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What is the point of a runny nose during a cold?
What is the biological purpose of having a runny nose during a cold?
Note, this is a different question than "What causes a runny nose" and other similar questions. Those question are about the cause, what starts the nose running. This question is about why? What is the body trying to do by making the nose run.
For example a cough, I'm guessing, is to help remove or loosen gunk in the lungs. Tears seem to have a point of cleaning the eyes. Diarrhea seems to have a point of clearing the bowels. Fevers have a point of killing viruses. Vomiting seems to have a point of getting rid of bad things in the stomach. Sweating seems to have a point of cooling the body down.
During a cold though, while reasons like inflammation etc cause a runny nose, what's the point? Why did we evolve to have runny noses during colds? What's the body trying to achieve by giving us a runny nose, specifically during a cold.

Does it need to be evolved? Can it not just be a side effect of some inflammatory process?

I don't know. That's the question. Tears seem to have a point. Coughing seems to have a point. Diarrhea seems to have a point. Fevers have a point. Vomiting seems to have a point. So, the question is does a runny noes have a point or as you suggest, is it just an unlucky side effect.

possible duplicate of If a trait would be advantageous to an organism, why hasn't it evolved?

This question is a duplicate because not everything needs to "have a point" in evolution.

This question is not asking why something hasn't evolved but, rather, why something has evolved. There's clearly potential for a scientific answer. In addition to AMR's answer, there's this idea: http://cmr.asm.org/content/24/1/210.full

@canadianer So the viruses are outflanking us again... Cause us to overproduce mucus to possibly induce a lower respiratory bacterial infection so that they can better infect the upper respiratory tract... I believe Homer Simpson would say "D'Oh!"

@AMR It's disappointing being outsmarted by something that's not even alive.

@canadianer one of my professors used to say that our genome is mostly viral anyway. If you can't beat'em, join'em I suppose.

Edited by request for clarity
The biological purpose of a runny nose is to clear pathogens and allergens trapped in the mucus out of the nasal cavity and sinuses as a result of rhinitis or sinusitis.

Mucus is considered to be part of the innate immune system and provides mechanical and chemical defenses against pathogens.

Mucus acts as a barrier protection that is difficult for pathogens to breach.
Mucus is capable of trapping pathogens in it and when that mucus is swept out of your upper respiratory track through your nose or down your esophagus, the pathogens are removed from those areas as well.
Defensive proteins called Mucins, Lysozymes, and Immunoglobulins are secreted into the mucus and provide additional protection, as they can lyse or opsonize pathogens.

Mucus keeps epithelial cells moist so that they do not dehydrate as air passes over them. This in turn keeps epithelial cells healthy so that they maintain a tight cell layer in order to protect the underlying tissue.

As part of the mechanical defenses against pathogens, epithelial cells are ciliated and they rhythmically sweep mucus from the sinuses and nasal cavity mainly into your esophagus and digestive system, but can also move mucus into your nose. Most of the time we aren't even aware this clearance of mucus is happening and it travels down our esophagus into our stomach's and intestines where it can be excreted from the body. This is the case when you do not have an infection and your mucus is not viscous.
When you have an infection the inflammatory response is triggered by cytokines from macrophages. Those cytokines induce cells in the area to do many things. One is to increase mucus production. This may cause epithelial cells in your nostrils and nasal cavity and sinuses to secrete more mucus as well, and this will be swept away through your nose, where you will notice it as a runny nose.
Usually your nose is runnier with rhinovirus infections or with allergens than it is when you have a bacterial infection where mucous tends to be thicker and more viscous. The ciliated epithelial cells have an easier time moving the thinner mucous of a viral infection or allergy than the thicker mucus of a bacterial infection, so you notice a runny nose more when you have a cold or hay fever.
So in short, the biological purpose of a runny nose is that it is part of the immune response to clear pathogens away and protect your uninfected epithelial cells from being infected. It also clears out much of the debris and inflammatory proteins that are found at the site of the infection so that they do not remain in the area to further inflame tissue that is trying to heal. When you have allergies your immune system reacts inappropriately to a benign substance, and if the allergen finds its way into your nasal cavity, it will generate rhinitis and cause your nose to run.

I agree with your last paragraph, but don't really follow the first. Why are you singling out the sinuses (do you think the main effect of a runny nose is to prevent sinusitis?) If so, that could be made more clear; if not, that should be made more clear as well.

@anongoodnurse I basically say sinuses because the mucus in you trachea and bronchi get swept up into your esophagus without going through your nose. For the most part the mucus that exits through the nose is from the sinuses and nasal cavity.

@gman I will add that our interaction with and adaptations to pathogens are significant drivers to evolution of the species.

Is this known through some sort of study, or conjecture?  I ask because I've heard it said that some symptoms, such as sneezing, are not the body's way of fighting a virus, but instead an effect that the virus has evolved to induce in the body to aid in spreading itself more readily.  A runny nose could be similar.  I have no idea, but am curious whether anyone really knows the answer.

Janeway's Immunobiology - 8th Edition. Chapter 2.

@anongoodnurse rhinitis is typically local, e.g., at the site of infection by a rhinovirus. So this answer is correct to focus on nasal and sinus production.

"When you have allergies your immune system reacts inappropriately to a benign substance, and if the allergen finds its way into your nasal cavity, it will generate rhinitis and cause your nose to run." <- What's the purpose of reacting inappropriately in so many humans?


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Short videos on evolutionary biology
What I am looking for
I'm considering to eventually start my teaching sessions with short emotional, awe-inspiring or exciting videos that are somehow related to evolutionary biology incl. diversity of life, history of evolution on earth, specific evolutionary processes (sexual conflict, evolution of ageing, evolution of mutation rate, speciation rate, ...), diversity in mating systems, major transitions, etc...
3-minute long movies would be perfect. 15 minutes would be too long. The videos should be easily accessible for Bachelor students having little background in evolutionary biology.
Examples
Asap Science video about the evolutionary history of life would be a good fit.
The beginning of We are all related by vsauce would be a good fit.
This video from SciShow is typically too long
This video on the evolution of human face would do but I am not quite sure how exact it is and it feels a little weird that the end product is a white male!
It'd be great if not all suggestions were about recent human history or about dinosaurs :)
Do you have any suggestions?

This question might very well be off-topic here. Let me know and I'll delete it. Advice on where to ask such questions would be very welcome.

The question is fine and will likely produce a good resource for the community.

Upvoted! Normally those kinds of questions get asked when an SE communitiy starts out so I would say it is high time :-)

@Remi.b I'm curious, is there anything wrong with your first example that you say is a good fit?

@Insane. No, it is a good fit but I am hoping to have several such good fits.

I think you should show your students a video by a creationist on why evolution is not true. That would certainly inspire them to appreciate the logic of evolution ;)

I lead a workshop on protein packing that opened with this video of the inner workings of the cell by Biovisions at Harvard. I narrated what is happening whilst the video was playing (I sometimes found it awkward when lecturers and teachers just watched the video too!). It's off topic at first glance, but It could set the tone for the complexity of life at a molecular level, and how evolution acts at a molecular level.

@biogirl Don't be so sure that intelligent design videos can't be compelling and inspiring. This clip is one of the prettiest and most informative ATP synthase videos available and it argues for intelligent design.

@James Oh you are right. But I think you can use that video in a productive way. Show it to "inspire" students and then prick the balloon by carefully explaining why the argument is not acceptable to biologists even if it is so seductive.

I suggest the Stated Clearly channel, but the videos are longer than 3 minutes

I find it discouraging that nobody else realizes that the subjectivity of this question (what you consider exciting is not necessary what I consider exciting) renders it off topic. Furthermore I think it is bad to try to appeal to the emotions rather than the intellect. That is the approach of the irrationalists. Evolution is yesterday's scientific news. Ignore the flat earthers and move on.

I saw this HHMI video today. It is called The Animated Life of A.R. Wallace, and it discusses the contributions that Alfred R. Wallace made to evolutionary theory. It is a little long for your stated time of 3-minutes. but it talks about how in fits of malaria he came up with his ideas on evolution.
HHMI also has a whole series of videos and modules on Evolution, though Wallace's came to mind as it showed his ambition and desire to solve the problem, even though he had not received formal training in the sciences.

Nice video. It is nice also to bring some fame to Wallace and not only to Darwin. I'm looking at the other videos on the website. +1

It is not really a video but it is a real life simulation in the browser about vehicles that evolve to master a race track. I project it onto the screen while I introduce genetic algorithms in my data science classes. I then ask people to identify key features of the evolutionary process and we talk about it while the "cars" are still evolving:
http://boxcar2d.com/
People told me that this is really motivating. After that we start programming our first genetic algorithm.
This is a video that I sometimes show additionally (5 min. about robots in an artificial world learning to walk):
https://www.youtube.com/watch?v=pgaEE27nsQw

Not quite what I expected but it is nice. I particularly appreciate the evolving car simulator. What population size, type of terrain and mutation rate do you recommend to maximize the speed of improvement? Can you maybe say a word about how you coded the information about the car and how to interpret a mutation? Would be great to have a snapshot of the parent population on the side to understand that we have a population and not just a series of random individuals. +1

@Remi.b: Thank you, I appreciate your feedback. I have to run now but I will answer your questions later!

BBC and other CG animation programs about Ediacaran life, trilobites, other old life forms, are very engaging to see. There are a lot of CG progams bringing to life ediacaran seas.
https://www.youtube.com/watch?v=znO8q5Ht17g
David Attenboroughs CG animation of the chinese microraptor, where it steps out of it's fossil and flies around the room.
microraptor chasing other flying reptile:
https://www.youtube.com/watch?v=-fyxUxGdrns
https://www.youtube.com/watch?v=SmcqnAWKLJQ

I like the David Attenboroughs link! Thanks +1. Note that the last link on 'Microraptor' is in french. Don't remove it but you should probably highlight it in your answer and explain what it is.

sry didn't have time to find the original english version.. https://www.youtube.com/watch?v=-fyxUxGdrns here it is, first result for "microraptor chase"... it's narrated by john hurt, the recently defunct actor of midnight expess and the storyteller series.

Here are a bunch of fun videos about evolution! They might not be very educative at first sight but they might still bring more than just a laugh to students.
MinuteEarth videos
The youtube channel MinuteEarth has plenty of evolution related videos of about 2-6 minutes each. Look for example at

Males vs. Females: Sexual Conflict
Why Do Animals Eat Their Babies?
Do We Have to Get Old and Die?
Are We Really 99% Chimp?
Why are Males often More Physically Aggressive?
Epigenetics: Why Inheritance Is Weirder Than We Thought

PBS Eons
PBS Eons have a lot of cool videos on the history of life on earth. Videos might be a bit long for your needs though, around 5-10 minutes long on average.
MaxBird feat Jamie

Les dinosaures ont disparu ? in 7'51'' (in french)

How is evolution often misrepresented

South Park - Mr. Garrison's Evolution Theory in 51''

and of course

Simpsons - Homer's evolution in 1'29''

One can also just type Evolution on google Image to get only this misleading and anthropocentric view of representation of evolution

Why Pokemon evolution is not like evolution in nature

Dirty Biology - Darwin chez les Pokemon (in french)

Song

Evo-Devo A capella on Despacito by acapellascience.

Creationist argument (although this is not really the way the OP wants to go to)

Simpsons - Missing link (start at 1'14'' to 2'10)

In the category 'Response to creationist argument' it is easy to find funny videos just by showing burlesque creationist argument such as

Ray Comfort - banana proves God (from 1'12'' to 2'20 although the whole video is pretty funny). The video mixes up questions of believing in God and of evolution which I don't mean to do myself and could (rightly) be taken as offensive by students so be careful.

https://youtu.be/hOfRN0KihOU Sorry, this video is not short, but perfect. From Kurzgesagt chanel youtube

Thanks a lot for the suggestion. I agree Kurzgesagt (a.k.a. In a nutshell) is a great channel. The video is a bit long though (as you said). It is also a little too introductory and too general and not very "emotional, awe-inspiring or exciting".

This Evo-Devo music video from A Capella Science is very good: https://www.youtube.com/watch?v=ydqReeTV_vk&feature=youtu.be

Thank you! The link is already present in my answer though.

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Why does blood come out of leach when salt is put on it?
I know osmosis is the reason for the water to come out of cells - When you sprinkle salt over a leech, it creates concentration gradient and forces the water out of the cells. But why does a lot of blood come out too ?

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What is (are) the medium of conduction for an electrical current with an external source in the human body?
I am trying to get some background for some personal research I am doing into the effects of Electro Convulsive Therapy. I don't understand how electric current from an external household source, say, flows through the body. There are no naturally occurring chains of metal atoms in the body, so it can't be electron flow, but my understanding is that the electric field around an electrode is very thin, so I can't see ion flow as accounting for electrical effects in the body at some distance from the electode - particularly with AC, as I would only expect a local oscillation. I am familiar with membrane depolarisation but that is essentially a cellular mechanism - is it (or saltatory conduction) activated by an external current? I know that the body as a whole (and cell membranes in particular) function as a dielectric, but I can't see how this fits into the global picture of current flow between two electrodes. Can anyone help or recommend me a paper?

Electric current flows rather rather easily through water that contains ions, which are electrically charged atoms. Since the human body is more than half water, and that water is filled with ions such as sodium, chlorine, potassium, etc., the body for the most part conducts electricity rather well.  The skin can have a high resistance to the flow of electricity, but it varies substantially, particularly being reduced when the skin is moist.  Medical electrodes, as for heatbeat measurements, are typically applied with conductive paste to overcome most of the skin's resistance.  You may want to look at this "Electricity And Human Body" page, or the article "Conduction of Electrical Current to and Through the Human Body: A Review".

In fact electrons do not flow through water: they are donated or received by ions at the electrodes.

@DonnardWhite, Yes, a particular electron probably doesn't flow further than an atom or three at a time. The reception of an electron by an ion does change the electric field near the ion, causing another electron to be donated to another ion further along. An enormously long chain of this happens through the ionic solution of the body's water and ions.  Eventually some electron pops out into the other electrode.  No particular electron flows from one electrode to the other, but rather each moves a minute distance along the path through the solution.

Ah, that I didn't know, and that is useful. I am trying to get a picture of an end to end passage of charge - problem is mmm - trying to imagine the energetics of this - my thermodynamics could do with some revision - but there is a directional electric field near the electrodes - but I'm guessing pretty random after that if you are saying there is a local electric field change for every electron exchange - would love to have a better idea of the medium - blood? membrane surface? but you have been a help. I'd read the second paper you mention, and: https://www.ncbi.nlm.nih.gov/pubmed/19212042


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Which species of rotifer is this?
If found this in a moss sample.

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

Also, for [tag:species-identification] questions, please be sure to include all relevant information mentioned here (which you saw when typing the question). specifically, please at least add an approximation of size of your specimen and indicate where you took your sample. Thanks.


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Inability of vultures to digest diclofenac
The population of Indian vultures has been rapidly declining since 2003. This is attributed to the diclofenac present in the carcasses which the vultures eat. Vultures seem to digest all sorts of food items but why can't they digest diclofenac? What is the mechanism which causes this?

Via: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1618889/

Post-mortem examination revealed extensive visceral gout in all diclofenac-treated birds (see electronic supplementary material). Histological examination revealed significant lesions in the kidneys, liver and spleen with extensive uric acid crystal deposition.

Via: https://repository.up.ac.za/bitstream/handle/2263/26027/Complete.pdf?sequence=7

From the mechanistic studies both diclofenac and meloxicam were directly toxic to chicken and vulture renal tubular epithelial cells following 48h of incubation. It was later shown that this toxicity was associated with an increased production of reactive oxygen species (ROS), which could be temporarily ameliorated by pre-incubation with uric acid due to its anti-oxidant activity. When cultures were incubated with either drug for only two hours, meloxicam showed no toxicity in contrast to the cellular toxicity present for diclofenac. In both cases no increase in ROS production was evident. In addition, diclofenac influenced the excretion of uric acid by interfering with p-amino-hippuric acid channels. The effect on uric acid excretion persisted after the removal of the diclofenac. It was therefore concluded that vulture susceptibility to diclofenac results from a combination of an increase in cellular ROS, a depletion of intracellular uric acid concentration and most importantly the drug’s long half-life in the vulture.

The second link posits three mechanisms for the cause of renal failure in vultures (ref., pg. 26):

Ischaemic nephropathy with secondary visceral gout
Organic Anion Transporter antagonism
Secondary renal toxicity with or without toxic activation

I'm just coming across this post now and I don't see any downvotes. As such, I'm going to remove your last comment as no longer necessary. Your post is well-linked/supported, so that aspect is great (thanks!) and should discourage downvoters. However, to further discourage downvoting, I would also encourage (if you'd like) to add a bit more non-quote context to your post. Some users downvote due to seeing answers that are primarily quotes of other sources. But as I said, you don't currently have any downvotes so you might be ok as is. Thanks!

I just seem to be the victim of some drive-by downvoters, lately, and am trying to head it off at the pass. Sorry if this annoys some.

Everyone is a "drive-by downvoter" by your definition. No one is ever supposed to comment on how they voted; votes are anonymous, and disclosing how you voted would defeat the anonymity of the system. Leaving comments does nothing to "head off" the problem because it isn't a problem. A downvote means someone who read your answer thought it was unclear or not useful. That's all.


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Can animals and humans be ranked in their ability to detect moisture?
One reason for insects being so successful - about 70% of all animal species - is their excellent ability to detect moisture. Take termites for instance. The soldiers boot out the flying reproductives only when it will rain within 24 hours. Because moisture will be needed to survive and make a new termite nest.
Humans by contrast are hopeless at detecting moisture; humans do not have the senses to be able to predict rain. Except by more indirect methods and science.
So my question is is there any way of ranking the different abilities to detect moisture? This is not a list question. Rather, it's steering for a formula or set of variables. Are there factors that make a dog better at detecting moisture than cat for instance, if that is the case?
I am surprised that nobody seems to have done this for something - water and moisture - that is so vital for life.

If you are going to downvote this at least have the guts to comment and say why; it seems like a valid question to me.

It sounds like you are talking about rain prediction, i.e. weather prediction of animals. And the title sounds like the ability to detect local water, like mosquitos when they lay eggs, which can be explained through scent. The phrases are more like BBQ convo than concise info statements and queries. A dog can smell water because water smells of algea and nitrogen and things. Air pressure can also predict rain, perhaps that's what termites sense. I'm not voting, I't difficult to answer a vague question. it's a cool topic to research though.

https://www.google.com/search?q=animal+sense+of+weather&oq=animal+sense+of+weather&aqs=chrome..69i57j0.5696j0j7&sourceid=chrome&ie=UTF-8

If it helps anything I have a shelf full of books about termites. I was keeping jargon to a minimum so that might sound ironically like "BBQ conco". The flying reproductives of termites are called aeletes. They have four fixed wings. I have beena round a lot of scientists who study termites.

So did you mean weather prediction or water location? Don't hesitate about to write formal, and even harvard/cambridge/academic English on this forum, it's quite a strict forum for science level. It helps others to learn good English and the ops like it.  I didn't have time to check the results for animal sense of weather prediction, but there are lots of examples and explanations of many animals.

Both if the animal is using their senses to find it.

The termites may not detect the moisture, only the pressure drop. same goes for most rain prediction in advance, the air would still have the same humiditiy.

Actually that is not true. Termite alletes will only be booted from their nest when [1] there is some increased humidity [2] the temperature is hot but not too much - 30 degrees centigrade approx, [3] little wind so they can fly better. I have observed first hand dozens of allete flights.

As a newcomer, a friendly word of advice regarding your response to the downvote (not from me). Be careful. Although I appreciate your frustration and have been in a similar situation, it is not obligatory to explain a downvote. Often, when I have done so, this had made the situation worse because the poster has objected to my criticism in an inappropriate and intemporate manner. From which you may see that an expression like "have the guts to comment" is inadvised and not in the "be nice" ethos (that the mods keep reminding me of).

Ok, thank you! It is not obligatory. But it helps.

I should have made a suggestion. You could grit your teeth and write “It would help me to improve my questions in the future if the person who downvoted me explained why”. You’re unlikely to get a response, though.

I think you simply Can't.
To design an experiment you need 2 things:
1- Something Common between Humen and Insect and can be measured.
2- Different scale to order the species.
And I Think here you just do NOT have both criteria.

One of the common factor one can use is "hygrosensation receptors" or their homologs. After that one can compare the technical properties of such receptors (like latency, sensitivity etc) to get rank list. Similar successful attempt have been made in the case of Vision. One can rank insects to humans for specific visual task based on their photoreceptors. [e.g. Visual Motion Processing (Clark and Demb 2017)]


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Nuclear vs Cytoplasmic Fluorescence
When staining transciption factor proteins with fluorescent antibodies (Alexa, etc.), why are the fluorescence signals stronger in the nucleus as compared to fluorescence signals in the cytoplasm (in context of transcription factor-activation?)
Is it simply spatial localization, that more fluoresence-marked proteins are at the same place, or are there other factors related?

Can you please clarify what you want to know. —— Do you find a strong signal in the nucleus surprising? Given their function, where would you expect to find transcription factors?

Yes, your hypothesis is correct. There are more of them.
A few terms need clarifying here, just in case...
First, fluorescence is due to the property of a dye that can be conjugated to the antibody. Different fluorophores have different properties, some are more efficient than others. Some display strong "solvatochromism", i.e. they are happier in the hydrophobic environment (brighter and red shifted).
Second, DNA is stained not with an antibody but with the UV fluorophore DAPI, which shines brighter in DNA —same thing with ethidium bromide and Sybr Safe.
Now, if you are labelling a TF and they ought to be in the nucleus you definitely will have a brighter signal as you suggest. There will be a way-ever-so slight difference as the environment is less aqueous, but the nucleus is not that packed as on pictures.


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How can paternal chromosomes be present in an egg cell during meiosis I or crossing over, if fertilisation has not yet occurred?
I am very confused about crossing over. It is said that crossing over increases genetic variation as it is a combination of paternal and maternal chromosomes. However, crossing over occurs in meiosis 1 but meiosis 1 occurs before fertilisation, so my question is how are there paternal chromosomes in an egg cell prior to fertilisation.

Maternal and paternal here are referring to the mother's parents, not the father that is fertilizing the egg.

when they say paternal chromosome, they mean chromosome of the father of the organism. Not the father of the offspring of the specific organism. During meiosis ,in order to form the gametes, the chromosomes of the mother and the father of a specific organism interact, because homologous chromosome pairs consists of a pair of the organism's fathers chromosomes, and the mother's.
please tell if you still don't get it.


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Is there anyway from which we can measure the viscosity of honey using a refractometer?
Is it possible to use a refractometer to measure the viscosity of honey because as we know, a refractometer is used to measure moisture and therefore water influences the viscosity of honey so is there a way that we can use to measure the viscosity of honey that way or using any other method apart from time since time has a high percentage of uncertainty?

Theoretically, if refractive index and viscosity are both simply functions of moisture content, you should be able to use one to approximate the other using an empirical standard curve. However, based on this paper, it looks like the relationship between moisture content and viscosity at 25C can vary quite a bit between different types of honey, expecially down below ~18% moisture. So I'd be pretty hesitant to rely on refractive index for acurate viscosity measurements unless you first rigerously validate your methodolgy against empirical viscosity measurements.


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Protein half-life regulating gene expression
Are there any instances in real life of protein half-life regulating gene expression? For example, in a cell, Gene A produces a starting population of protein P, after which the expression of the gene is turned off. The starting population then degrades over time. When the numbers of protein P are reduced to roughly half, the transcription of Gene B, which had been repressed until then, is turned on (perhaps a byproduct of the protein degradation acts as a transcription factor for Gene B?)
My apologies if the question does not make sense. I am a sci-fi author, trying to design a synthetic virus for my novel - a bioweapon of sorts. The scenario is that the viral genome, upon making its way into the nucleus of a human cell, goes into a lysogenic phase, where the genes for its replication are turned off.  The virus needs to initiate its replication only after a certain amount of time has elapsed, say X days. X is the half-life of protein P, which is produced by the viral genome while lysogenic. After X days, transcription of the rest of the viral genome is turned on, and the virus starts making copies of itself. Only this time, the copies go straight into lytic mode upon infecting a cell and start multiplying exponentially. My fictional virus has mechanisms to suppress interferon signalling and evade the immune system (for some time at least, until it gets out of control in the host body).
I am aware that some real-life viruses that infect bacteria can switch between the two phases, but the trigger for the switch is always an external event - like UV damage - and not something controlled by the virus itself. In my scenario, I want the virus to behave like a programmed timer, turning itself on after a fixed elapsed time.

Some variation on quorum sensing based autoregulation maybe?

Many processes are mediated by (usually active or catalyzed) degradation of proteins. For example, cyclin proteins are degraded by the ubiquitin pathway as part of the cell cycle, allowing the cell cycle to proceed. They are however helped along on this by catalysis via ubiquitin ligases.
I was not able to find any examples of a "passive" degradation of a protein regulating anything, but it might be very difficult to demonstrate in any biological system that a degradation process was truly passive.
It seems that the main thing you are interested in is epigenetic memory of a cell- e.g. a way of measuring time lapse in a biological system.
It's not exactly the same, but you may be interested in processes like the cyclomorphosis of Daphnia, which are effectively transgenerational epigenetic memory. I'm hazy on the molecular details though.
Another option might be something like a DNA methylation clock.


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Why are these nesting magpies building another nest
Pair if eurasian magpies occupy a nest visible from my balcony. It's the nesting season for them here, and I assumed they have laid eggs. I can't see the eggs directly, but one of the magpies has been regularly sitting inside the nest (at least for last two or three weeks) and they always attack other birds that come too close.
Today, they've started building a new nest on another tree. It's pretty close, the nests are about 20 meters apart. They still visit their original nest.
What does it mean? Is it a sign of nesting failure? Does it mean their original nest is no longer sufficient?

I found an article that explains secondary nests as backups in case of nest usurpation by other birds:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4858914/
This is for black sparrowhawks losing nests to Egyptian geese around Cape Town. They measured number of nests built per breeding pair of sparrowhawks and found it to correlate with number of Egyptian geese present and especially their nest usurpation behaviour.
That article mentions brood parasitism (e.g. cuckoos) as another possibility for other birds, and I've seen references to duplicate nests with eggs in each. ( https://www.tandfonline.com/doi/pdf/10.1071/MU939286a )


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Recommended books and articles on the origin and evolution of sexual reproduction?
I'm interested in learning about the origin and evolution of life on Earth. In particular, one topic that puzzles me a lot as a layman is the evolution of sexual reproduction, since the DNA mutations have to be such that they affect both female and male in a coordinated way so that their reproductive organs match with each other in order to make the sexual reproduction viable. Would you guys kindly recommend me high quality books and peer-reviewed articles on the matter that hopefully can clear these questions out? Thanks in advance.


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Where does the pain from headaches come from
I may be wrong but I have always thought that the brain doesnt have any nerve endings, so why is it we get headaches and where does this pain come from?
I have heard lack of sleep, hydration or stress can causes headaches but I am interested in why and where the pain comes from this.

I knew it would be somewhere, I just couldnt find it .. Thanks

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Looking for dataset of proteotypic and non-proteotypic peptide
I doing experimentation for peptide prediction using machine learning. I need some data for testing. My background is Computer Science.
Any advice how to find proteotypic and non-proteotypic peptides. I already got one dataset "Y.pestis". However, I'm looking for another dataset (for verification). For example, S.typhimurium or S.oneidensis, but any other peptides will be OK.
I tried PRIDE archive, but I couldn't figure out how to get two datasets; one for proteotypic and another for non-proteotypic
Any advice is appreciated!
Thanks!

I suppose anyone answering this question would already know what a proteotypic peptide was. I don't find the definition totally clear from brief literature searching. From your question it would seem to mean a peptide that is unique for the proteome of one organism. Is that so? Do you know how the Y.Pestis dataset was prepared? I should imagine it was done computationally, in which case it would presumably be easy to apply to any other characterized bacterial genome.

Yes, peptide that is unique for the proteome of one organism e.x E.coli


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Are there computational models verifying the feasibility that complex biological systems can emerge by random mutations plus natural selection?
I am interested in studying the theoretical feasibility that very complex systems such as the vascular system, the respiratory system, the nervous system, the digestive system, among others, could have emerged by means of random mutations plus natural selection. Are there computational models that have successfully verified (via simulation or other means) the theoretical feasibility of the Darwinian hypothesis that random mutations plus natural selection can indeed give rise to sophisticated systems under the time constraint and the environmental constraints life on Earth probably had to face? What is the state of the art (as of 2020 and later) on this regard?

Yes, those exist.  Look up "Artificial Life" , "Genetic Algorithms"  and "Evolutionary Computation".

Thanks for the search keywords, but do you know if they have been able to successfully simulate DNA mutations in a population and see if new organs or new systems can emerge from that? Maybe asking for a 100% accurate simulation of a biological organism can be too much, but at least an approximate simulation, as close to reality as possible. Do you know if anything like that has been done?

Eyes have been evolved digitally.  I dont know about ohher organs.  Starting from DNA per se has not been done, because we don't yet know how to calculate the process of producing an organ from DNA instructions.  However, the principles of evolution have been extremely well verified digitally as well as in the lab, as in "directed evolution".

Awesome. Can you share some references to learn more about this? Especially on the evolution of eyes digitally.

Here is one.  Really, a Google search will get you pretty far down this road.  https://ieeexplore.ieee.org/abstract/document/8790284


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Ants and their love for sweet and sugar
I have observed many times that ants are able to reach the box where sweet items are kept even if the box is kept in secret.
How do they identify 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). At very least please search on this site for before posting — there are several related questions with decent answers present.——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and either delete or [edit] your question accordingly. Thanks!


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Radiation mutation breeding in plant seeds: practical aspects
I did read some seed irradiation papers and they all use Gy as unit of measure, however I have never seen seed weights reported.
How did they calculate that, since Gy is J/kg?
Differencies aside between using gamma and X-rays, is there any equivalent dose I can apply using an X-ray tube fitted with a dose area product meter?
I am not sure if I can assume that spreading seeds in an area and then irradiating up to a certain dose area product would mean that each of those seeds was exposed to a certain amount of radiation.
Suggestions welcome, thank you.

It might help if you shared a link to one of the papers you're talking about. I don't work with seeds, but I wouldn't expect to see the actual weights reported since the unit is already normalized to weight. For example, if I'm reporting on arsenic concentrations in the liver, I'm analyzing the normalized data in units like ng of arsenic per gram of tissue, and my methods section describes how those values were calculated prior to analysis. I would imagine that whoever makes the instruments used for irradiating seeds have standard protocols available online.

I see. So should I assume that they weighted the seeds and irradiated until they reached a certain amount of J/kg, hence being Gy?

Here are some links: http://en.cnki.com.cn/Article_en/CJFDTotal-JXNY200709006.htm https://inis.iaea.org/search/search.aspx?orig_q=RN:41095572 https://www.actahort.org/books/1067/1067_9.htm

As a general rule, you shouldn't have to assume things when reading a scientific research article. They should include some indication of the methodology or protocols used. Saddly, that's often not the case. I'd try reaching out by email to the corresponding author on a paper your interested in and politely requesting their protocol. Most people are usually willing to help. You could also try contacting the manufacturer of the instrument you are working with for support. Sorry this didn't really answer your question.


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Why is a cell in anaphase (without a nuclear envelope) be considered as a eukaryotic cell?
Can anyone shed some light on this? All I can think of is that it has something to do with the chromosomes being paired

Related, possibly could be considered a duplicate though it's a bit parallel rather than directly duplicated: https://biology.stackexchange.com/questions/10404/are-mature-erythrocytes-prokaryotic

Does this answer your question? Are mature erythrocytes prokaryotic?

Organisms are classified as either eukaryotic or non-eukaryotic, not individual cells. This organismal classification does not change with momentary alterations of cell physiology during the cell cycle.

It is still considered a Eukaryotic cell because the daughter cells and mother cell are both Eukaryotic; the chromosomes will condense and be contained in a Nucleus after Telophase and Cytokinesis. Furthermore, Prokaryotic binary fission does not involve the assembly of Spindle Fibers, whereas dividing Eukaryotic cells in Anaphase use Spindle fibers to transport the Chromosomes towards the poles of the dividing cell.
I hope this answers your question!! :)

Only eukaryotic cells are able to under go a mitotic/meiotic cell cycle, in which, after an interphase of variable time length, such cells enter M-phase, and one of the regarded phases of such stage is anaphase, so in order for a cell to undergo chromosome segregation in the form of anaphase, it has to be eukaryotic.


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How effective is rinsing in removing microbes from surfaces
Microbes including viruses stay alive on surfaces depending upon the type of the surface like steel, wood, plastic, glass, marble etc. How effective is rinsing these surfaces with tap water in removing the existing microbes. I couldn't find this information on internet. Please provide source for your answer.

I am not asking answer for every microbe and every surface. Whatever research and information is available on the subject is valuable and can be used to theorize.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and then [edit] or delete your question accordingly. In particular, avoid "questions with too many possible answers or that would require an extremely long answer".  ——— We also expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

Rinsing the surface will make the micro organism growth static on the surface i.e it removes the micro organisms from the surface,but it is only for time being.But it is not effective in killing the micro organism.Mostly in labs,70% Alchohol is used to disinfect the surface.It is more effective in killing the organism.

As you are a new contributor, can I make the friendly suggestion that you would benefit from reviewing the Help on Answering questions. One key point is that stating an opinion is not sufficient. Evidence should be cited in support of your answer, generally in the form of references to papers or websites, preferably with links. Otherwise nobody can judge. Otherwise, how can the poster or readers judge whether your answer is correct or not? And it's worthwhile reading the section on only answering well-asked questions.


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How can prokaryotes repair double strand breaks by homologous recombination if they're haploids?
Title says it all, I must be going crazy.

Several answers to this question:

Much of the time what bacteria are doing to repair DSBs is actually non-homologous end-joining, which does not require strict homology. This is the more likely mechanism earlier in the cell cycle when copy number is more likely to be ~1.
If cells have completed DNA replication (later in the cell cycle), there are at minimum 2 copies of all DNAs present in the cell. These can be used for homologous recombination.
Bacterial chromosome copy number can be overreplicated in some situations, such that DNA replication is not synchronized to the cell cycle and is more than normal for a cell. In these situations copy number can be >2.


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How is energy stored in the cotransport of molecules down to its electrochemical gradient?
I am talking about symporters and antiporters, that transport usually an amino acid against its concentration gradient while at the same time transport another molecule down its electrochemical or concentration gradient or both. It is said that "cotransporters use the energy stored in electrochemical gradient", but I do not understand what do they refer to when talking about storing energy.
Thanks in advance.

Hey Laura not sure what exactly your question means. Please read the theory about electrochemical potentials in general and ask your question again.

Please give a source for your quotation, with a link if possible.  For one thing, it lacks context, and for another the lack of an article before “electrochemical” suggests you are paraphrasing or quoting from memory. We need more and precise information if we are to help you.


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What are the limiting factors of pathogen population size in human populations?
I understand that one limiting factor in non-human animal populations is that increased pathogen populations decrease animal populations from killing them, which decreases the density of the animals, which makes it harder for pathogens to infect other animals. However, pathogens, at least in developed nations, don't seem to kill a large enough number of people for this to be the main limiting factor. So what else are the limiting factors?

One of the limiting factors is how many uninfected hosts exist. As a pathogen becomes more widespread, the probability of someone infected with it infecting someone else decreases, as it's more likely that the person will spread the disease to someone who already has it instead of someone who doesn't have it, preventing the virus's population size from increasing. See this for more information.
Also the more common a pathogen is, the more likely it is that people will take actions against it, for example by being more sanitary or getting vaccinated against it.


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books for beginners in research in mathematical biology
I am a M.SC(mathematics) student. I have no subject like mathematically modelling.But  i'm interesting in research in mathematical biology.Initially which book i should study.
Please guide me.THANKS...

This is far too broad to answer effectively.  We don't know anything about which specific areas you are interested in or what your level of ability is, aside from that you haven't had any mathematical modeling coursework.  Most books would probably be accessible for someone with a background in ODEs, and I'm sure you've had experience with those.

additional info is needed for sure. Everything can be mathematically modeled.

Beside the Otto & Day book, also consider Murray's Mathematical Biology: I. An Introduction (also Mathematical Biology II: Spatial and Biomedical Applications). It covers different applications and is written for people coming from a math background.

Probably the best contemporary book taking a broad view of mathematical biology modeling is Otto and Day's 2007 book A Biologist's Guide to Mathematical Modeling in Ecology and Evolution published by Princeton University Press.
There are also a number of books that focus on more specific areas e.g. mathematical population genetics, ecological modeling, infectious disease epidemiology, etc. But without knowing which areas of modeling interest you it is difficult to recommend at this level.

sorry for too late comment ...i'm interesting in mathematical population genetics

The post is too broad. Mathematics is used in tons of different fields of biology.
Population genetics is one of the main field of biology that is contains quite a lot of mathematical formulations. This post gives a list of references for books in population genetics.

was this perhaps intended to be a comment?

You are right. It should have been a comment. Too late to add comments though.


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Yeast absorption of different spectra of light
I'd like to monitor the growth of a yeast population by shining light through it and monitoring the change in light that gets through as it grows. I'm not sure if I should use IR, or any particular colour of light.
Are there any charts that show the light absorption of brewers yeast to different spectra of light?

Usually the growth of microorganisms is monitored at 600nm.

Why not just run a spectrum of a yeast suspension and zero it to blank growth media?

You can also use a plate reader and 96 well plates it its feasible for your experiment.

Thanks for the comments. I am going to use Chris's information and try with a 600nm LED.

Here I have "Kilju" made with two different yeast. On is a blend of wild yeast and d47 I made wine with last year, and the other is bread yeast. One (the bread yeast) has additive light reflection (as in it appears to be brighter) while the other is subtractive and looks as if it absorbs light. https://i.sstatic.net/Ffp5I.jpg

Most of the loss of light being transmitted through individual cells is not absorbed, rather it is scattered (redirected from its original direction to a new one without loss of energy).  There is actually not very much in cells that can absorb visible light, and virtually nothing at all that can absorb many red or near-infrared wavelengths.
Scattering does depend on wavelength, but the relationship is very complex.  For scattering from small cellular components (mitochondria for example), Rayleigh scattering dominates, which will decrease with the 4th power of wavelength, so that green light will scatter much more strongly than red.  For larger components that are comparable or larger than a wavelength (nuclei or whole cells), scattering will increase much more slowly.  The relationship between the direction of scattering and the size/wavelength is even more complex, but is very useful in applications like label-free cytometry where cells can be sorted based on scattered light.
600-800 nm light is a reasonable choice because it will not damage the cells unless the power level is very high, although using shorter wavelengths may give you more sensitive measurements.

authors: Александр Званцев


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Are nucleic acids found in cell membranes?
I've found various results online and I was recently marked in on an important test as wrong when I made the assumption they were not found in the cell membrane. Does anyone know what the correct answer is in this case?  Thanks in advance.

Nucleic acids are not structural components of cell membranes (ribosomes and nucleus are the main places where they are found).
However, being open system, cell exchanges chemicals with its surrounding and cellular membrane can transport nucleic acids as well. This is why these acids can potentially be detected in the cell membranes.
If you have the exact question expression it can help with more precise answer.

Heterochromatin is anchored to the nuclear envelope by lamins, and they actually found here that this is important in expression and differentiation during development. Not saying that nucleic acid is a core component, but the interactions between that particular membrane and nucleic acid is important. An interesting tidbit to consider, IMO.

No, plasma membrane does not contain any nucleic acids – DNA and RNA. The main components of plasma membrane are lipids, glycol- lipids, phospho lipid bilayer and cholesterol.

Also contains proteins: https://www.nature.com/scitable/topicpage/cell-membranes-14052567/


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During the process of correcting mutations via gene therapy, is the defective gene removed?
Just recently started learning about gene therapy, many websites explain that the corrected DNA can be added to the genome using a vector and all that. I just don't understand what happens to the other sequence of nitrogenous bases that codes for the incorrect protein.
Thanks in advance for any answers :)

To be specific: I am talking about adult, somatic gene therapy here, and germline gene therapy experiments is still a landmine when considering ethical reasons.
The defective gene codes for a defective protein, that usually plays a part in pathways. Since the protein is also defective, that pathway is also rendered defective because of this protein, and usually when pathways go defective, bad things happen.
There are three target approaches to gene therapy:

Gene silencing by Antisense Oligonucleotide Therapy
Genome Surgery by ZFN, Crispr/Cas9 etc..
Gene Replacement by viral vectors

The only method that corrects the defective gene here is the genome surgery method. By using Zinc Finger Nucleases, or Crispr/Cas9s, TALENS or other methods like that, the defective protein is corrected at the genome level, which automatically corrects the mRNA and protein, and everything works as it should.

Other methods like Antisense, just prevent the incorrect protein from forming. This is really useful if the defective protein is itself toxic to the body, and a replacement protein can be achieved by masking the defective region to produce a truncated but functional protein.

Gene replacement usually puts in a healthy copy of the gene in, that functions along with the defective copy, and this solves majority of the problems as the affected pathway is no longer rendered inactive, as the healthy protein takes over the defective pathway. The defective protein is still produced, but doesnt do anything (or rather, is rendered moot as the healthy protein takes over) and gets removed during regular maintenance of the cell.

Now depending on the type of disease the individual has, gene replacement may also take place along with gene knockout (depending on if the defective gene is toxic), but obviously many considerations have to be thought about before the combinatorial therapy can be used (toxicity of treatment itself being the primary concern, followed closely by efficacy).
Now obvious question with gene replacement, antisense or any other form of gene therapy is how we get the therapeutic agent to all cells, and yes that is a major challenge, and that's why gene therapy is expensive. And no, the therapy doesn't correct all the cells in your affected tissue, but it aims to correct majority of the cells, and that should restore function (atleast in myopathies like the muscular dystrophies)
As you can see here, in DMD, dystrophin gets muated due to a mutation We can either mask the mutation by Antisense therapy at the level of the RNA (which leads to a functional protein forming), put in an alternative form of dystrophin (mini or micro dystrophin) that takes over the function of dystrophin in majority (if we are so lucky) of the cells, and the overall phenotype of the individual improves. Recent advances in genome surgery are also being investigated for ameliorating disease symptoms. The reason I concentrated on DMD is that, gene therapy for DMD is my PhD. So apologies for the bias.

Very informative and helpful response, I really appreciate when people go above and beyond, and give well written answers such as this.


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Hybrid seed production requires a male sterile parent. Why?
Hybridization is the process of crossing two plant species or varieties. In this case, two varieties of plants. In plant breeding, crossing is a very useful technique to improve the features of the offspring. For example, if a maize corn variety has lost yield over the years, it can be crossed to a variety with a higher yield and the offspring will also have a higher yield.
In order to cross these two varieties, the male needs to be sterile. Why is that? I don't understand how the process works and I cannot find the reason anywhere. The answer should be pretty basic, and I think I am missing something that everybody assumes I should know.

male-sterility is not required for breeding.
Male-sterility means that the female acting plant (the plant that will bear the fruit) has sterile male organs (either dysfunctional anthers or sterile pollen). and won't self pollinate. The male-acting plant is fertile.
In monoecious plants this is helpful for breeding because we can't easily provide a controlled pollinating environment by separating the female and male organs
Tomatoes are monoecious (hermaphrodites), self-pollinated. The pollination occurs (usually) before the flower opens. Male-sterility prevents pollination and allows the breeder to pollinate.
Corn is a cross-pollinated plant with some capacity for self-pollination, male-sterility in corn helps ensure that the corn plant is not pollinated by itself.
Male-sterility gives peace of mind and easier breeding techniques but is not a requirement.
You can expand your knowledge using Principles of Plant Genetics and Breeding, Second Edition by George Acquaah. Check chapters 5: Introduction to Reproduction and Autogamy.
Searching "male sterility in plants explained" in google yielded many relevant pdfs.

To get a hybrid you need pollen from a different plant. Corn is likely to self-pollinate if some action is not taken to prevent it. I don't know of sterile males plants - in the US corn belt the self-pollination is prevented by detasseling. Many young people get summer jobs detasseling (cutting off the tassels) for seed corn.

My kids did some tasseling ; It was a good paying summer job. Maybe I can get one to post what they did. I took their word for what they did. I just saw a group of teens in the corn rows ( if they were near the edge of a field.).


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Infectious deadly disease among free animals?
Sorry for the presumably naive question, I'm not a biologist and searched for that but didn't find a clear answer to this question.
What I would like to know if deadly infectious diseases are common also among free animals (I mean living free in nature, not in captivity)? Therefore I'm NOT referring to the transmission from animals to humans like covid, bird or swine flu, rather infections that have caused several deaths among animals living in a natural environment without affecting humans? Is that something quite normal in the animal kingdom too? Presumably also before the appearance of humans? Or does it not happen? Or is it rare but exists? Eventually a link to some article or paper on this would be welcome.

Just as a brief response, yes, it happens all the time. There are endemic infectious diseases in wild populations all over the planet. We are definitely not unique in that. Here is an interesting BBC story about some of them from several years ago.

As far as scholarly articles go, here is a collection of them from Acta Veterinaria Scandinavica on BioMedCentral.


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Evolution: what were we doing for 100.000 years?
I'm not a biologist/anthropologist but there is a question that comes up again and again and which I couldn't find any deeper thought, even not a speculation. As far as I understand it, according to modern evolutionary science, the anatomically modern Homo Sapiens Sapiens exists since about 100-300.000 years. Lets be conservative and take 100.000. However, human's ability to build a culture, a society, a civilization that uses the rational mind, an analytic thinking that gives birth to philosophies and, even more recently, to science and technology showed up only very late compared to the human's history. Lets say with the Sumer civilization about 3.000 BC. Now, this implies that, despite having anatomically a fully developed brain, for about 95.000 we were doing not much with our intelligence other than hunting, surviving, develop very rudimentary tools, migrate and not much more but without any cultural development which one should assume is proper of a human brain such as thinking, developing increasingly sophisticated tools, develop philosophies, religions, arts, music, sciences, math, technologies, etc. The latter even not much developed before the scientific and industrial revolution in the last few centuries.
This doesn't make much sense to me. One might argue people were busy with surviving, there was no education and we couldn't develop our IQ, there were no books for cultural transmission, etc. This might be part of the answer explaining a stop of cultural evolution for some centuries, even some thousand years, but for 100.000 Years? This doesn't look to be the fully picture.
So, my question is if there is something (article, book, etc.) of someone who pondered on this aspect in more detail? Is there a possible explanation why evolution produces a brain without using its full capacities for 95% of its existence so far? Are we 100% sure that the brain humans had 50.000 ago are the same we have nowadays?

If you think hunter gathering does not fully utilize the brain I suggest you try it for a month, if you survive I think you will understand just how much thought needs to go it survival. I also suggest studying history to see just how slow technological progress was before the advent of science. this question is one big misunderstanding of a person in a very privileged position in time and location.

This question contains potentially interesting aspects (although I think there are several false presumptions in the post - for example, go and look up the Lascaux cave paintings), but I think it's off topic for biology. Biology can't give you the answer to the question you have.

I’m voting to close this question because it's not about biology.

If you gave paleolithic people some neolithic age F1 crop choices, corn/potatoes/sheep/beef/wheat, they could have enough food for thousand strong tribes, and civilizations 45000 years ago. Just imagine giving aborigines and papuans some cows, melons and corn and letting them form civilizations.

I can think of two factors that could explain why a civilization took so long to appear despite humans having fully developed their capabilities.

Civilization is built into previous achievements: this generates an exponential growth in technologies making it easier to improve or create technologies giving that you already have the tools to create it. Think about a simple light bulb, how long it would take you to build one from scratch having to build any tool you use? Having this into account is not surprising that a fully articulated language could take thousands of years to be built from scratch.
Population size: 100-10K years ago the human population was a fraction of what it is now. This would slowdown civilization if we consider that development is proportional to the population.

The measures and reasons for the evolution of behavioural modernity https://en.wikipedia.org/wiki/Behavioral_modernity?wprov=sfla1 have generated many theories, like for the FOXP2 gene that works on human speech.
Biologically we can consider the evolution of crop species and their yields and docile livestock as a non-human evolutionary change which has massively boosted human culture into civilizations i.e. wheat, potato, corn, grape yields
If you study "the evolution of stone tools", there are theories of the full planning and workflow to shape difficult stones into fine craftmanship, which give an intuitive grasp of cultural and biological increments in technology. The crafted tools of humans changed gradually and radically over the last 70k years. That study doesnt overlap much with biology though, because of sparse biological evidence.
There are also mathematical formulas to chart the evolution of intelligence / noogenesis as a sum of the total synapses in many individuals communicating together, something that changed exponentially recently when humans made tribes of many thousands.
Tribal humanity becamy civilization. Aborigines and Maori and Papuans and tribal north Americans and Eskimo all represent different cultures of technologies and tribes.
There seems to be a synergy of many synapses communicating, when tribes group into civilized cultures of 1000ds of humans, further boosted by emergent technologies like agriculture, which is represented in indus valley/egyptian/mayan cities, which accelerates the technologies in a confusingly exponential way.


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Homology ratio comparison between different species
I found the following homology ratio:
protein coding genes of the organism with an homolog in mouse / all protein coding genes in the organism
I have done this for all protein coding genes between several organisms and mouse using a phylogenetic-based approach. I have noticed that the ratio found between an organism and mouse is greater than the ratio between another organism and mouse! On the other hand the second is evolutionary closer to mouse than the first.So:
1.Is such an approach trying to quantify homology? Which i know is not correct as homology is qualitive measure.
2.Can we compare the ratio of homology between the above 2 couples od species or such a comparison is biased?
3.Shouldn't the ratio of homology be proportional to the evolutionary distance of the organisms (according to conservation)?
As you can understand, in the way i calculate the above ratio, i don't take into account the one-to-many or many-to many relationships! I just take into account the genes that have at least one homolog in mouse..is that the bias of my calculation?

You want to compare the homology of proteins between species? To do so, see how phylogenetic trees are built.

There is the path of gene trees and species trees though! I am checking genes so i should care about the gene trees,correct? For example :  It is very possible that in my analysis of gene X, species A is closest to mouse, while for gene Y species B is closest to mouse and that's where a bias is introduced!

I don't understand your example, sorry.

Phylogenetic trees are usually much more complicated statistically/mathematically than simply ranking based on coding DNA homologies. Not going into the details (because I don't know enough about it) but in essence they try to reconstruct the best fitting tree amongst multiple organisms taking in account effects such as horizontal gene transfers and sequence conservations. Bottom line it is not a simple pairwise comparison between two organisms coding sequences and I am not too surprise you see an organism being closer than you would expect. My advice to you is trust the phylogenetic tree.

1.Is such an approach trying to quantify homology? Which i know is not correct as homology is qualitive measure.

A common approach to identify orthologs (homology between two genes resulting from a speciation event) it 'best bidirectional match': if you blast gene A (in species 1) against all genes of species 2 the best match is gene B, and if you blast gene B against all genes of species 1 the best match is gene A.

2.Can we compare the ratio of homology between the above 2 couples od species or such a comparison is biased?
3.Shouldn't the ratio of homology be proportional to the evolutionary distance of the organisms (according to conservation)?

Not necessarly. The fact that two genes diverged a very long time ago does not prevent them from being homologous. Homology is about shared ancestry (here of two genes) and not about evolutionary distance.
Could you clarify how you get the homologies? Did you compute them yourself (if so how) or did you use a specific database?


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Can you do better than "Sock-Wasp"?
I met this beautiful fellow when I was choosing my socks this morning. It seems I had found her cozy place. A stowaway, supposedly sneaked into my bag while camping, and me taking her all the way home. She just sat there for about a minute (probably just as tired as me, thinking "Duuuuuude, why did you wake me?"), then stretched her neck and and set off, searching for a calm spot to get her 5 more minutes.

Ca. 3 cm long. At home in Austria/Southern Germany.
I searched the internet a bit, and I think it's a female wasp, possibly Dolichovespula because of the pointy snout(?). I don't think it's a commom wasp, due to its size. Also no median wasp queen, because there's no red.
Maybe a tree wasp?
TL;DR: Can you help me identify this buzzer?

End of story:
After a lot of buzzing on her side, me chasing her with glass and cardboard in hand, and she dozing off two times in very uncomfy places (I was a bit embarassed about how un-hospitably dusty everything was), she settled for a box of clothing and snuggled her way into my shirts. I praised her sense of Cozyness, but then carefully emptied the box piece by piece outside and found her inbetween a flowery garment. She slowly stuck her head out from the folds ("DUUUUUUDE, again?!") and flew around the terrace for a while. I hope she's found a snug place out there.

It really is beautiful.

I presume it is a female Dolichovespula adulterina living in the Palearctic (Austria and Germany) and Nearctic regions.


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What would be the difference if I use the Web server instead of dedicated server for protein modeling and docking?
We know that software tools like I-tasser etc have a web server and a standalone option too. Is there any difference to protein C-scores or efficiency or accuracy if you do it on standalone instead of web server?
What would be the difference if I use the Web server instead of dedicated server for protein modeling and docking?. Available from: https://www.researchgate.net/post/What_would_be_the_difference_if_I_use_the_Web_server_instead_of_dedicated_server_for_protein_modeling_and_docking [accessed Apr 27, 2017].

I don't understand the link to Research Gate. Please explain.

There should be no difference in output.*** The big difference is likely going to be in the size of the analysis you can perform, and how fast the analysis is performed. A lot of web-servers have a job size limit to prevent one person from hogging resources unless you buy greater access. On a public web-server, your job is queued with everyone else's. If the server is in high demand, you may have to wait along time for your analysis to kick off.
***: I said there should be no difference in output and that is true if you set up your server the same as the public webserver with the same parameters used for analysis execution. This could be a good or bad thing depending on what you are trying to accomplish. Some public webservices do not give you access to all parameters, so setting up your own may give you the ability to tune your analysis to a greater degree.

Good answer, but it could be made better with some references. This community asks that answers cite reputable sources so as to ensure higher quality (and hopefully accurate) answers across the community. Thanks.


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Do organs or any structure in the human body shrink/shorten if it's function is no longer useful?

Charles Darwin was one of the first scientists to theorize on the function of the appendix, which in his day had been identified only in humans and other great apes. He hypothesized that the distant ancestors of these animals survived on a diet of leaves, and so they required a large cecum, a portion of the gut that houses bacteria that can break down stubborn plant tissue. Later, he speculated, these ancestors shifted to a largely fruit-based diet that was easier to digest. A large cecum was no longer necessary, and it began to shrink...Darwin thought the appendix, which juts off of the cecum, is one of its former folds that shriveled up as the cecum shrank. Consequently, he thought it carried no function.

I recently read a source which states the above. It made me wonder that if there is some other organ/part in our body which may shrink as further evolution progresses and it's use diminishes, just like our appendix. I'd like to know if this 'theory of shrinking' applies to any organ that may become useless.

If you read the Wikipedia article on the appendix, you'll see that the hypothesis of vestigiality is simply incorrect. It is quite important in maintaining the balance of flora in the gut, and also plays an important role in immunity. Remember, Darwin lived 150 years ago, and not everything he proposed was correct. Even Einstein was wrong on occasion.

Reading your title you seem to be talking about development, while the post is about evolution. You should check the definitions of these two terms if they are unclear to you.

If you were interested about development (but I doubt you are), muscles and bones would be good examples.

You should link to the original article you are quoting.

@MattDMo I've read this article thrice but nowhere does it state for sure that the appendix DOES HAVE THIS FUNCTION ONLY and without it our body will suffer complications. Not just Wikipedia, but almost every site uses the phrase '...may have this function' or 'may house good bacteria...' far too much. And Huffington Post still states it's function to be 'in much debate'.

You're using the Huffington Post for scientific information??? Could you maybe try journal articles from the past few years instead?

And you're actually trusting Wikipedia on this??

It's not just Huffington Post it's practically every alternate web result that states this.

First of all, our appendix isn't 'useless'. Their is a high concentration of lymph nodes (higher than anywhere else in your gut), so it might not be needed for digestion anymore, but it's function somewhat shifted to a more immunological role.
Secondly, yes there are other organs/body parts that shrink over time. In evolutionary time, look at our tailbone. In monkeys it's still a full tail, in apes it's almost nothing, and in humans it's still present in the skeleton, but not visible on the 'outside' anymore. Probably in a few (hundred/thousand/..) years it will be completely reduced until it is no longer present in the human skeleton (because since we don't have a tail anymore, it doesn't have any function anymore).
Over a much shorter timescale it is also possible. For example the thymus expands in puberty, and afterwards it shrinks until it is almost completely gone.

The thymus does not shrink because of vestigiality or lack of use. It is simply part of the development of the immune system, that T cell maturation and development moves from it elsewhere, like the lymph nodes, spleen, and bone marrow. You already repeated what I said much earlier about the appendix. Finally, the coccyx is certainly not without function. It serves as an attachment site for ligaments, muscles, and tendons, and is an insertion point for muscles in the pelvic floor. It is also important for stabilization when you're sitting.


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Why does the rabies virus have such a long incubation period?
So there was a case in India, where a man developed rabies 25 yrs after the dog bite. Source:
https://www.google.co.in/amp/s/m.timesofindia.com/city/goa/25-yrs-after-dog-bite-man-gets-dies-of-rabies/amp_articleshow/16415870.cms
I have the following questions:
1) what are the reasons behind such a long incubation pd?
2) in such cases, can vaccines taken years after the dog bite save the person? (Even though it’s advised to take it immediately)

I think the article described that the virus was sequested in the tissue, and that is why it did not spread. Also I think one can do treatment after exposured although 25 years sound long. I think it depends on if the patient had been vaccinated previously as well. source: https://academic.oup.com/cid/article/30/1/4/323391

This question may not be particularly answerable.
The only available information about this specific case is in the original article (Shankar et al. Ann Indian Acad Neurol. 2012 Jul-Sep; 15(3): 221–223. doi:  10.4103/0972-2327.99728); they say only:

The anatomical site of viral latency and the mechanism of reactivation of rabies, a neurotropic virus, remains an enigma to be unraveled.

Other reports in the literature of long incubation periods (>7 years, the previously reported maximum seems to be 14 years) are scattered/old/speculative, e.g. Gavrila et al.  Ann. Inst. Pasteur 1967 Vol.112 No.4 pp.504-15:

Discussing these cases of prolonged incubation periods, the authors point out that in rabies the incubation period can vary within very wide limits and that it is possible in areas where the disease is enzootic that, in very exceptional cases, the disease can develop after an incubation period which may sometimes greatly exceed the maximal limits now admitted, and that, as for example in cats [this Bulletin, 1965, v. 62, (1106)], stress conditions and so forth may lead to the generalization of the virus until then quiescent at the point of entry.

Plotkin 2000 Clinical Inf Dis 30:1 says

the reasons for this long latency are unknown ...
   in the absence of specific prophylaxis, the virus becomes hidden, only to invade the CNS weeks, months, or years later. Where is the virus during this period? There is some evidence for slow replication in muscle cells and for latency in macrophages, but there is no certainty that these account for the long incubation periods.

There has been an experimental study on skunks (Charlton et al. Acta Neuropathologica June 1997, Volume 94, Issue 1, pp 73–77) that suggests there is some infection of muscle cells at the injection site, but otherwise not much is known about the mechanism.
I would guess that vaccination would be effective if it were administered soon enough, but it will probably be hard in these surprising cases to identify the disease soon enough.

The incubation period for the rabies virus is typically not that long - usually under 1 month.  The reasons for longer incubation period include site of virus entry (where on body the infection occurs) and the viral load (how much virus enters at the infected site). Although there are examples of very long incubation (many months or years), reasons for this are unknown.  You may find the link below helpful - see under "symptoms".
http://www.who.int/mediacentre/factsheets/fs099/en/


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Why do we see better on stretching our eyelids to the side?
I've often noticed that on stretching my eyes to the side I see a lot better. On searching, I read that this happens because the cornea reshapes itself (due to the ciliary muscles). But is that all, or is there a more accurate biological explanation for this?

It is indeed because you're distorting the cornea. I don't think the ciliary muscles are involved (source?) Also, it depends on your vision. Some people with perfect vision will see less perfectly.

You might get pinhole effects in some circumstances, but for me this technique just makes my vision much much worse (and certainly wouldn't be the best way to introduce a pinhole).

@BryanKrause - Although changing the transmission of lightwaves is altered in both pulling the eyelid and looking through a pinhole, the mechanisms are very different. Pulling your eyelid is akin to squinting in the effect it has on the cornea. Pinholes limit the area over which lightwaves can reach the retina.

@anongoodnurse Squinting does both; a quick look around the interwebs suggests the pinhole effect predominates, though I didn't look for actual peer reviewed publications.

@BryanKrause - You're right! "So basically, squinting allows us to see better in two ways: by changing the shape of our eye and letting in a limited amount of light that is more easily focused." TIL. (And I didn't look on Scholar either. But two science pages stated this. Good enough for me for comments. :))


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Do male skunks have teats?
Simple question.  Do male skunks (striped skunk, eastern US/Canada if it matters) have teats?  Occasionally want to identify road-kill, but don't know if teats are diagnostic for females.  I believe they are for racoons.

Petrides, 1950, writes:

Male skunks have tiny nipples which are considerably smaller than those of juvenile females.

and also:

Female skunks which had bred could easily be distinguished from those which had not by differences in the size of the teats

So it sounds like the mere presence of teats is not sufficient to sex skunks, but the size is sexually dimorphic and is probably a reasonable guide with practice, though the differences may be more subtle for female juveniles vs. males.
For pelts, Petrides recommends sexing based on the presence of a penis scar; I presume that genitalia is likely a more reliable guideline than teats.
For roadkill where damage might make it hard to sex animals based on genitalia, Fuller et al found canine size to be highly predictive, though they suggest that a comparison group of sizes from animals of known sex be used for a particular region, so that might not be too helpful for sporadic sexing.
Casey & Webster 1975 discuss sex identification based on presence of Barr bodies in the hippocampus, but their technique would probably not be applicable to your use case.

Casey, G. A., & Webster, W. A. (1975). Age and sex determination of striped skunks (Mephitis mephitis) from Ontario, Manitoba, and Quebec. Canadian journal of zoology, 53(3), 223-226.
Fuller, T. K., Hobson, D. P., Gunson, J. R., & Schowalter, D. B. (1984). Sexual dimorphism in mandibular canines of striped skunks. The Journal of wildlife management, 48(4), 1444-1446.
Petrides, G. A. (1950). The determination of sex and age ratios in fur animals. American Midland Naturalist, 355-382.


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Explain asymptomatic viral infection (ie covid) with no symptoms
There are a lot of people that are testing positive for covid that have no symptoms (ie they are asymptomatic).  This raises the question - does the current test have an unacceptably high rate of false positives?  From a physiological point of view, doesn't an active viral infection of any sort generate tissue damage and hence some sort of response (immunological, inflamatory, histochemical, etc) that DOES lead to outward symptomology?  Viral replication necessarily causes tissue damage (is there a human virus of any sort that does not?).  Tissue damage, especially in the upper airway and lungs, would (it seems to me) cause a response (coughing, perhaps fever, etc) yet we are told that covid is capable of causing asymptomatic infection.  Is this really plausible?  We seem to only have these swab tests as the only indicator telling us these asymptomatic people have the covid infection (or the virus is present in their airways).  This is, naturally, a huge public health and social problem if these tests are false-positives.

Typhoid is an example of an infection that even when it causes symptoms - the symptoms are not readily visible by a bystander (ie caughing by someone with covid).  Is there any other example of an upper respiratory or lung infection that does not cause symptoms ?  The covid test was necessarily rushed into production and that leaves a reasonable chance that it may give false positive results.  And even if covid is somehow able to replicate in the lungs and upper respiratory tract without eliciting an inflamatory response, then how can that person be contageous IF THEY ARE NOT COUGHING?

Pine Street Inn homeless shelter in Boston - Of the 397 people tested, 146 people tested positive. Not a single one had any symptoms.  Testing of the entire crew of the aircraft carrier Theodore Roosevelt - at least 655 Roosevelt sailors have now tested positive - the majority have displayed no symptoms.

Widespread testing of asymptomatic people has until now not been a priority or even seen as necessary or needed or useful.  When it is done, however, it is turning up lots of positive results.  This to me is unexplainable.

'how can that person be contageous IF THEY ARE NOT COUGHING?' because they are breathing and speaking.

As far as asymptomatic caries of other respiratory diseases: in one study Asymptomatic rhinovirus infection outnumbers symptomatic infection four to one among university students

@Peggy Do you want an answer or not? Your responses in comments lean towards "not", which makes this a bad question.

@Bryan Krause: what you consider "bad" about the question could be implying that tests should indicate "symptomatic infections" only - at the same time, it's been said that there are asymptomatic infections that are "infectious". So, the question seem unclear about "infectious infections" that are not symptomatic. Am I allowed to set up some "draft answer" based on definitions? To me, Stackexchange has got all the forms and frames needed to discuss - peers should be more tolerant towards "draft" questions. e.g.  answers her  to me "do not answer the question", however, they are (answers).

There are many examples of asymptomatic virus infections.  For instance,  person can be infected with HIV for years before noticable symptoms appear.  Then there's the varicella-zoster virus that gave you chicken pox when you were a kid, only to lie dormant for half a century before reappearing as shingles.

@jamesqf In fact even flu can be (and often is) asymptomatic.

It isn't just Sars-Cov-2. Many diseases and medical conditions are known to be asymptomatic in some people. The most famous asymptomatic carrier of a bacterial disease was Mary Mallon ("Typhoid Mary"), a woman who was permanently infected by the Salmonella typhi bacteria. She had no ill effects from the infection but spread it to many other people until she was forced into quarantine.
The underlying issue is that our immune systems are highly variable from person to person.

Tissue damage, especially in the upper airway and lungs, would (it
  seems to me) cause a response (coughing, perhaps fever, etc)

It isn't that binary. Your respiratory system is constantly being damaged by pathogens and pollutants, but your body is constantly repairing the damage.. As long as the rate of repairs can keep up with the rate of damage, you may not notice anything. When you feel sick from something like Sars-Cov-2, it's an indication that the pathogen is causing damage faster then it can be repaired. The balance between these depends both on how fast your immune system responds, and how efficiently your repair mechanisms work. Both of these can vary widely between individuals, depending on both genetics and the environment.

First, the 60% asymptomatic numbers for the Roosevelt are fairly consistent (adjusting for age) with those from the Diamond Princess: about 50% at the peak of the infection, but in a much older population. (Also you can be pretty sure the Japanese were using a different test kit [in February] than the US.)
Second, asymptomatic when tested, doesn't mean you won't develop symptoms later, as the damage accumulates. (In fact, accumulated lung damage is the main problem with Covid-19; see q on Skeptics on the death of Rooselvelt sailor.) Nonetheless, the presymptomatic people can shed enough virus to infect others:

We report temporal patterns of viral shedding in 94 patients with laboratory-confirmed COVID-19 and modeled COVID-19 infectiousness profiles from a separate sample of 77 infector–infectee transmission pairs. We observed the highest viral load in throat swabs at the time of symptom onset, and inferred that infectiousness peaked on or before symptom onset. We estimated that 44% (95% confidence interval, 25–69%) of secondary cases were infected during the index cases’ presymptomatic stage, in settings with substantial household clustering, active case finding and quarantine outside the home. Disease control measures should be adjusted to account for probable substantial presymptomatic transmission.

And yeah, this asymptomatic presentation is not unique to Covid-19 among respiratory diseases. Influenzas cause this too:

We identified 235 virologically confirmed secondary cases of influenza virus infection in the household setting, including 31 (13%) paucisymptomatic and 25 (11%) asymptomatic cases. The duration of viral RNA shedding was shorter and declined more rapidly in paucisymptomatic and asymptomatic than in symptomatic cases. The mean levels of influenza viral RNA shedding in asymptomatic and paucisymptomatic cases were approximately 1–2 log10 copies lower than in symptomatic cases.

It does seem to be that case that the less "sick"/symptomatic shed less virus, in influenza at least, and probably by analogy in Covid-19 as well.
The degree of asymptomatic presentation can vary between strains (and likewise by age group) even for viruses that are pretty similar, like the "common cold" CoVs:

(If you want to know more about the specificity of Covid-19 tests, ask on med SE. Your question was pretty broad, and I can't touch all the angles here. I've only shown you that asymptomatic cases in other viral respiratory illnesses are not uncommon.)

To answer your question  it is necessary to distinguish the concepts of:

infection
symptom
test set up

The term infection might even denote the swallowing of a "dose from a  nose", without any replication of virus. On the other side of the ladder, "infection" might refer to a symptomatic disease.  However, "to explain infection without symptoms" implies that there does exist some stage  in between -  and "replication of virus within individual cells of the body" might "explain infection without symptoms" in the sense of the question.
Moreover, defining infection by "infection of single cells"  is the basis for  test set ups: "take" a "dose of the nose": a test would not run the risk of false positive results just to include that rare case of an infection that has not reached the stage of viral replication. (And a test should not run the risk of false negative by setting the minimum that high  that viral replication surely leads to symptoms).
Most important, the key concept "viral replication" explains why there may be contagiousness (there is no such term as "infectiousness", but a contagious person "always" is considered "infected", of course) without symptoms: viral replication does not imply symptoms of the disease.
The above should explain why there is infection=disease without symptoms, in principle.
Cp. https://www.verywellhealth.com/how-do-you-define-asymptomatic-2721956 where they talk of "over-diagnosis" which might be the opposite to "symptomless spread", as you might get treated not because of being sick "just a little bit" (without being infectious). For Diseases that do not exhibit symptoms cp. https://en.wikipedia.org/wiki/Asymptomatic. Maybe you speak of "asymptomatic disease" if there are some persons that do not show symptoms compared to persons that do exhibit symptoms, both groups refering to a common denominator, "viral load" for instance.
To answer the question which refers to Covid-19 one must look at the symptoms of covid. How can it be that viral replication in the case of CoV-19 does not INSTANTANEOUSLY lead to symptoms - if AT ALL?
A common concept is  to differentiate symptoms that  result from the activity of immune cells from those symptoms that result from the destruction of the infected individual body cells, which is a common differentiation.
It seems difficult to find reputable sources googling as with Covid it is mostly "explaining asymptomatic spreading" that is the main issue. Your question pertains to that as well, but focuses on "explain asymptomatic disease" - which might be considered a self-contradictory concepts as it denotes some "hidden disease" that should have certain symptoms that are just not being unveiled.
To "explain asymptomatic infectiousness", compare for instance
https://www.nejm.org/doi/full/10.1056/NEJMe2009758
"A key factor in the transmissibility of Covid-19 is the high level of SARS-CoV-2 shedding in the upper respiratory tract,1 even among presymptomatic patients, which distinguishes it from SARS-CoV-1, where replication occurs mainly in the lower respiratory tract."
One more link: https://www.nejm.org/doi/full/10.1056/NEJMe2009758 refering to influenza (the more viral load in the upper tract the more symptoms - which should not explain asymptomatic transmission)
Some reputable source on "asymptomatic disease" (i.e. not on asymptomatic spread):
"Clinical and immunological assessment of asymptomatic SARS-CoV-2 infections" https://www.nature.com/articles/s41591-020-0965-6
There are attempts at explaining "asymptomatic covid-disease" specifically.
However, for instance, https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(20)30460-6/fulltext specifically names "Lactate dehydrogenase" which seems to refer to the immune system in a corona-unspecific way, i.e. seems to  refer to individuals' being different in strength of their immune systems.
Here is my own personal approach based on the type of target cells of Covid, which are epithelial cells called "pneumocytes II" (target antigen of the spike is ACE2)

As target cells are stem cells their loss of function in  replacing dead epithelial cells (whose apoptosis is a regular one and, interestingly, not caused by the virus!)  might be felt only very late or not at all

The second function of Covid's target cells, pneumocytes II, besides their function as stem cells renewing epthelium, ist the production of surfactant. Hereby, I  tentatively  hypthesize that loss of that function of only leads to symptoms of shortage of breath if the  muscle activity of breathing in (which is supported by surfactant) does not overcompensate the loss of surfactant when the breathing activity of the patient in general is low.

I had to rule out my idea that the inflammatory reaction, in asymptomatic cases, might even be less in degree than with common cold caused by corona virus because stem cells as such should be lesser in number compared to differentiated epithelial cells  - this idea is wrong: counterintuitively, stem cells, i.e. pneumocytes II are much higher in number than pneumocytes type I.

For whom it may concern some explanatory remarks on  "infection and symptoms" in abstract terms:
The term symptom according to commmon usage refers to the signs sick person present with when they feel at uneas.  However, in a more intricate way,   "symptomatic" might be  defined as: infection of single body cells causing replication of virus. In that case, there would not exist any "asymptomatic infection" as that would be self-contradictory: if "symptom" does come with "infection" - of one single cell.
To explain asymptomatic infection the underlying concepts of "symptom" and "infection" must clearly be set apart. The replication of the virus (infection) is different from the symptoms as consequences of this event. Viruses only replicate in cells, thus turning a test to a positive result, and only then (not before infection of single cell, "after contact".)
On the other hand, tests are not set up to turn positive before this replication starts, as it is the basis for contagiousness. Your question may seem to  blame tests for being "false positive". However, tests are not set up to show negative results when it's only the symptoms that do not show, but the cells have harboured viruses that have replicated, thus causing contagiousness. Test are truly positive when they indicate virus replication only, and, on the other hand, presumably only turn positive if there ,in fact, has been some minimal infection of single cells, thus indicating some more virus than has been inhaled.
If there is "infection without symptoms" this might quite easily be explained by the symptoms being caused be the reaction of the immune system, not by the loss of function of body cells. There may be a common situation where epithelial cells  are infected already, implying virus replication, thus contagiousness - without the immune system causing the symptoms, and no  defunct epithelial cells either, thus  resulting in a  test being positive showing "symptomless infection".
For a very up-to-date and surprising alternative answer to your question that refers to insertion of viral RNA as DNA into the genome (retroviral like mechanism ) that is detected by positive testing "without symptoms" see the following reference.
https://www.sciencemag.org/news/2020/12/coronavirus-may-sometimes-slip-its-genetic-material-human-chromosomes-what-does-mean
which is like a review of the reference in some other question at stackexchange Does SARS-CoV-2 kill its host cell or not?

This is a (not very good) criticism of the question, but by no stretch of the imagination an answer to it. Answers should be answers. If you have

By adding some "no stretching" to your comment it becomes much more "substantial" (don't know how to say in English) than what I have gotten used to around here - so sad....

@David Please see - I coorected the criticism you criticized as - yes, indeed - it is incoherent to my commenting on "first comment" of question. Let me know if this is being unclear to you.

This still doesn't answer the question. Symptoms are defined, for xample see here. It does not mean the infection of the body with a pathogen.

@user1136 All this flagging makes me look important. So I should get along alone very well as soon as you have skipped me out :-) What you're saying suits me fine! You are right. I haven't said anything to the contrary. Your reproach is that I haven not answered what the question is about, and you have?

@Chris . "I agree" :-) With your link,  I expected some page with precise definition of covid-19. Then, that page was on general principles. Still, you are right! "Explaining" in the sense of the question needs specifity.  I will edit and elaborate on "replication without symptoms in case of Covid-19".You do not want me to clarify a question that might in strict terms of peerness be an "unfocused question"? I took your job?

Haven''t read yet all what's in your link - I think it's a good link, as "Alzheimer" might illustrate what I was talking about. It should be clear what the test is testing for: for the symptoms that define the disease which are "just" certain effects of certain causes or for, I'd say, pre-effects of symptoms - which, interestingly, in the case of anti-bodies, may be post-symptom-effects as well.

user1136 Please see my comment above, refering to the link you gave. What are you flagging me for? Is it for not answering the question as it is put? If yes I would like to retaliate to just the opposite: your comment does not fit the question as formulated. What I've been trying to do was interpreting the question according to its explanatory text, then answer it as it was put.