNA polymerase selects for the D-enantiomer: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4121797/
Other nucleoside antiviral drugs appear to have L-stereochemistry (ibid.) for this reason, to reduce toxicity, so I'd assume the same about remdesivir, as well. I tried looking through a paper on the organic chemistry of remdesivir synthesis, but I don't know enough about that subject to see whether there was a specific step or steps along the drug's synthesis, which involve separation and purification of enantiomers. Perhaps someone with more expertise there can comment.

Don't you think it is much more about proofreading mechanisms of human polymerases than enantiomers. CoV has a proofreading mechanism but it is much less efficient than ours.

Remdesvir cannot interfere with human transcription as it is DNA dependent whereas viral transcription is RNA dependent. And this drug is adensoine analouge which blocks the addition of further nucleotide performed by RNA dependent RNA polymerase.The RNA dependent RNA polymerase is used to replicate viral RNA-based genomes. This competes with adenosine triphosphate to add into the nascent RNA strand. This substitution results in early termination of RNA synthesis and thus prevents the viral genome transcription.
https://www.sciencedirect.com/science/article/pii/S2352771420300380
And this invitro study has shown that Remdesvir discriminates between viral and human RNA polymerase.


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Does it make sense to express membrane transporters as concentration?
Let's assume a situation where a molecule, S, is transported out of the cell by membrane transporter T. For simplicity we do not consider any other synthesis or production processes. Furthermore, we assume Michaelis-Menten (but another enzyme mechanism would lead to the same question, I think).
Mass balance concentration:
$\frac{d  [S]}{dt} = - [T] \; kcat \; \frac{[S]}{[S] + Km} $
Mass balance amount (moles):
$\frac{d  S}{dt} = - T \; kcat \; \frac{[S]}{[S] + Km} $
In both mass-balances the square brackets [.] indicate concentration.
In order for the units to match, the first mass balance equation expresses the transporter term as concentration (i.e. $\frac{T}{Volume_{cell}}$). Does that make sense? After all, these transporters are stuck in the membrane and not 'floating around' in the cell like the S molecules. Expressing T as concentration assumes that the transporter molecules are equally distributed across the volume, which is not the case. Does this not lead to an overestimation of the reaction rate?
Or did I make a mistake somewhere?


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Best fundamental literature about genetics
I'm seeking for good genetics literature. I'm not afraid of it's complexity, because I want to have relevant knowledges about molecular genetics. After Wikipedia articles and basic molecular-biology books I need something, that can explain some aspects more detailed. I need something fundamental, but not abstract or scientifically popular. I understand, that question probably will be closed, but I don't know any other place to ask.

Finding something more fundamental and more detailed than Wikipedia might be a challenge.

For textbooks, I think Gene X is very detailed, very comprehensive.

"genetics" is extremely broad. Could you identify a specific discipline? e.g. molecular genetics/molecular biology, human population genetics, evolutionary genetics, genomics, plant genetics, developmental genetics, biotechnology...? The obvious answer would be "a genetics textbook" but I suspect you want something more specific.

@Maximilian Press Probably, molecular genetics is what i need.

I can think of a few different sources that might be interesting to you, focusing specifically on so-called "Central Dogma" ideas.
My personal bias is I think that knowing a bit of the history is invaluable for understanding the concepts, because a lot of the concepts turn out to be tied up in how they were discovered. Most of the big-picture stuff in molecular biology was figured out by 1980 or so, and molecular genetics followed closely behind.
Matthew Cobb has written a number of good books about how famous discoveries were made- I've read Life's Greatest Secret, which I found very readable and also informative about the discovery of the genetic code.
Sean Carroll wrote a good book about molecular mechanisms in developmental biology.
Both of these are "pop science" books but they are written by PhD biologists with a lot of technical details.
I am very fond of Erwin Chargaff's books as well but he is not to everyone's taste; he missed a few things early on in the history of molecular biology by being over-cautious, and was rather bitter about it later, which bled through in his writing. Most relevant probably are "Essays on Nucleic Acids" and "That Heraclitean Fire".
You could also read Jim Watson's book Molecular Biology of the Gene, which is rather old (though updated) but is a lot better on the technical aspects than most textbooks by my understanding. (He's a bad person but the book is good.)
And of course MIT has online molecular genetics courses.


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Can swarming locusts act as a vector for any human pathogens?
What human pathogens can the locusts currently swarming in Africa act as a vector for?
E.g. can the locust swarm 'become a reservoir for' SARS-CoV-2? Measles? Ebola?

I'm not sure why you're getting close votes -- this post is not asking for an opinion. Close-voters, please review the guidelines for voting to close. Thanks.

we ask that all posters do their own research before posting here and indicate what research you've done. I invite you to explore coronaviruses in general to better understand their regular infection patterns.. Report back what you've found (by editing your post) and let us know what is still unsure to you

I have not heard of locusts being a vector for any pathogen. For immunocompromised people, they can on rare occasions be infected by bacteria carried in the guts of insects. For desert locusts, their main gut bacteria is Pantoea agglomerans (Enterococcus agglomerans). This species has been listed as a pathogen of immunocompromised patients.

Should I delete?


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Can single-cell organisms have through-holes? (Are donut-cells a thing?)
I've watched a YouTube video about microorganisms, which featured a shot (below) of a single-cell organism, that looked like it had several through-holes in its body. Somehow I have a pretty steady mental image of a single-cell organisms being basically blobs: a sphere, an ellipse, a branching tree-like structure, all seem like plausible single-cell creature shapes to me, but something like a donut just doesn't. Is my intuition wrong and this is just a normal thing cells do? If so, how do those holes form? And if not, why does this shot look like a cell with holes?
I thought that those holes might be just me wrongly interpreting the image. One idea was that this might be a result of the cell's complex 3D structure being projected on a 2D screen, but the movement of particles inside of the cell (which you can see in the video) seems to support the "cell with holes" interpretation. The other one, that was suggested in YouTube comments, is that those "holes" might be vacuoles inside of the cell. It seems that for that to be true, the image would have to be more like an MRI scan, revealing only a "slice" of the cell. But you can see some of 3D structure there, so it doesn't seem right either.

Wow this is a good question.

Yeah, holes seem to happen in leptomyxa:

L[eptomyxa] reticulata is an edaphic protozoan and a predator of bacteria and amoebae. [...] The plasmodium is very polymorphic; its size varies between 50 .mu.m and 1 cm. It generally spreads in the form of a very thin transparent protoplasmic layer. It may have the shape of a full blade, sometimes perforated with holes, or of a network; the pseudopodial zones with active locomotion present a typical fan-shaped contour.

There are some hi-res images from other sources showing the same

Image source: http://penard.de/Amoebozoa/Tubulinea/Leptomyxida/
It seems that what happens is that branches "merge back" after touching "at the tips" leaving holes in such organisms, but that's just speculation on my behalf. I haven't (yet) found a source discussing the dynamics of how these holes get formed.
And a couple more images from  a different source--a broader review of leptomyxidae.

[Above] Light microscopy of Leptomyxa arborea n. sp. and L. variabilis n. sp. (by S.
Geisen and C. Burberg) on the plastic bottom of a Petri dish (Phaco). A-F: Leptomyxa arborea,
various shapes and specimens of different size. G-M: Leptomyxa variabilis, various shapes of
trophozoites (G-K and M); cysts (L-M). Arrows indicate the most pronounced bunches of
adhesive filaments; arrowheads indicate pore like structures in cysts. Scale bar is 100 μm in A-E
50 μm in F-K and 25 μm in L-M.

[Above] Isolate of Leptomyxa sp. (by morphology of trophozoite indistinguishable from
L. reticulata) observed in the sample from Valamo Island, North-West Russia (by A.Smirnov).
A: usual appearance of a trophozoite. B-D: subsequent stages of contraction of the cell on the
object slide under the bright light beam. Figure D shows pseudopodia very similar to those or
Rhizamoeba; polypodial cell like this one can move relatively rapidly for some distance.
Molecualar data from this strain were not obtained. Scale bar is 50 μm.

By the way, the "branches" are more or less "legs"/"limbs" used in locomotion; but also this species is multinucleate:

Leptomyxa reticulata is the type species of the genus Leptomyxa. It is a
multinucleate, expanded organism with plasmodia-like organization of its ramose body,
possessing a simple life cycle [...] Moving amoebae usually form adhesive uroidal filaments along the posterior end of the body or an uroidal structure consisting of a pack(s) of such filaments (the latter often is seen when the locomotive cell adopts a shape of
an irregular ramose triangle, with the base directed anteriorly).

A more diagrammatic explanation:

Main morphological traits of leptomyxid amoebae. A-E: Leptomyxa cf. reticulata
(Valamo Island strain by AS). A: expanded, plasmodium-like ramose cell, slowly moving on the
substrate. This is the “textbook” appearance of Leptomyxa. B – more compact, faster moving and
actively feeding cell. C: Disturbed cell showing compact lobose pseudopodia. Leptomyxa accepts
shapes like this under certain influence (light, temperature, etc. in order to relocate rapidly). D:
solitary cyst with double wall. E: several cysts covered with the shared outer cyst wall (D-E are
drawn based on photos by Pussard and Pons 1976a)

(So yes, creepin' amoeba with holes and "limbs"!)
A more interesting question at this point is whether there are any (naturally occurring) single-nucleus examples of "cells with holes".

Human macrophages don't seem to able to quite get holes in themselves but they can contort quite a bit, as you ca see in this video: https://youtu.be/rgFeL3jd9X0?t=54

The short answer seems to be "yes", you can get single cells that are toroidal (donut-like) in shape. This seems to be done in the lab by various manipulations. This was first done in 1961. Notably, the cells in question seem to be eggs or single cells of multicellular organisms.
Update: see @Fizz's answer about natural occurrence of holes
I am guessing that what you are seeing in the micrograph you show is not a hole. I think that a vacuole is a good guess, contractile vacuoles are common in protist organisms. Here is another example of a protist with a contractile vacuole "hole" in 2D. The cell image library is a good resource if you want to investigate further.
I think that you are unlikely to be able to see enough of the 3D structure there to ascertain that there is a hole through the cell from that image. A 3D projection of the cell could be reconstructed by confocal microscopy, but it would be actually a 3D structure- it's made up a bunch of 2D section images like the one you show.


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What functions other than spore dispersal does a fruiting body serve in a mycelial network?
I'm not exactly sure if this is the appropriate forum to ask this, so apologies in advance.
My question is both technical and general: what are the less obvious functions that the individual mushroom might serve in a network of mycelia. My knowledge of biology is pretty limited but I know that, for example, some mushrooms absorb radiation with some effects on the underlying network or that the network might generally shift itself underground overtime based on the signals that the individual fruiting bodies "gather" over their above-ground lifespan on.. whatever, humidity, predators, other conditions of relevance.
This is not to mystify it too much, but i'm really interested in the biological dynamic where a "node in the network" contributes something to the decentralized network, this probably sounds familiar, fungi are just the most obvious example. I was wondering what would be the term for this to begin with if there is one and if somebody could point me to some work on it at any level of resolution: from ecology to genetics or mathematics.
Thank you very much.

A cheeky answer would be that for poisonous mushrooms, the fruiting body provides vomit, faeces and corpses for nutrients.


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Where can I find SARS-CoV-2 genome sequences for the UK?
I have downloaded and analysed the sequences of 832 complete samples from the European Nucleotide Archive but I cannot find a single one that was from the UK. I have also tried Genbank and they do not seem to have any UK ones either. I'm still waiting for my logon for Gisaid - looks like they may have some. Is there anywhere else I can try?

European Nucleotide Archive has only the genbank sequences but they have a link to download them all.
Gisaid refuses to make the sequences at disposal. On https://bigd.big.ac.cn/ncov/variation/analysis https://bigd.big.ac.cn/gbrowse/2019-nCoV/?gbgff=1;s=0;f=save+gff3;format=gff3;l=hCoV-19/France/B2337/2020 you can find all the high quality sequences in a diff form, except they didn't take the N in account.

@reuns i think this is a reasonable answer that you could add, probably more helpful than mine.

Thanks for the bigd link. Over 10,000 sequences but unfortunately most of them are stored on Gisaid and they don't let you download these. I thought this information would be in the public domain.

GISAID certainly does allow downloads. You need to register and follow their guidelines for acknowledgement if you publish, but it’s completely false to say they don’t allow downloads.

Just to clarify, if you go to the bigd link you cannot download any of the sequences held on Gisaid. I'm still waiting to see if my registration for Gisaid gets approved - it's been over a week since I filled in the form. I don't understand why this information is not in the public domain. The irony is that Chine (and most other countries) has been open and shared its genome information with the world, but the UK has not.

I deleted my answer as there are now better answers posted here.

https://twitter.com/arambaut/status/1254809662257606656

Oxford University's Bugbank project is designed to collect SARS-CoV-2 samples (and other microbial cultures) from UK Biobank participants for sequencing. Once completed this data will be available to researchers through the UK Biobank:

We originally developed this system as a pilot study to determine the feasibility of prospective microbiological culture collection from UKB participants to create a microbiological biobank (‘bugbank’) for joint studies of epidemiological, human genetic and pathogen genomic risk factors for infection. In light of the COVID-19 pandemic, we have repurposed the system to provide near-to-real-time data on SARS-CoV-2 positive and negative test results for UKB participants.

Dynamic linkage of COVID-19 test results between Public Health England’s Second Generation Surveillance System and UK Biobank (2020) *

* Disclaimer: I have worked on this project.

Thanks for this. Unfortunately I don't meet the admission criteria - I'm not a researcher, just a curious member of the public.


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T-cell "exhaustion" in patients with Covid-19
Following up on my previously asked question, which asks how COVID infects T-cells in immune system.
Here's a study that shows that recovered covid patients have "exausted t-cells". To quote:

T cell counts are reduced significantly in COVID-19 patients, and the
  surviving T cells appear functionally exhausted. Non-ICU patients,
  with total T cells, CD8+T cells CD4+T cells counts lower than 800/μL,
  300/μL, and 400/μL, respectively, may still require aggressive
  intervention even in the immediate absence of more severe symptoms due
  to a high risk for further deterioration in condition.

Is this normal for other coronaviruses (like the common cold)? Also is it possible that this immune damage can be a long-term effect, similar to HIV?

It's not a flu-like virus! Symptoms may be similar, since they are not specific, though flu doesn't cause interstitial inflammations and pulmonary embolism!

I edited this so that it's more clear. In a previous question people said that it's normal for coronaviruses to infect T-cells. By "flu-like" I was referring to other coronaviruses like the common cold that spread through airborn droplets like the flu.


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When did bison exchange smartness for larger skeletal muscles or a digestive system that can ferment grass?
Patricia Churchland (2019) writes:

From time to time, evolution favors a dumbing down; sacrifice some smartness in exchange for larger skeletal muscles, like bison, or for a digestive system that can ferment grass, again like bison.

Roughly when did these evolutionary changes occur?

Patricia Churchland is wrong there.
Bison are very big deer/goats, and they are not dumber than deer and goats, you know how clever sheep are! There is a theory that they are related to a rabbit sized early ruminant about 40 million years ago.
Bison and deer have common ancestors about 17 million years ago.
Goats and deer have common ancestors about 22 million years ago, they have a similar digestive system to bison, your book is being vague there.
Oligocene epoch:
The formation of the Himalayas and the Alps brought about significant geographic changes. This was the chief reason behind the extensive diversification of deer-like forms and the emergence of cervids from the Oligocene to the early Pliocene.[50] The latter half of the Oligocene (28–34 Mya) saw the appearance of the European Eumeryx and the North American Leptomeryx. The latter resembled modern-day bovids and cervids in dental morphology (for instance, it had brachyodont molars), while the former was more advanced.[51] Other deer-like forms included the North American Blastomeryx and the European Dremotherium; these sabre-toothed animals are believed to have been the direct ancestors of all modern antlered deer, though they themselves lacked antlers.[52] Another contemporaneous form was the four-horned protoceratid Protoceras, that was replaced by Syndyoceras in the Miocene; these animals were unique in having a horn on the nose.[45] Late Eocene fossils dated approximately 35 million years ago, which were found in North America, show that Syndyoceras had bony skull outgrowths that resembled non-deciduous antlers.[53]
https://en.wikipedia.org/wiki/Deer#Eocene_epoch
This science mag study contradicts with the wiki references by about 20 million years:

https://science.sciencemag.org/content/364/6446/eaav6202
Here's a giant book on the topic of ungulate radiation based on their teeth, it doesn't give an easy answer to your questions though, it implies that there have been many genera of ungulates the size of cats and dogs and larger in the paleocene: https://www.researchgate.net/publication/36248483_Adaptive_radiation_of_early_Paleocene_ungulates/link/0c96051683bae86a84000000/download
Bison are at the top of the ruminants, after the cervus (deer):

That book is sociology and neuroscience, and it lacks depth for evolution. Evolution is fabulous at providing evidence and physical details, so she should demonstrate some examples ( bat digits, hand structure of primates, sea mammals, resemblances ).


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How to determine the most likely reading frame of a DNA sequence?
This question is from a past exam paper for an introductory bioinformatics module. I'm a computer scientist doing biology for the first time.
"A short bacterial gene has been sequenced, giving the following DNA sequence. Write out the 6 possible reading frames for this sequence and indicate which is the most likely protein translation of this sequence. Explain your reasoning for picking the given translation, and write all the translations in single letter amino acid code form.
5' - ttattcatccgccagcgccatgcgcgccat - 3'  "
I think I understand the 6 possible reading frames: three from the 5' end starting tta, tat and att; and three from the 3' end starting tac, acc and ccg.
I could also write out the translations for a given reading frame with a codon usage table.
It's the most probable reading frame part I don't get. I thought perhaps I was looking for the longest open reading frame. I can only see one start codon (atg). What is the correct way to recognize the most probable reading frame?
I can't find this problem exactly on Biology Stack Exchange. I did find:
Help reading chromatogram
It made me wonder if I'm getting confused between "reading frame" and "open reading frame", this question only asks or the former.
Thanks!

This is a terribly artificial question, but assuming that the sequence represents the whole reading frame, what do you need to consider as well as start codons? I like your suggestion of codon usage, but it's not as sophisticated as that.

Thanks for getting back to me so quickly. I'm still not sure but I had a few ideas.

Length of the frame, long enough to code something useful - but that would still be length between a start and stop codon.
Presence of expressed sequence tags - though I wouldn't know how to tell you if some sequence contained an EST and I suspect they are longer than 30 bases.
The presence of more or less "likely" amino acids eg, does the sequence have more of the most frequent amino acids (which I think are serine and leucine) - but I don't think we'd be expected to know this.

The presence of common subsequences that might indicate, say, common secondary structures - again, this is not something we've talked about in our course. 5) Sequence reading errors in the lab. Look for where there could be start and stop codons if you just changed one (or two) bases. For example, in the reading frame starting "att" from the 5' end, you could change that first triple to "atg" to make it a start codon, then perhaps the last "cca" should have been a tta stop codon. 6) Promoter sites?

Given that you've said it's easy, (2) to (6) all seem harder than what I was originally thinking about. More generally, I can't see how it can't have a stop codon and still be a gene.Thanks again.

OK, I've provided an answer.

The 3 reading frames from the 3' end use the "other" strand of dna, that is ATG and two others. Experts from mathematical and computational sciences contribute greatly to bioinformatics after a bit of education. Good luck!

This is what we classify as a homework question, but as it satisfies the criterion of the poster demonstrating an attempt to answer it, I provide the following suggestion of an answer.
I assume that as it appeared in an introductory bioinformatics module the exam question is just testing reading frames (obviously) and the punctuation of the genetic code. The meaning is not entirely clear, but as one reading frame would start with the initiation codon ATG/AUG (reverse complement of: cat - 3′)† and end with the termination codon TAA/UAA (reverse complement of: 5′ - tta) that will presumably produce “the most likely protein translation”.
This is reading frame F4 in the output from EMBOSS Sixpack, below, in which termination codons are indicated by an asterisk.
      L  F  I  R  Q  R  H  A  R  H                                   F1
       Y  S  S  A  S  A  M  R  A  X                                  F2
        I  H  P  P  A  P  C  A  P  X                                 F3
    1 ttattcatccgccagcgccatgcgcgccat 30
      ----:----|----:----|----:----|
    1 aataagtaggcggtcgcggtacgcgcggta 30
       X  N  M  R  W  R  W  A  R  W                                  F6
      X  I  *  G  G  A  G  H  A  G                                   F5
        *  E  D  A  L  A  M  R  A  M                                 F4

The conceptual translation, reading N to C, is MARMALADE, which is obviously meant to be humorous and suggests that it is indeed the intended answer.
Open Reading Frames
The poster asks for clarification of the difference between reading frame and open reading frame. There is a Wikipedia entry for open reading frame but I provide an explanation of my own to relate it to the example.
There are always six reading-frames for the conceptual translation of a piece of double-stranded DNA, as shown in the example.
I would define an open reading frame as one that is not excluded from being translated by the punctuation of the genetic code. It has the theoretical potential to be translated considering only the punctuation of the code, although it may not actual be translated. It can start either with the first AUG after a termination codon (even though it cannot be certain that this is the actual AUG used) or the start of a sequenced fragment of DNA (with the assumption that an AUG is possible preceding the 5′ end of the fragment). It can end either with a termination codon or the end of the sequenced fragment (with the assumption that a termination codon will lie 5′ to the end of the fragment).
By these criteria, reading frames F1, F2, F3 and F6, above are completely open (even though the internal methionine could theoretically be an initiation codon), F5 contains the open reading frame GAHGAGG, and F4 is a complete open reading frame, perhaps excluding the termination codon (depending on your semantic definition of the precise end of an open reading frame).
† Reverse Complement
If we take a section of DNA written in the 5′-to-3′ direction — according to standard convention — and use the Watson–Crick base-pairing equivalences (A=T, G=C) to generate the complementary strand, this will be in the 3′-to-5′ direction. For the strand in the question,
5′ - ttattcatccgccagcgccatgcgcgccat - 3′

the complementary strand is:
3′ - aataagtaggcggtcgcggtacgcgcggta - 5′

As shown above.
For ease of translation manually — and for any computer program that manipulates sequences — one needs to reverse this to the  5′-to-3′ direction:
5′ - atggcgcgcatggcgctggcggatgaataa - 3′

This is the reverse complement. Now the starts of the three reverse reading frames are easy to read as:
ATG...
 TGG...
  GGC...

Could be helpful (especially for someone without a solid biology background) to expand on the reverse complement subject. Based on the question it seems that this was most likely the part that was giving the OP trouble.

@David Well I feel silly, but also grateful for the excellent answer. I had tunnel vision but it's obvious now. Out of interest, what made you describe the question initially as "terribly artificial"?

@azure_reflection — Most proteins are much longer than nine amino acids, and programs predicting genes usually have a cut-off of perhaps 30. (Someone else might be able to give you precise size distributions.) There are exceptions (in biology there are always exceptions). In eukaryotes some small peptides are generated by translation of small orfs that precede the predominant AUG. But, from experience, I sympathize with lecturers setting problem-type exam questions.

@Astrolamb — done.


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To what exten do children produce antibodies against covid-19?
Here in Sweden all kindergartens and schools up to the month of June the year people turn 16 remain open. In almost all other European country schools are closed.
I do not really know why our schools are open, the official policy is unclear. One idea though is to get the children to catch the disease while the elders remain in hiding in order to acquire more immunity in the society.
However, according to some Chinese study younger people seem to be able to fight the disease without antibodies. In the age group 15-39 the number of antibodies found were less then a third of the number of antibodies found in the age group 60-85.
https://www.scmp.com/news/china/science/article/3078840/coronavirus-low-antibody-levels-raise-questions-about
Question: To what extent does infected people in the age group 0-16 develop antibodies against covid-19?
I know that presence of antibodies do not necessarily guarantee immunity against reinfection but if children do not produce enough antibodies they will obviously not be immune.

There are many levels in the word immune, children are mostly immune against the disease and their innate immune system has to do something with it. That said they often develop a benign infection and a question is if they are contagious (a single children probably not much, due to Chinese studies not finding any single case where contagion from a children was obvious, but as a population, in schools with many close contacts and poor hygiene it might be very different).

One report stated that closing schools only has a marginal effect. If they are not sneezing and coughing and putting snot in rags, it limits their viral output. people who don't even have a temperature don't have as high numbers of a virus as people who have flu symptoms. For antibodies, it seems that children's immune system does actively fight the virus very efficiently, and that would be with antibodies. studies will take a while.