text:
Why does cutting onions cause tears?
Why does cutting onions cause tears? From a couple of sites, I found that it is because of sulfuric acid produced by onions. But I could not find more details. What is the biochemical pathway by which onions cause tears? Also, which compound is responsible for it? If it is enzyme-catalyzed reaction, can we just stop the production of this enzyme without causing any side-effects?

Your last sentence refers to the Vidalia Onion, IIRC.  Lacking sufficient sulpher, it doesn’t produce significant quantities of the irritating sulfoxide.

Related advice: https://cooking.stackexchange.com/q/567/28937

Interesting question! The cause of tears and itching is the chemicals produced by onion (Allium cepa). Lets go into some details.
Onions, coming from the family Liliaceae (also containing garlic, chives, scallions and leeks) store compounds known as amino acid sulfoxides, and the one we are talking about here is S-1-propenyl-L-cysteine sulfoxide (abbreviated as PRENCSO), also calles isoalliin (due to its similarity with alliin found in garlic). When onion is damaged (cut, chewed, etc.), an enzyme alliinase converts PRENCSO into 1-propenyl sulfenic acid. This compound is then converted into propanethial-S-oxide by an enzyme lachrymatory factor synthase (earlier this reaction was considered spontaneous). The reaction looks like this:

Propanethial-S-oxide is the major cause of the flavor and aroma of onion. However, it is a volatile compound i.e. vaporizes very quickly. When its vapors reach the eye, it causes tears because of being a lachrymator (aka tear gas) i.e. as soon as it comes in contact with cornea, it triggers a nervous response which leads to activation of lachrymal (tear) glands.
PS: when propanethial-S-oxide comes in contact with cornea, a small amount of it reacts with water to form sulfuric acid. This sulfuric acid is the cause of itching and irritation in eyes due to onion. Also, scientists are now trying to genetically either modify or stop the production of lachrymatory factor synthase enzyme to produce tearless onions. This (modification) has even been achieved to a high efficiency, as another answer discusses. However, making tearless onions could prove harmful to the crop in several ways, as discussed here.
EDIT: As asked in comments, I will add some details about how the sulfuric acid is produced from the reaction between propanethial-S-oxide and water.
The only resource I could find giving some details about this was Marta Corzo-Martínez, 2014. They summarize the complete pathway in the following diagram:

After applying some common chemistry principles, the concerned reaction turns out to be:
$\ce{4~C_3H_6SO~+~4~H_2O \rightarrow 4~C_3H_6O~+~H_2SO_4~+~3~H_2S}$
As you see, one of the products of hydrolysis of propanethial-S-oxide is hydrogen sulfide ($\ce{H_2S}$). Just like $\ce{H_2SO_4}$, $\ce{H_2S}$ also causes irritation in the eyes (its effect on eyes has been well documented, see Lambert et al, 2006 as an example). Thus, the produced $\ce{H_2S}$ only increases the irritation and itching in the eyes caused due to $\ce{H_2SO_4}$.
BONUS: Another interesting point here is runny nose. propanethial-S-oxide is actually the compound responsible for the smell and flavor of onions. But, it causes tears by exciting the lachrymal glands i.e. reflexive lachrymation. propanethial-S-oxide excites the trigeminal nerve (the fifth cranial nerve) causing activation of lachrymal glands. Interestingly, the nerve endings of trigeminal nerve are also present in the nose, along with the eyes. So, this compound can also activate the lachrymal glands from your nose, and since the lachrymal duct is joined from eyes to nose, you can also experience runny nose along with tears and irritation in eyes.
References:

Propanethial-S-oxide | University of Bristol
Alliin | Wikipedia
Tear Gas | Wikipedia
Timothy William Lambert, Verona Marie Goodwin, Dennis Stefani, Lisa Strosher, Hydrogen sulfide ($\ce{H_2S}$) and sour gas effects on the eye. A historical perspective, Science of The Total Environment, Volume 367, Issue 1, 15 August 2006, Pages 1-22, ISSN 0048-9697, https://doi.org/10.1016/j.scitotenv.2006.01.034
Encyclopedia of Perception, Volume 1 -
E. Bruce Goldstein,
SAGE, 2010
The Neurology of Lacrimation – How an Ear Infection Can Cause Dry Eye -
by Noelle La Croix, DVM, Dip. ACVO

I'm curious about the sulfuric acid. The oxidation number of S is rather low in propanethial S-oxide, are you certain that sulfuric and not sulfurous acid is produced? I know about the relatively low stability of the latter.

This is due to a lachrymatory agent called as syn-propanethial-S-oxide.
The process goes as follows:

Lachrymatory-factor synthase is released into the air when we cut an onion.
The synthase enzyme converts the amino acids sulfoxides of the onion into sulfenic acid.
The unstable sulfenic acid rearranges itself into syn-ropanethial-S-oxide.
Syn-propanethial-S-oxide gets into the air and comes in contact with our eyes. The gas diffuses through the air and, on contact with the eye, it stimulates sensory neurons creating a stinging, painful sensation.
The lachrymal glands become irritated and produces the tears.
Tears are released from the tear glands to dilute and flush out the irritant. In this case it is to reduce the effects of sulfuric acid,a chemical that could damage the eye if it was not for the tear reflex that renders the sulphuric acid largely harmless.

So, we can stop tear production by not irritating our eyes by using the onions which produce less irritants.

Through a single genetic transformation in onion (Allium cepa), a crop recalcitrant to genetic transformation, we suppressed the lachrymatory factor synthase gene using RNA interference silencing in six plants. This reduced lachrymatory synthase activity by up to 1,544-fold, so that when wounded the onions produced significantly reduced levels of tear-inducing lachrymatory factor.

Sources: https://www.loc.gov/rr/scitech/mysteries/onion.html
https://www.ncbi.nlm.nih.gov/pubmed/18583530

Interesting. I was wondering, though, if it has to come in contact specifically with the eyes? As it seems for myself that the smell alone (well, the irritating gas actually) starts the tears, and the painful feeling comes from my sinuses rather than the eyes? I also noticed I sustain the feeling much longer if I pinch my nose. Yet that might be confirmation bias ^^

@spectras I believe so; I have a pair of goggles that I wear when cutting onions and it seems to prevent the effect.

Just because it's a random thing I learned working in fast-food for 3 months at the ripe age of 16 before being fired, soaking onions in ice water dramatically reduces irritation. Maybe the ice isn't needed, can't recall.

@ChrisSchneider As temperature decreases enzyme activity and diffusion decreases.

@chrisschneider also the propanethial-S-oxide and sulfuric acid are water soluble, so it prevents their vaoprization

@spectras In my experience, your observation is not confirmation bias, it's simply true. Whatever causes the tears, it makes its way through the nose. Pinch your nose for good (f.ex. with a clothespin and from the start to the end of the process) and there will be almost no tears at all. I got this tip from someone who cooks all the time, I tried and it just works.

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Do the primers used for Covid-19 test work with all new strains?
We keep reading news of new Sars-CoV-2 strains, some of them allegedly able to evade vaccine-induced Igs. That's not unexpected, specially for a single-stranded RNA virus. However, it seems to me that the tests (RT-PCR) are being done exactly as they've been since early 2020, all around the world.
Therefore, my question is about the primers used: how can we be sure that there are not new strains with sequences not complementary to the primers? Does the current covid19 test target highly conserved RNA regions? If that is correct, how do we know that those regions are highly conserved?

Just for completeness, these Q/A provided no relevant clue: What specific markers does a Covid-19 PCR test look for? and Are specific primers or detectors, or both, used in COVID-19 tests?.

Here's a good resource for anyone that wants to try answering: http://covid-19.dnageography.com/. This is the SARS-CoV-2 Mutation Browser, which, as of writing this, includes data on >82k mutations at >6k positions across >10k complete SARS-CoV-2 genomes. Conveniently, the data can be subset to look at position-specific mutation frequency across genes and regions, including the regions primed by the most popular diagnostic primers, like the primers from the CDC's diagnostic panel.

accompanying preprint: COVID-19 Variants Database: A repository for Human SARS-CoV-2 Polymorphism Data

I TRY to answer. First of all, no we cannot be 100% sure that the primers are effective against all strains.
However, the strains that are under media attention right now are due to variants in the spike protein, while RT-PCR primers are designed on different genes.
One WHO document (I do not know if it's the official guideline) targets RdRp (RNA-dependent RNA polymerase) and a gene called E gene.
While the document itself nor the paper on which it is based explicitly addressed conservation of the target genes, I found evidence for relatively high conservation of at least RDRP in this paper.
Personal opinion here: in looking for RT-PCR primers, you always need a balance between targeting genes that do not vary in the species, and targeting genes that may aspecifically amplify in different species (e.g. SARS-CoV).
Final answers:

how can we be sure that there are not new strains with sequences not complementary to the primers?

We cannot. However, as far as the variants media are talking about, we know that RT-PCR has some ability to detect them, since they have been sequenced as a consequence of some patient testing positive to RT-PCR.
We cannot exclude the existence of unknown strain. They could be identified by e.g. sequencing patients with COVID-2 symptoms testing negative to RT-PCR (and possibly testing positive to the antigenic test). I don't know if such cases have been observed.

Does the current covid19 test target highly conserved RNA regions?

Yes, the current RT-PCR based tests target conserved genes (although I wouldn't call the highly conserved, because of the caveat I expressed above as a personal opinion)

If that is correct, how do we know that those regions are highly conserved?

Mostly by sequence similarity. Regions that have the same sequence in all the individuals of a species and in related (or distant) species are conserved.

No, some strains contain mutations causing partial or complete failure of amplification of at least one of the test targets.
Here's an FDA bulletin on the issue from January:
https://www.fda.gov/medical-devices/letters-health-care-providers/genetic-variants-sars-cov-2-may-lead-false-negative-results-molecular-tests-detection-sars-cov-2
As the bulletin notes, most tests have multiple targets, so the test result remains positive with a virus variant even if one of the targets doesn't amplify.  In fact, the UK B.1.1.7 variant prevalence has been estimated using RT-PCR by looking for a one-target failure result.
Different tests use different primer sequences and even target different Sars-CoV-2 genes. That's a lot of different mutations that would have to happen to evade all detection by even one test, let alone the many different ones. If Covid-19 symptoms started showing up in many people testing as "negative", it would be quickly be investigated in more detail.

source: Stack Exchange

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

sort: votes


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What keeps a virus from spreading from one species to the other, when it can infect both?
I have read that there have been cases where animals (some tigers, also a dog) have been infected by Covid-19 through a human host. At the same time, I read that currently it is deemed unlikely that the virus can spread back from those animals to humans (in the same source). Regarding the infection of other animals like tigers there is also this question which has some sources.
That makes no sense for me, I would think outside of the body, a virus is the same independent of the source and so any species that can catch it should be able to spread it to any other species that can also catch it. Are there any reasons why this would not be the case, in general?

One reference for the human-to-tiger transmission: https://www.nytimes.com/2020/04/06/nyregion/coronavirus-new-york-update.html (scroll down towards the bottom)

Your question would be improved if you could cite the things you've read.

@UuDdLrLrSs That seems to be a news ticker that updates constantly. The tiger thing doesn't seem to be there anymore.

I'm pretty forgiving when it comes to questions, probably more so than a few would like, but there are a lot of uncited assertions in this that make it really difficult to answer.

@BryanKrause Added a link to the german news page where I read it. It is about the tigers, but also contains a bit about dogs and house cats which can be infected, but that at the same time the virus couldn't spread back to humans.

@AlexReynolds Sure I am interested in this particular disease, but I don't expect a definitive answer here. But the general case can probably be answered - are there viruses which jump from one host species to the other, but can't jump back? If so, why?

@kutschkem its still there - search for "tiger" in the text of the page

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What is the role of increased cytosolic calcium concentration after firing, in neuronal cell bodies?
I've come across several studies in which scientists were investigating various questions related to neural activity by focusing on neuronal cell bodies using Calcium imaging. As this article suggests for example, cytosolic Ca concentration in the soma will significantly increase if the neuron fires. I understand the process behind this. But I'd like to find out if this somatic Ca increase has significant downstream effects inside the soma.
Could anyone shed some light on such known processes/pathways?
I've thought of one possibility based on an article that showed Calcium would upregulate mitochondrial enzymes, such as PDH and OGDC, responsible for TCA reactions. Considering that there's a coupling (source) between cytosolic and mitochondrial Ca concentrations, this could lead to a very quick increase in metabolic activity that covers up for the ATP loss related to neuron firing. However, I'm a bit skeptical about this idea. I'd think that the lack of ATP and low NADH/NAD ratio should speed up the TCA enough already and Ca might be more critical somewhere else instead.

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The attached article happens to be the exact same article that led me ask this question above. It clearly states that we can observe a Calcium increase in the soma related to action potential, but doesn't seem to discuss at all what the function of this Ca increase is. And that's what I'm asking here.
I've done my research before asking. Of course, I could spend a few more days going through articles (that are often behind paywalls) and would eventually find the answer (if there is). But having to do this is exactly what I wanted to avoid by asking a clear question in a specialized community.

I think it's a good question (+1). It could be improved by a citation (e.g., to the one tyersome suggested and that you found), and also by better clarity of what exactly you are asking (I think your comment helps but comments are ephemeral). The biggest issue that you can improve is the ambiguity of the question "why": several times you ask why but why is often misinterpreted. It seems you are not interested in how the calcium gets into the cell but rather what the purpose of calcium influx is near the soma rather than at an axon terminal. If true, can you edit to make this clear?

(these edits will help you get an answer that's actually what you want, otherwise someone could come and write an excellent answer about voltage gated calcium channels and then they will find they wasted their time if this wasn't what you wanted)

Fair point. Thank you for your well-thought comments. I edited my question accordingly. I hope now it aligns up with the standards and readers can interpret what I'm after exactly.

Thanks for the edits! I've already upvoted so can't do it again, but I do hope you get a good answer. I have some ideas myself, at least one of which is mentioned here (it was in the 'related questions' on the right): https://biology.stackexchange.com/questions/36646/doubling-the-concentration-of-extracellular-calcium-hyperpolarizes-a-neuron-why?rq=1 but it will take me some time to collect references that talk about other purposes. Calcium is quite a diverse messenger so it's likely an answer will only point you in a couple directions for future research rather than give a definitive answer.

I see. Appreciate the upvote. It makes things even more interesting, if there really is not a definitive answer to this question. I'll jump back into the literature then and do some exploring. I'll start by reading into the idea brought up in that question you pointed out. Thank you for all your help. I'll keep an eye out on this thread so maybe we can discuss the findings.

After doing some further research, my conclusion is that intracellular Ca levels play a role in regulating synaptic vesicle exocytosis, LTP, redox signaling, and the krebs cycle. The latter effect seems to be the most relevant one in neuronal cell bodies.


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How would blocking Na/K ATPase affect the ability of a neuron to exhibit a series of action potentials?
Neural firing usually occurs in the form of spike series. Several action potentials are happening in a quick succession. Whereas Na/K pumps (and other pumps) restore ion gradients to allow processes that take place during an action potential.
Now my question is, what would happen if we completely blocked these pumps and immediately after, we started exciting a neuron? Would the neuron be able to fire a few times before losing the gradients? Or, would one single spike completely diminish the gradients and without restoration by pumps, a second AP would be impossible?

For those who might wonder about the same problem, I've found an answer to my question. During a single AP in the soma, transmembrane currents are so brief in time that only small fractions of the ion gradients are being used up. Theoretically, the cell should be able to exhibit numerous APs before exhausting its ion gradients to the point where it can no longer fire.


text:
How does lipoid pneumonia lead to acute respiratory distress syndrome (ARDS)?
How does lipoid pneumonia lead to acute respiratory distress syndrome (ARDS)?
The vaping illnesses that have been happening on the news in the United States are being caused by the federal prohibition on marijuana. Smugglers will legally go to recreational marijuana dispensaries in legal states and purchase cartridges that contain about a gram of "wax". Proper cartridges will use polyethylene glycol, polypropylene glycol, or vegetable glycerin to suspend the THC for vaporizing, but the smugglers have been known to open up the tank and remove some of the wax and refill the remaining volume with Vitamin E Oil. These tampered cartridges are then sold on the black market to recreational and medical consumers in illegal states.
The CDC Report: "Outbreak of Lung Injury Associated with the Use of E-Cigarette, or Vaping, Products"
Edit: So, I was on some conspiracy shtuff when I wrote this post because I was worried about impurities in my vapes killing me. I don't want to take this down because I want my cognitive distortion to remain visible as a reminder of how we can succumb to biased reasoning. Also, the answer I marked correct contextualized the fragmented information of which I was aware and attempted to give me an improved framework for understanding the terms I was using incorrectly as a layman.

Welcome to Biology.SE! This appears to be a reasonable question, but the inclusion of unsubstantiated or irrelevant claims detracts from this. Specifically, the entire middle of your post seems to be a distraction from the biology. Instead, please summarize the relevant information from the CDC report and add any other relevant information you can find about ARDS and lipoid pneumonia (with references from reliable sources). ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and edit your question accordingly. Thanks!

There are several ways to get ARDS (sepsis, pneumonia, trauma, pancreatitis, etc).  Pathophysiologically, they all converge at alveolar insult.  So however it happens, there's alveolar insult, cytokine release that recruits neutrophils, and the activated neutrophils release toxic mediators that destroy the alveolar membranes.  So for your question specifically, the mineral oil in the vape cartridges (theoretically) is instigating an inflammatory reaction that destroys alveolar membranes.


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Pedigree - Dealing With Unknown Parent Genotypes
I'm dealing with a pedigree problem, and I'm having some trouble dealing with problems of unknown parental genotypes (where there are multiple possibilities). This is not a homework question; it's an exam practice problem.

The question asks: Suppose brother and sister 6 and 7 are mated. What is the probability that their first pup will be albino?
The answer choices are 1/4, 1/8, 1/16, 1/32, or Not Enough Info.
Here's my attempt at the problem:
Since #2 is black, and some of its offsprings ended up sepia, #2 must carry the sepia gene (since the male mate is cream, and sepia is dominant over cream). So, we know that #2 is $Cc^k$.
Now, the male mate can be either $c^d c^d$, or $c^d c^a$.
This means that in order for the offspring of #6 and #7 to be albino, we need:
1) Male parent needs to carry the albino gene (i.e. male needs to be $c^d c^a$).
2) Male parent needs to pass on the albino gene to both #6 and #7.
3) #6 and #7 both need to pass on the albino gene.
I think the probability that the male is $c^d c^a$ is $\frac{1}{2}$, since the male parent can be either $c^d c^a$ or $c^d c^d$.
If we draw out a punnett square, the probability that the albino gene gets passed onto 1 individual is $\frac{1}{2}$ (since we already know the offsprings are sepia, we only need to consider the genotypes that contain $c^d$).
The probability that #6 and #7 pass on the albino gene is $\frac{1}{4}$.
This led me to think that the final probability is then P(male parent has albino gene) * P(#6 inherits albino gene) * P(#7 inherits albino gene) * P(#6 and #7 pass on the albino gene), which is $\frac{1}{2}$ * $\frac{1}{2}$ * $\frac{1}{2}$ * $\frac{1}{4}$, which gives us $\frac{1}{32}$, but I do not feel confident in my answer. Specifically, I do not know how to account for the fact that the male parent can be either $c^d c^d$ or $c^d c^a$.
Is my thought process correct? If not, where in my logic did I go wrong? Thank you for your help.

Based on the information given in the pedigree, you can actually be certain that #2's mate has a genotype of CdCa because of the following:
Two of 5's siblings are albinos. Since albino is a recessive trait (lowest in hierarchy of dominance), both parents (4 and 4's mate) must have the Ca allele. Let's call 4's mate "8". Since 8 has the Ca allele, at least one of 8's parents must also have the Ca allele. Since you have already (correctly) determined that #2 is CCk, #2's mate must have the Ca allele, and must therefore have a genotype of CdCa.
Thus you can eliminate the extra (1/2) from your calculation, making the answer (1/2) * (1/2) * (1/4), or (1/16).


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Breeder's equation and equivalent expressions for narrow-sense heritability
I am trying to model the phenotype of a trait as $X = G + E$, where $G$ and $E$ are the genetic and environmental effects. (I'll ignore the distinction between broad-sense and narrow-sense heritability in this question.) Wikipedia tells me that $$h^2 = \frac{\mathrm{Var}(G)}{\mathrm{Var}(X)}$$ The same page also gives the breeder's equation $R = h^2S$ but also says "Note that heritability in the [breeder's equation] is equal to the ratio [${\mathrm  {Var}}(G)/{\mathrm  {Var}}(X)$] only if the genotype and the environmental noise follow Gaussian distributions." So let $G \sim N(0, \sigma_G^2)$ and $E \sim N(0, \sigma_E^2)$ be distributed according to normal distributions. Then $X \sim N(0, \sigma_G^2 + \sigma_E^2)$ so $$h^2 = \frac{\mathrm{Var}(G)}{\mathrm{Var}(X)} = \frac{\sigma_G^2}{\sigma_G^2 + \sigma_E^2}$$
Now I want to perform a selection, choosing a parent with $X=a$. We can expect the child to have the trait $\mathbb E[G \mid X=a] + E'$ where $E' \sim N(0, \sigma_E^2)$ is some other environmental effect. (I don't want to bother with recombination and multiple parents, so we can just think of it as cloning the parent: given that $X=a$, we expect the parent's genetic part to have been $\mathbb E[G \mid X=a]$.)
To find $\mathbb E[G \mid X=a]$, note that $\mathbb E[X \mid X=a] = a$ and by linearity of expectation, $\mathbb E[X \mid X=a] = \mathbb E[G \mid X=a] + \mathbb E[E \mid X=a]$. To get the terms to cancel, we want to write $E$ as $\alpha E$ where $\alpha E$ has the same distribution as $G$. Since $\alpha E \sim N(0, \alpha^2 \sigma_E^2)$, we want $\alpha^2 \sigma_E^2 = \sigma_G^2$, so $\alpha = \sigma_G/\sigma_E$. Thus we have $$\begin{align}a &= \mathbb E[G \mid X=a] + \frac1\alpha\mathbb E[\alpha E \mid X=a] \\ &= \mathbb E[G \mid X=a] + \frac1\alpha\mathbb E[G \mid X=a] \\ &= \left(1+\frac1\alpha\right)\mathbb E[G \mid X=a]\end{align}$$ Hence $$\mathbb E[G \mid X=a] = \frac{a}{1+\frac1\alpha} = \frac{a}{1+\frac{\sigma_E}{\sigma_G}}$$
Since the parent was selected at $X=a$ and the child has mean $\frac{a}{1+\frac{\sigma_E}{\sigma_G}}$, we have $$h^2=\frac{R}{S} = \frac{1}{1+\frac{\sigma_E}{\sigma_G}} = \frac{\sigma_G}{\sigma_G+\sigma_E}$$
Now my problem is that the two expressions for $h^2$ don't match. They look pretty similar, but one of them has all the terms squared while the other one doesn't. What's going on/where did I go wrong?
ETA: To give a concrete example, suppose 80% of variance in the trait is explained by genes. Then the breeder's equation predicts the child to have $0.8a$. But computing $\mathbb E[G \mid X=a]$ gives $a/(1 + \sqrt{0.8^{-1} - 1}) = (2/3)a$. So the two approaches predict different things (although if it was 50% they would give the same prediction).

I found my mistake, which is where I said "To get the terms to cancel, we want to write $E$ as $\alpha E$ where $\alpha E$ has the same distribution as $G$." What we actually want is to find a constant $\alpha$ such that $\mathbb E[\alpha E\mid X=a] = \mathbb E[G\mid X=a]$. In my question, I assumed that this was the same thing as finding $\alpha$ such that $\mathbb E[\alpha E] = \mathbb E[G]$; hence I was trying to find $\alpha$ to make the distributions of $\alpha E$ and $G$ the same (the means are both 0, so I just needed to get the variances to equal each other). But actually, conditioning on $X=a$ shifts the distributions so the $\alpha$ I found in my question doesn't work.
Since my previous strategy doesn't work, I ended up skipping the step of finding $\alpha$ entirely. I realized that the random vector $(G, X)=(G,G+E)$ is a bivariate normal, because we can write $$\begin{pmatrix}G \\ G+E\end{pmatrix} = \begin{pmatrix}\sigma_G & 0\\ \sigma_G & \sigma_E\end{pmatrix}\begin{pmatrix}Z_1 \\ Z_2\end{pmatrix}$$ where $Z_1,Z_2$ are standard normal random variables.
Now Wikipedia gives the conditional distribution for bivariate normals, which in our case is $G\mid X=a$. We only need the mean, which is $\mu_G + \frac{\sigma_G}{\sigma_X}\rho (a - \mu_X)$. Both $\mu_G$ and $\mu_X$ are zero, and $\rho$ is the correlation which is $$\rho = \rho_{G,X} = \frac{\mathrm{cov}(G,X)}{\sigma_G \sigma_X} = \frac{\mathrm{cov}(G,G) + \mathrm{cov}(G,E)}{\sigma_G \sigma_X} = \frac{\sigma_G^2}{\sigma_G \sigma_X} = \frac{\sigma_G}{\sigma_X}$$ Thus we end up with $$\mu_G + \frac{\sigma_G}{\sigma_X}\rho (a - \mu_X) = \frac{\sigma_G^2}{\sigma_X^2}a$$ which is exactly what we want.


text:
how the coronavirus was distinguished?
I have read a lot about the outbreak of the coronavirus, I know that in january scientists had already sequenced the viral genome.
How was the virus identified prior to the sequencing
Given that viruses are not like germs that you can see and distinguish readily in microscope, how could scientists know that there was something new about the new disease and how could they purify the pathogen that cause that disease without knowing what it is and without knowing its genetic code?
Where can I find information about procedures that are used to identify new viral pathogens?
Given that there is a group of people with suspicious desease, what are the laboratory procedures used to eliminate known pathogens and how you discover that you have a novel virus without knowing its genetic sequence (and without the ability to extract it - as far as I know you can not isolate virus particle with tweezers...).
Thank you!

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, you seem to be asking for someone to summarize an entire field, which may not be practical on this site. ——— We also encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

This is basic epidemiology. When medical professionals notice that a group of people with some characteristic in common, are being seen for a similar disease, they ask if there's a connection. In this case, several people in Wuhan were diagnosed with severe pneumonia, and the doctors noticed that they worked in the same location.

Three adult patients presented with severe pneumonia and were admitted to a hospital in Wuhan on December 27, 2019. ... Her occupation was retailer in the seafood wholesale market. ... He had been a frequent visitor to the seafood wholesale market.

--A Novel Coronavirus from Patients with Pneumonia in China, 2019
You're more likely to follow up when the disease is unusual or severe, and when the connecting factor is unusual or suspicious. In this case, the severe pneumonia was presumably unexpected, and live animal markets always have potential for disease transmission.
(In fact, it's quite possible that the virus had been circulating in the region for weeks before this cluster was noticed, and that previous cases had not been surprising enough to trigger the research needed to identify a new virus; though it's also likely that the medical personnel in Wuhan had noticed that there were an usually high number of pneumonia cases and were already looking for a connection.)
See also the answers to How did scientists discover HIV?. Old-fashioned epidemiology is always critical.
The same article explains how the virus was sequenced:

Bronchoalveolar-lavage fluid samples were collected in sterile cups to which virus transport medium was added. ... RNA extracted from bronchoalveolar-lavage fluid and culture supernatants was used as a template to clone and sequence the genome. We used a combination of Illumina sequencing and nanopore sequencing to characterize the virus genome.

And isolated:

... supernatant from bronchoalveolar-lavage fluid samples was inoculated onto the apical surface of the cell cultures. ...  After three passages, apical samples and human airway epithelial cells were prepared for transmission electron microscopy. ...

So briefly, they took patient samples, grew them on cultured cells, used electron microscopy to check the kind of virus. They sequenced fluid (not cells, since the virus would be secreted into the fluid, making it a relatively pure source of virus RNA) and then sequenced using a standard high-throughput sequencing approach; knowing the likely kind of virus would make this easier but isn't essential. There would have been lots of human RNA in the sequence, but it's easy to bioinformatically separate that out and limit your analysis to the viral sequences. The virus isolate was also not essential for the identification; knowing the sequence is the critical information today. But having a virus isolate certainly makes all the subsequent work much easier.
This is pretty standard modern molecular biology, not an esoteric skill.

it doesn't answer my question. i didn't ask about that stage. i'm asking after you understand that there is a group of people with suspicious desease, what are the laboratory procedures used to eliminate known pathogenes and how you discover that you have a novel virus without knowing it's genetic sequence (and without the ability to extract it- as far as i know you can not isolate virus particle with twizzers...).

The article I linked also explained the isolation in detail. I've edited it into the answer. These are standard modern molecular biology techniques and most reasonably modern infectious disease labs would be able to do them.

thank you............!

@ iayork    'RNA extracted from bronchoalveolar-lavage fluid and culture supernatants was used as a template to clone and sequence the genome' i still don't understand how could they know wich of the templates is that of the suspected virus. also, when extracting RNA from tissue you get a lot of different sequences, many of them belong to the patient's own genome or to other unharming viruses and microbes. how can you know which primer is the one you are looking for? . (i've learned MB of the cell, still i don't know how to approach this issue)  thank you!

Not much human RNA in the fluid, but the virus gets secreted there. In any case, it’s easy to bioinformatically drop out the human sequences in your computer after the fact, leaving just the virus.


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What animal is this?
I have seen this bug/worm twice on my dog's leg after taking him for a walk this week. I think that this is a leech, but my mom disagrees because she says leeches are not found where we live but are found around beaches. We live in Carmel Mountain San Diego: Google Maps.
The closest beach is around 15 minutes away.
The bug is approximately the size of a fingernail, and it did not do anything when I picked it up.

EDIT: We were just walking around my neighborhood, nowhere jungle-ish at all.

Welcome to Biology.SE! What kind of environment(s) are you walking through? There are definitely leeches in California, but leeches are typically associated with wetlands ...

I added an edit, with details about the environment of the walks.

Leeches are found other places than beaches. Some live in streams, lakes, rainforests, mountains, and even aquatic locations in deserts

@theforestecologist interesting. I guess San Diego can be considered a Desert, but I do not think there are any aquatic locations around where we live.


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Is there any evolutionary reason why male traits appear in the heterogametic sex and female traits in the homogametic sex?
If you define male as the heterogametic sex, and female as the homogametic sex, then my question sounds like a tautology. But, what I'm trying to get at is why is it that the traits we associate with "males" (e.g. having an unlimited amount of possible offspring, greater average height, etc) appear in the heterogametic sex, and why traits that we associate with "females" (e.g. having a limited amount of possible offspring, shorter average height, etc) appear in the homogametic sex. Or, is it simply by chance that the homogametic sex became the female sex and the heterogametic sex the opposite?
As far as I understand it, heterogametic chromones allow for a greater chance of mutations being displayed, so I wonder whether there is something advantageous about this occurring in the male sex rather than the female sex. Perhaps it is because males are more "expendable" since they can have an unlimited number of offspring? Is this line of reasoning accurate, and are there any alternative explanations that go deeper than this?

The title question,

Is there any evolutionary reason why male traits appear in the heterogametic sex and female traits in the homogametic sex?,

suggests that male always is the heterogametic sex, but this is not true.  ("Male" is usually defined as the sex with the small, mobile gametes, i.e. sperm, as contrasted with the large, nutritive gametes, i.e. ova.) There are many species where females are the heterogametic sex, such as birds, most snakes, some fish, crustaceans, and insects.[a] These species use the "ZW" sex-determination system, which is essentially the inverse of the more familiar "XY" system.[a]  Other species don't have a heterogametic sex, but rather use lack of one chromosome as the determiner ("XO", "ZO"), and yet others use lack of one half of all chromosomes as the determiner ("haplodiploidy"). Others don't distinguish sexes by chromosomes, but use environmental stimuli.[b]
All this variety in forms of sex determination suggests that there are not substantial evolutionary advantages to having the heterogametic sex be the male.
[a] "ZW sex-determination system", Wikipedia.
[b] "Sex-determination system", Wikipedia.

+1 OP's whole question is based on a false premise. Mammal-centrism strikes again.


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How do viruses die outside of host cells?
I am posting a question that a friend of mine has asked.  My friend wrongly assumes that SARS-CoV-2 virus can be transmitted through blood, although there is no such evidence.  However, his question remains a valid one.

With so much news about COVID-19 all around us, I have been doing some
      study on viruses.  I do understand that viruses are not really living
      creatures.  They just have some genetic information, which they can
      pass on to the host cell, causing the virus to proliferate, and in some
      cases interfere with the normal functioning of the cell.  Outside of a
      host cell they are completely inert.  In fact they show all the traits
      of a non-living entity.  I get that.
My question is based on the following scenario.  Imagine there are two
      doors, next to each other.  Let’s call them A and B.  There is a door
      knob on each.  A COVID-19 patient sneezes near the doors, and some SARS-
      CoV-2 viruses land on each door knob (i.e. door A and door B).
      Unfortunately within a few hours someone with a cut finger touches the
      knob of door A and gets infected.  So far no dispute.
Fast forward 5 years.  In the meantime the knob on door B never got
      cleaned/wiped.  In other words, the inert viruses are still on the door
      knob.  Again someone with a cut finger touches the knob of door B but
      in this case the person does not get infected.  Why?
Obviously something happened to the virus during these 5 years that
      caused it to lose the ability to pass on its genetic information to the
      host cell and replicate.  What exactly happened?

Addendum:
We received a response for the query that seemed reasonable to us but was voted down, and presumably deleted by the author.  Fortunately I was able to recover a screen capture.  To keep the discussion going, I would like to temporarily include the response here till a better response is posted.  Here it goes:

This isn't very professional, but there are the basics. Viruses are obligate parasites, which means they can't live outside a host (in this case, a cell) for long. Viruses get damaged as everything else, the damage taking many forms, such as hydrolysis, photolysis, free radical damage, reaction with other molecules (like detergent), conformation changes, dehydration, maillard reactions, and changes induced by heat of labile molecules (like decomposition). All types of damaging processes happen at an increased reaction rate with increasing light and heat. Viruses have rudimentary repair mechanisms if any, so it's a matter of time before they become inactivated. A damaged virus entering the body wouldn't be able to do much harm if any, as their genetic information would be damaged beyond repair, and so, not able to be replicated to make more viruses. Their proteins and genetic bits would still trigger an immune reaction and immunize against intact and not very damaged viruses (which is why damaged viruses are used in vaccines). Those damaged viruses that remained outside just become microbe food.

Yes, disputed. The virus is not circulating in the blood stream (as far as we know), it is replicating in the cells of the airways.

Any answer for the basic question: what causes (non-living) viruses to die outside of host cells?

They don't die since they are not alive.

Please do not post text as images as these cannot be indexed by the search and found.

I don’t think that including a deleted response in a question is appropriate. If the person deleted it you should respect that. And a question is a question, not a discussion to “keep going”. Finally, it is not acceptable to post text as images as it discriminates against those with visual difficulties.

What exactly are you looking for in an answer? As far as I can see, the response you received (and added a screenshot of) looks like a good enough answer to the question in your title. But if it doesn't answer the question in your mind, you should probably edit your question a bit.

A similar question has been answered here: https://biology.stackexchange.com/a/89953/55506


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

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

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

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

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


text:
Poor Hygiene vs. Cross-species transmission?
Did a poor hygiene at wet Chinese markets add anything to equation to trigger critical mutation of COVID-19 helping it to transmit the virus from bats/pangolins to humans?
If not, would it spread to humans anyway (even if those markets were clean and spotless) since people over there were in frequent contact with such viruses (right before preparing those wild animals as meals), which would give the virus enough time for necessary adjustment/mutation?

Even though I mentioned COVID-19, I think the question could be
  generally applied to any mutation of a virus right before it transmits
  from animals to humans. It happened many times in our past and I am
  quite confident there are many researches out there related to this
  topic.

I'm specifically interested in deciphering whether poor hygiene on those wet markets helps propelling such cross-species transmission.
Could it be the virus was already transmittable to humans whilst it was still in those bats/pangolins without any prior mutation whatsoever?
Please elaborate. Thanks.

I just discovered this most recent study that fully answers my question.
The reason appears not to be related with the hygiene itself, but the high stress level of animals that are put into cages close to humans. Therefore, the hygiene level seems irrelevant for such virus transmission from animals to humans, as long as it doesn't increase the stress level of each individual animal:
Global shifts in mammalian population trends reveal key predictors of virus spillover risk


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Could blood transfusions from COVID19 surviver be worth researching as a possible form of treatment
As a general viral immunology question (rather than seeking personal medical advice).
Would a blood transfusion from a COVID19 surviver to a sufferer be worth researching as a possible form of treatment? There is evidence in other animals (elephants) that blood transfusions are beneficial against viruses.
BBC Chester zoo
More specifically would lymphocytes and other cells able to attack the virus from the donor outweigh the resulting increase in virus burden caused by adding the donors blood into the sufferer? and how does the is change over time from the time of the survivers recovery?
Needless to say this procedure risks crossing strains of COVID19 and other risks so would need thorough analysis of such risks before being practiced.

Please see here.

ok reworded they question

I don't know why this was closed; it is easily answered: https://www.nbcnews.com/health/health-care/doctors-push-treatment-coronavirus-blood-recovered-patients-n1158476  https://www.reuters.com/article/us-china-health-hospital-idUSKBN20B1M6  This is "convalescent serum" - a form of passive immunity


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Could phytoplankton in the Poles have a baseline photosynthesis activity during polar nights using auroras as a light source?
Polar nights refer to the phenomenon where there are extended periods of darkness where the Sun hardly arises from the horizon in the polar winter.
However, there are other dim light dources like auroras. Could photosynthetic microorganisms (such as phytoplankton) use this as a source for a very basic photosynthetic activity and primary production of sugars?
Also in this article (https://www.science.org/doi/10.1126/sciadv.abc2678) the authors indicate that microalgae could grow in extremely low light conditions during the Arctic polar night.
My question is: Can these organisms use very dim light sources like aurora borealis to produce a very basic photosynthetic activity and produce sugars or fats to survive?
Related: https://www.sciencenews.org/article/algae-light-phytoplankton-grow-dark-arctic-winter-ice

This question is similar to: Could plants do photosynthesis at moonlight?. If you believe it’s different, please [edit] the question, make it clear how it’s different and/or how the answers on that question are not helpful for your problem.


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

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

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

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

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

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


text:
What is the name of this part in plants, fruits, vegetables?
What is the name of this part of the plant, fruit, vegetable? The thing that the plant is connected with the tree and gets nutrients with? The part we usually cut out when eat fruit.
Examples below
Papaya

Banana

Mango

google the word stem.

@John that's not a stem. What is the name of the plant part that stem gets into in the plant. This part of the fruit is not a stem.

'Stalk' or 'pedicel' would be an appropriate term (see, for example, this paper or this one). Specifically, you could say 'terminal part of the stalk/pedicel', though I don't know if there is a word for that.
Note that the term pedicel is commonly used for the stalk of a flower; it makes sense to use it for fruits too as they are derived from flowers.


text:
COVID-19 Infection rate related to population size?
Recently, in the UK's daily government briefing they started showing the graphs that compare national death rates, adjusted by the population size of each country.

I understand the various reasons why comparisons between countries are difficult and might not make sense right now.
I understand that a country's population places an upper bound on the number of people who
can become infected.
I can see why population density might affect the rate of infection.

But, why would the rate of infection be different because of the population size?  Surely, when a virus reaches the shores of a new country, it doesn't think to itself "hey, there are a lot of people here, I'd better spread faster"...?
I hate to sound like a conspiracy theorist, but right now we in the UK might be the worst-hit in Europe, and I wonder if showing these graphs adjusted by population size might be a political attempt to make us look "not quite so bad".
But, I am very ignorant of biology and epidemiology, so maybe there is a sensible reason for adjusting these graphs by population size.  Can somebody explain it to me?
Update: I have noticed that over the last few days, the UK government briefing has stopped including the charts that are adjusted by population size.

Perhaps the rates are similar, but a high rate of testing is revealing more cases.

What really matters is the per-capita infection rate.  2800 total cases in New York City (or London) would be almost negligible.  2800 cases on the Navajo Reservation (or say in the Hebrides) would affect a large part of the population: https://www.abc4.com/coronavirus/navajo-nation-reports-seven-confirmed-deaths-174-positive-tests-from-coronavirus/

It depends on what you want the graph to show you (and not just whether it makes the epidemic look more or less scary).  For example, if viewers are interested in the overall impact of the epidemic, they might want to know about per capita deaths rather than total deaths (here I will only use "rate" to mean "number per unit time" rather than "number per  individuals").
You're right that (1) we don't expect the epidemic growth rate (measured by cases or hospitalizations or deaths) to depend on population size (initially - once enough people have been infected to significantly deplete the pool of susceptibles, the population size does matter) and (2) naively plotting per capita deaths of regions with widely differing  population sizes can be misleading.
A good solution, used by the widely redistributed Financial Times COVID-19 plots, is to plot the time axis as the number of days since 0.1 average deaths (per million) first recorded (obviously you can pick a different per capita threshold); this sets the scale appropriately for regions of different sizes.
For example this chart:

It looks from The Guardian's story that the government's plots are adjusted to "number of days since 50 deaths".  It would seem better to use a threshold based on a per capita threshold (larger countries will hit the 50-death threshold sooner) ...

Thanks!  I was also using "rate" to mean "number per unit time", so your answer makes sense to me.


text:
fibrous skeleton of the heart
is it true to say that "fibrous skeleton is between all of the myocardium and most of the cardiac muscle attach to that"? cause I can't get this that how can it be between all the muscles.

Where is this quote from? The phrase "myocardium muscle" is strange usage (muscle is redundant with myocardium).

edited it. I wrote it wrong sorry


text:
Removing DNA from a cell
Stupid question perhaps but what does happen if one completely removes DNA from a single cell organism? As far as I know DNA is only needed for propagating information to descendants doing it's removed from a grown up cell and put some artificial source of protein there will it just lose ability to mate or will it die immediately?

Welcome to SE Biology! It is helpful when asking questions to do a minimal level of research first to help you focus your question. For instance, there is a huge amount of information if you google "role of DNA in a cell".

@MaximilianPress well, I did actually. I knew from school and from research that DNA is essential for producing proteins and thus life. I should have specified the question perhaps.

@SPr thanks for your answer.

@SPr would suggest putting your comment into an answer.

@s0nicYouth I mean... I think with a quick due-diligence search you would have easily found what @S Pr commented. But maybe I am overestimating the usefulness of science information on the internet.

That depends on the status and activity of the cell. Red blood cells purge their nuclei and DNA contents and continue to perform their function quite well, though they lose their ability to split and form new cells (i.e. are terminally differentiated). Most cells, however, require the genome to transcribe and translate genetic information into protein to maintain their metabolic and functional activities. As you say, DNA would also be required to divide and build new cells, so that would be one major downside of removing all DNA. Adding exogenous proteins or amino acids will not help with ensuring correct protein production and maintenance, because proteins are coded for by mRNA which act as mobile transcripts of DNA. They are dependent on DNA transcription, without which they cannot exist. Proteins do not spontaneously form. Long story short, DNA is almost always absolutely essential, and it is the case that if you removed the nucleus from most cells, they would die very shortly thereafter.

(migrated comment to answer by request)


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What is the mass of a single erythrocyte?
I really have been searching through internet on different languages, but can’t find any article that answers on the question what is the single erythrocyte mass. I don’t know, I think it’s pretty easy to calculate experimentally, but I didn’t find anything.
Has anyone measured single erythrocyte mass, and if yes, what is the value?
My try
Experimentally
I am not biologist or medical student. What do I know: blood consists of liquid part(water, salt) and solid part(red blood cells, white blood cells and thrombocytes). If It is possible, the white cells and thrombocytes can be moved off the blood in some test tube, so that will left only erythrocytes. Then, there should be medical statistical value like erythrocyte density or number of erythrocytes per liter.
We have some blood with only erythrocytes, we know how many erythrocyte are there. We can measure that blood weight, substrate the liquid weight(somehow), divide by erythrocyte number and will get the mass of a single erythrocyte.
Theoretically
About 90% of erythrocyte mass is hemoglobin. Hemoglobin is a molecule. Molecule is a countable thing, so, perhaps there is information about how many hemoglobin molecules, in average, is in one erythrocyte.
According to Angelo D’Alessandro, Monika Dzieciatkowska, Travis Nemkov, and Kirk C. Hansen article Red blood cell proteomics update: is there more to discover? it is about 270 millions per red blood cell. Molecular mass of hemoglobin is about $64 kDa$, absolute mass equals $1.106*10^{-22} kg$.
If my assumptions are correct, then 90% of erythrocyte mass is about
$$2.97*10^{-14} kg$$

If you can’t find the mass (and I wouldn’t imagine there’s a lot of interest in that, but obviously it interests you) you could presumably calculate it from the cell dimensions, assuming a density of about 1. Not a simple sphere, I know, but it should be possible.

Is your problem that you wish (or have been asked) to separate them? If so, you need to search for a term like "centrifugation of blood" or "fractionation of blood". Is this Wikipedia article any use as a starting point? And the English in your title is misleading: I would suggest you replace "separate" by "individual" or "single".

@David, I am not a biologist, or medical worker, I can’t do that

The volume and the density of erythrocytes should be known.

OK, I've made a calculation. You could check the arithmetic. But do tell me, why do you wish to know this?

@David doing some modeling for diploma work

Had another try. Checking the paper I see I misread the figure legend.

About 90% of erythrocyte mass is hemoglobin.
According to Angelo D’Alessandro, Monika Dzieciatkowska, Travis Nemkov, and Kirk C. Hansen article Red blood cell proteomics update: is there more to discover? there are about 270 millions hemoglobin molecules per red blood cell. Molecular mass of hemoglobin is about $64 kDa$, or $1.106*10^{-22} kg$.
From the given, 90% of erythrocyte mass is about
$$2.97*10^{-14} kg$$
Now, using the proportion, calculate that the average erythrocyte mass is
$$m=\dfrac{2.97*10^{-14}kg*100\%}{90\%}=3.3*10^{-14} kg$$
$$erythocyte\space mass=33 pg$$

@David calculations result is also pretty similar to mine, He got $83 pg$

It’s not my kind of biology, and I tend to make mistakes in arithmetic, I’ll have a go…
I found a paper by Leblond and Shoucri published in the Journal of Microscopy (1978) 113, 161-170, entitled Calculation of surface area and volume of human erythrocytes from scanning electron micrographs. You need institutional access to read it, but for the human erythrocyte shown below they calculated:
Volume = 85.5 μm3

They found a range of sizes (65 μm3 in another image) so I shall take an average value of 75 μm3.
75 μm3 =  75 × 10–18 m3
Assuming a density of 1.1 g/cm3 for erythrocytes, i.e. 1.1 × 106 g/m3
Mass of an erythrocyte = 83 × 10–12 g (0.08 ng)
This is the same order of magnitude as that calculated later by the poster.
(Apologies for initially quoting the volume in pm3. No idea how I did that — it’s clearly μm3.)

Unfortunately, wrong. $75pm^3=7.5*10^{-35} m^3$.

RBCs have a density of approx 1.110g/mL. Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5516969/

Also, volume, that equals $85 pm^3$ is interesting, because I found range $70-100 um^3$

According, to that(another) “article “https://en.m.wikipedia.org/wiki/Mean_corpuscular_volume, average volume is $92.8 fL=92 um^3=9.2*10^{19} pm^3$

@ArturKlochko  Mea culpa. I see now, it's the pm as a whole that are cubed. Hunting down papers I can do, simple arithmetic as another matter... However now I seem to get an impossibly low answer of the order 10^–29g. Am adjourning for the moment.

Yeah, it’s impossible because it less then any atom mass

Discovered it was cubic micrometers not picometers. Now corrected, and correct, I hope.

Pretty similar to what did I calculate. I think the fact that this two different ways gives very similar values proves that mass of an average erythrocyte is about tens of picograms. But, still I think, Your method is not as accurate as mine, because it depends on simultaneously two various value - erythrocyte volume, and blood density(much more various then erythrocyte volume). Thank You for help


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Century old trees and evolution
We always think of natural selection as occurring at the level of populations not individuals. how about century old trees where germline is being produced from constantly dividing cells. Are all meristems in an old tree sharing the same genetic material, or enough mutations occur that different meristems have a different genetic background and are being selected differentially? Do different cells in a tree behave evolutionary more like different populations?
Added Note: The point I was trying to make is that for multicellular organisms in which the germline/somatic separation does not occur early in life, maybe Lamarck was not that wrong. In school we always learn to ridicule Lamarck with the giraffe story. But maybe in some instances Lamarckism makes at least as much sense as Darwinism.

The population of cells within a single tree can definitely be subject to selection. It still remain that it is a population of which selection is applied, you just shifted the level of selection. See evo101 > The hierarchy of selection for a quick introduction.

Note btw that this concept relates to formation of cancer.

Yes, indeed, somatic mutations can and do occur on different branches of a plant. Here is a recent study exploring this concept in an annual herb (rather than an old tree), and showing that selection is active in filtering these mutations during growth of the plant. From the end of the abstract:

These results support the hypothesis that somatic mutations accumulate during vegetative growth, but they are filtered by different forms of selection that occur throughout development, resulting in the culling of expressed deleterious mutations and the retention of beneficial mutations.

Interesting. In mammalian systems you can also get heritable, but non-permanent modifications on DNA such as methylation as a result of environmental factors. These presumably have some influence on selective fitness too. Any idea about this in plants?


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Is the coronavirus getting less dangerous?
Please note

This question is based on data from the UK government's web site (data from the ONS). I am not taking this data as accurate, but am using this as it is the only source of data I can find, and is what (presumably) the government themselves use when deciding what to do. My question is about trends, not the accuracy of the government's data.

I'm also not asking about the wisdom of government policy, that is a political issue, and I'm only interested in biology and statistics here.

Finally, I realise that my analysis is all quite rough and ready, as there are many indeterminate factors involved. Again, I'm interested in an overall picture, so a rough analysis is probably reasonably informative.

Here in the UK, the data on new virus cases seems to imply we have a serious problem...

This was plotted using data from the government's web site, and shows that the number of new cases has risen dramatically since the beginning of September. I used a 5-day average to smooth the line (same for the other graphs below)
However, if you look at the number of deaths, it seems that the increase is nothing like as rapid...

Whilst there has been an increase since the beginning of September, it is very much more modest, and not necessarily indicative of a serious problem.
Now, I'm not a medical expert in any way, but it seems to me that the fact that the number of deaths is growing more so much more slowly than the number of new cases indicates that things may be not actually be getting worse, but may be getting better. Sure, more people are getting the virus, but the percentage of those who are dying (which I would have thought is the most important issue we need to consider) is not increasing.
To check this, I divided the number of deaths by the number of new cases, and it showed a very different picture...

As you can see, there isn't a noticeable increase since the beginning of September. To examine this more closely, you can zoom in on the past 8 weeks or so...

Whilst there was a jump in the middle of Sept, it hasn't really increased since then, and may even be decreasing.
So, is my analysis wrong, or is the virus actually becoming less of a problem in the UK?

One obvious problem with your graph is that people don't die immediately after diagnosis.  Many people diagnosed in September will die in October, but you aren't counting them.  You can see possibly the beginning of an October death spike in what data you do have.

@swbarnes2 That would also make the beginning of a good answer.

@AvrohomYisroel, The UK's coronavirus stistics are some of the least thorough and systematic, because of their lack of a pandemic preparation and free test centers. S. Korea and Germany give better data and wildly different data than the UK.

This would be improved by cutting out some of the rhetoric, e.g. "winding people up into a panic", which suggests that you already have an answer in mind.  You might also consider that (if the UK was like the US) many of the early deaths were among extremely vulnerable populations such as older people in nursing homes.  Those people having been killed off already, so they aren't a factor in ongoing statistics.

@jamesqf I agree with the first part of your comment, but definitely not with the second. There are still plenty of very vulnerable people around (at least in the US) that avoided being infected during the first round, but are still quite susceptible to disease should they be exposed to it. Round I was certainly not a clear-cutting operation among the sick and elderly by any stretch of the imagination.

@jamesqf I tried to edit that part out, but it got rejected for some reason. I'm keen on cutting out any kind of political or emotive language in these kind of discussions,

I have voted to close this as it is not a question about biology in terms of SE Biology but an analysis of a public health situation in one country at one time presented to start a discussion or as a “I think this, try to refute it?” shot.

@swbarnes2 Good point, I hadn't thought of that.

@jamesqf You're right, I did have an answer in mind, but was trying to ask objectively, as I'm quite prepared to be proven wrong. I've edited the answer to remove the comment you mentioned.

@MattDMo: I have no data beyond news reports (e.g. mass deaths in nursing homes &c), but I think we might be talking about different degrees of vulnerability.  I didn't actually intend to imply that it was a clear-cutting, as you put it, but rather a thinning, which reduces later mortality.

The issue is using the number of positive tests as a measure for the total number of active cases at a given time. At least in the U.K., the early testing capacity was much lower than it was now:
Because of this, many people who were infected were not being tested and so weren't included in the total number of infections. Therefore, the total number of infections in April/May time was likely a large underestimate. It's been estimated that there was something in the range of 150,000-200,000 new cases per day in that time period.
On the other hand, testing capacity in the U.K. at the moment is much higher and will catch a much higher proportion of the total cases.
Therefore, your crude calculation of 'death rate' = deaths / cases is skewed by the error in the estimated number of cases, making it appear the 'death rate' is going down because we underestimated the total number of cases early in the pandemic.
The other thing to note is that the 'death rate' is dependent upon demographic factors, most obviously age. Early in the pandemic in the U.K., a large number of cases occurred in care homes, where the residents were particularly vulnerable. On the other hand, cases are high in students at the moment, who are a low-risk group. If the age distribution of cases is relatively skewed towards older people, then the 'death rate' will appear higher than vice versa, even though nothing may have biologically changed with the virus.
Note: Sorry, I don't have citations for a lot of this. I will try and find them and add them at a later point.

Thanks for that, very informative answer. My only comment would be that while everything you say makes sense when comparing data from the spring to now, but if you only consider data from (say) the beginning of Sept, as I did in my question, your points wouldn't make such a big difference. Or would they? I would be interested to hear what you think. Thanks again

Just by looking at the data, I would say that those deviations could well be within the margin of error (i.e. confidence intervals) of the numbers of cases and deaths recorded. Of course, there is a large amount of error in the estimation of the number of cases, so I expect those confidence intervals to be quite large. IN that case, the deviations we see may well just be 'random noise' that don't correspond to anything meaningful.

Fair comment, thanks

Schools opened
What happens in the beginning of September. Something that would expose a large number of people to the virus, particularly people young and healthy enough to have a low risk of death due to virus but who still have decent chance to catch the virus.

Excellent observation, never thought if that. I wonder if there is any data showing deaths by age, as that would help confirm or contradict your suggestion.

@AvrohomYisroel you also have to keep in mind that the death rate amongst young people is a lot lower than for older folks, but young people can pick up the virus and spread it to older people they come in contact with, while not necessarily getting very sick or dying themselves. I think one lesson out of this is that there are all sorts of variables at play here, and you can't necessarily draw universal conclusions just out of the data you've analyzed so far.

@MattDMo Agreed, very valid observation. I said right from the start that my analysis was rough and ready, I'm now seeing quite how rough it was!


text:
What does vaccine efficacy mean?
In the last few weeks, Pfizer/BionTech, Moderna and AstraZeneca have each released preliminary estimates of the efficacy of their SARS-COV-2 vaccines.
But what do their respective efficacy percentages actually mean? Is the Pfizer/BioNTech vaccine 95% effective in any person? Or is the success of provoking the desired immune response limited to 95% of the population?
Put very simply: is it 100% effective in 95% of the population, or 95% effective in 100% of the population?

Summarizing, it means 95% fewer infections than the placebo group. How is not yet explained. Whether 95% become immune, or everyone becomes 95% tougher to infect. More importantly, the main purpose of corona vaccines is the old herd immunity. Like extinguishing a fire by hosing down all of the surrounding wood. See below for excellent detail and further reading.

Vaccine efficacy
Pfizer's target measures for efficacy (see the study on clinicaltrials.gov) seem to be:

Confirmed COVID-19 in Phase 2/3 participants without evidence of infection before vaccination

Confirmed COVID-19 in Phase 2/3 participants with and without evidence of infection before vaccination

From Pfizer's study plan (VE = vaccine efficacy):

VE will be estimated by 100 × (1 – IRR), where IRR is the calculated
ratio of confirmed COVID-19 illness per 1000 person-years follow-up
in the active vaccine group to the corresponding illness rate in the
placebo group from 7 days after the second dose. VE will be analyzed
using a beta-binomial model.

(note: they also have other time windows and checkpoints in their analysis plan; which one is reported will shift from press release to press release as they get more data. If you are interested in the details the study plan also describes the planned interim analyses, and some of the press releases discuss deviations they've made from their original interim plans in consultation with regulatory agencies)
This measure is called relative risk, and can be written like this:
%InfectedPerTimeplacebo = NInfectedplacebo / (NStudiedplacebo * AverageFollowUpTime)
%InfectedPerTimevaccine = NInfectedvaccine / (NStudiedvaccine * AverageFollowUpTime)
Efficacy aka VE = %Infectedvaccine / %Infectedplacebo
If you assume risks are the same in the placebo and vaccine groups (they "should" be, but might vary if, for example, people who experience vaccine side effects change their behavior) and the average follow-up time is the same (they should be approximately the same, because they are giving the vaccine and placebo to patients enrolled at the same time), this ratio would tell you that a vaccine efficacy of 95% means that if you took 20 people who would have had a positive test after the placebo, you would only expect 1 of them to test positive if they instead got the vaccine.
Population vs. individual statistics

Put very simply: is it 100% effective in 95% of the population, or 95% effective in 100% of the population?

These are population-based measures. They can't say anything about efficacy in particular individuals by these outcome measures. For example, there is no way to know from a study like this whether the vaccine is 100% effective in 95% of the population, or if it raises the infective dose in everyone by some amount which causes the number of people exposed to this critical viral dose in their environment to decrease by 95% (or some other effect with the same end result).
Other approaches like challenge studies, where vaccinated individuals (or animal models) are intentionally exposed to a certain dose of the virus, can help understand the individual effects of vaccination, as can indirect measures of immune response like antibody titers. These approaches have other drawbacks, however (safety, translating animal results to humans, translating a given immune response to an infection chance, etc).
Beyond just 'vaccine efficacy': disease severity, real-world efficacy
These particular outcomes also say nothing about disease severity. It could be that the people who do test positive despite getting the vaccine get just as sick as the sickest people who don't (interpretation would be that the vaccine protects mostly against mild illness). It could also be the reverse, and that people who get the vaccine and still test positive have a milder illness than they would have otherwise. Efficacy defined by this relative risk ratio does not say anything about this, it only compares positive vs negative rates.
An additional note: these numbers report efficacy in the trial environment. "Real-world" effectiveness (the same measure of effect, but in real world use rather than under trial conditions) might depend on other factors such as differences in the people enrolling in trials vs the general population (both in terms of things like age and preexisting conditions as well as behavior and exposure risks), failure to administer the vaccine properly (including improper storage), failure to complete both doses in timely fashion, etc. This measure of effectiveness also refers only to "primary" effectiveness. One would expect that if enough people were vaccinated, the effect on the population could far exceed the primary effectiveness, because not only do vaccinated individuals have a lower chance of infection, but everyone else in the population also has a lower risk if there are fewer people available to transmit the infection.

Should also note that (as with flu vaccines, which are only around 40-60% effective for the individual) a major purpose of the vaccine is not to provide 100% protection to the person that receives it.  It's to reduce the transmission rate so that the virus doesn't spread.

@jamesqf Meant to include that in my final paragraph but it slipped my mind; included now.

"Efficacy aka VE = %Infected_vaccine / %Infected_placebo" -- did you mean IRR here?

AFAIK the Pfizer vaccine showed that the disease severity was also lowered in the group that did catch Corona despite being vaccinated; none of those developed a severe form. The control group apparently had a few people hospitalized.

It means protection against the virus brought to you by the vaccination.
Around 45.000 people participate in the trial; 50% of these are vaccinated with the trial vaccine and 50% receive a placebo. Additionally, you exclude people from the trial who had had COVID-19 before. Because infecting people with a potentially deadly disease is not possible ethically, you watch both groups for occurrence of the disease.
I have numbers only for the Biontech/Pfizer vaccine, but the principle is the same for the others as well. In this trial 170 cases of COVID-19 were seen: 162 in the placebo group and only 8 in the vaccine group. If the vaccine were to do nothing at all, then you would expect to see similar numbers in both groups, which means that these 8 cases from the vaccine group represent a reduction (or efficacy) of about 95%.
With the vaccine, only 5% will catch the disease, while there is no protection for unvaccinated persons. For the numbers, see the press release from Pfizer and the database entry on clinical trials for this trial.

To further clarify the statement that "with the vaccine, only 5% will catch the disease", this means that 5% of vaccinated people who would have otherwise caught the disease will become infected, not that 5% of all vaccinated individuals will catch the disease (only about 0.01% of vaccinated people did).

@NuclearHoagie Exactly. Without the vaccine you would expect similar numbers of infections in both groups, which is reduced by 95%.

How do you get .05 out of this though? 166/168 is about .988.

@Timkinsella You are right, I somehow added two wrong numbers, which are corrected now. It should be 8 people for the vaccinated group vs. 162 in the control group. See the original publication. Thanks for pointing out.

@Chris There is one more “2” to change to “8” in the third paragraph.  I tried to change it but it’s below the character limit for edits at my rep level, apparently.

@Timkinsella Right, missed that one, too. Now it should be correct. Thanks again.

Saying that a vaccine is $95\%$ efficacious/effective is neither claiming that the probability that it works is $95\%,$ nor that it has a $95\%$ chance of blocking infection or conferring immunity against disease development, nor that it works $95\%$ of the time, nor that it protects $95\%$ of its recipients.
And vaccine efficacy/effectiveness is certainly not the recipient's probability of not contracting the pathogen, since this obviously depends on its prevalence, their health and exposure, and other factors.
Rather, vaccine efficacy just measures the increase in protection conferred by the vaccine under ideal conditions (while vaccine effectivenss measures the same in “real-world” settings): a vaccine efficacy of $95\%$ means that during a controlled clinical trial in which half the subjects had been vaccinated and half hadn't, among those who eventually developed the disease, the ratio of those who had been vaccinated to those who hadn't is $5 : 100.$ Technically, vaccine efficacy is the proportionate reduction in disease occurrence conferred by the vaccine during the clinical trial.

efficacy
among those who developed the disease,the ratio ofvaccinated to unvaccinated participants
(relative risk)assuming that effectiveness = efficacy,contracting the diseaseis ___ times as likelywith the vaccine than without

$100\%$
$0 : 100$
$0$

$95\%$
$5 : 100$
$0.05$

$60\%$
$40 : 100$
$0.4$

$50\%$
$50 : 100$
$0.5$

$0\%$
$100 : 100$
$1$  (the vaccine has no effect)

$-20\%$
$120 : 100$
$1.2$  (the vaccine makes you more susceptible to the disease)

If exactly half the subjects had initially gotten the vaccination, then mathematically $$\text{vaccine effcacy}=\frac{U-V}U=1-R,$$
where $U$ and $V$ are the respective numbers of unvaccinated and vaccinated subjects who developed the disease, and $R=\dfrac VU$ is the relative risk (the rightmost column in the table above).
Do note that if the clinical trial was short (as was the case with the first Pfizer-BioNTech COVID-19 vaccine), then the published vaccine efficacy could not have taken immunity duration҂. into account. Therefore the figure may vary—perhaps significantly—as the subjects continue to be monitored over the coming months/years.
 ҂Follow-up data since this Answer was originally written indicates that the first Pfizer-BioNTech vaccine's real-world effectiveness waned by $10-35$ percentage points six months following vaccination. These figures are complicated by the predominance of a more infectious virus variant, Delta, which wasn't around during the clinical trial.
P.S. For the Pfizer-BioNTech trial (in which $43661$ subjects were split evenly between the placebo and vaccine groups), $U=162$ and $V=8,$ so \begin{align}\text{vaccine efficacy}&=\frac{162-8}{162}\\&=95.1\%.\end{align}
P.P.S. Note that the Pfizer-BioNTech trial checked only for symptomatic disease: the $U=162$ and $V=8$ figures do not account for the asymptomatic cases of COVID-19 among the study subjects.

Vaccine efficacy is the percent change in the percent of individuals who test positive in the vaccinated group versus the placebo group in a trial. The CDC website explains it here
So a 95% efficacy means the vaccinated group had 95% less percentage of people test positive than in the placebo group. So if the placebo group had a 20% positive rate, the vaccinated group had a 1% positive rate (5% of 20%). If this 95% efficacy is deemed to be statistically significant, it likely means that the positive rate in the vaccinated portion of the population will be 5% of the positive rate in the unvaccinated population.
Normally, if 100% of the population takes a vaccine, a 60% vaccine efficacy is considered enough to cause enough decrease in positivity rate to stop the spread of COVID-19 so 95% is really good. This paper goes into what the vaccine efficacy needs to be if less than 100% of the population takes the vaccine.

I'm sure you'll have seen the recent results of the Oxford vaccine by now! The headlines stated 70% efficacy at first, with the intended regimen of two full doses two week(?) apart, but found (by accident, apparently) that if the first dose was a half dose, the efficacy rose to 90%.

More intriguingly, Professor Jonathan Van-Tam, Deputy Chief Medical Officer for England, said today that of the 24,000 (I think) trial participants who were given the vaccine in either regimen, none of them needed to be admitted to hospital. Does this, I wonder, mean that although the efficacy in terms of not contracting the virus at all was 70% or 90%, the people that did get the virus had milder symptoms than usual, and thus the efficacy in terms of preventing hospitalisation and death is closer to 100%? What would the name for that be?


text:
HPV. How do viruses persist outside the body?
The main route of transmission of human papillomavirus (HPV) is generally believed to be sexual. While fomites have been postulated for inexplicable infections, sexual health professionals regularly counter that lying respondents are the more likely explanation.
Research into HPV seems to have mostly stalled and there are few in depth in-vitro studies into viability of the virus outside the body, the infectivity of fomites or their infective dose that I could find.
There are some footnotes and references to animal models, with claims that HPV can remain infective at least 7 days after desiccation but no upper limits. There is some more precise research but understanding the significance is difficult for layman.
For example research published in Nature stated HPV-16 "can remain viable and capable of transducing the reporter construct upon stimulation of cell cycle re-entry for at least 2 weeks, but most likely for no longer than 4 weeks."
How can one understand the viability and limits of viruses, and HPV in particular, outside the body?
To clarify: Despite the fanciful language of the bounty I'm not looking for certainty, but general principles of environmental virology and an overview of statistical observations in regards to HPV in particular.
Note: The various aspects which influence the persistence of viruses in the environment spoken of below are summarized with some additional detail in a literature review published in 2010 in Food and Environmental Virology.

Good question - but I think it could be improved by including some links to the studies you mention. Thanks

Please [edit] your post to include references documenting the persistence of infectious HPV outside of the body. Without that evidence you may very well be asking about a phenomenon that doesn't actually occur. In the future please also make sure to write out abbreviations in full at least once. Thanks!

Refined the question as suggested.

As far as I can tell this topic, specifically for human papillomavirus (HPV), hasn't been fully investigated. There is some literature on it (as cited by OP), but it is sparse, making this an open field for someone to investigate. As such there is no certainty about how long a sample can persist in the environment as a huge number of factors come into it.
However, this is a difficult topic to investigate - how do you mimic in the laboratory the conditions under which you would find the virus in a natural shedding? In terms of HPV, no-one seems to have fully investigated just how the virus is deposited in terms of how it is shed in a natural manner from warts. It is assumed in the literature that it is in the form of keratinised squamous epithelial cells with virus inside, and probably naked virus too. These will have different profiles of decay in the various environments because of the natures of the different forms.
In terms of environments for persistence, there are a huge number of factors that might play into it. Here are a few of the known significant ones: heat (max temperature and min temperature as well as freeze/thaw cycles), light (particularly UV from sun), humidity (overall in environment and local to the place were the virions are), salinity (beach?), chemical (e.g. chlorine at a pool), how the virus is deposited, and last but not least, what the virus is in (a skin cell? mucus? naked virion?)
HPV is a non-enveloped virion containing double-stranded DNA. The virion is composed of 72 capsomers each consisting of 5 copies of the structural protein L1 and forms a strucutre with icosahedral symmetry. The capsid is capable of self-assembly under the right conditions, which means that it is likely quite stable (relative to some other viruses), as it can potentially re-form if damaged by heat or something similar.
The virus enters the cell through abrasions or micro-traumas of the skin surface, where it invades the squamous epithelium and only grows in those keratinized cells. It can also invade and grow in epithelial tissues of some mucosa such as the nasal passages, throat and vagina. Some of these tissues are shed containing virus through abrasion and natural shedding of the epithelial surfaces.
Now that we have a bit of the biology out of the way:
How do we test for persistence of a virus in the laboratory? Actually it is quite simple, generally you grow and purify the virus (or a surrogate similar virus) and then place some as droplets on the surface you wish to test. You then subject it to the conditions that you want to mimic and see how long you can detect it for.
The methods of detection vary depending on the virus and study. Some will use molecular detection methods like the ability to PCR amplify genetic material from the virus as a surrogate for genetic damage making the virus incapable of replication. The other most commonly used is to try to propagate the virus from swabs taken from the surface it was applied to. This doesn't work for all viruses, as some are not culturable, or are very difficult to culture (e.g. for SARS-CoV-2, only about 30% of positive samples can be cultured, but for measles virus very close to 100% can be cultured). If the virus is not culturable, it may be that it can get into the cell and either replicate but not escape the cell, or that replication is incomplete, so genes are expressed, but no virions formed. If either of those two options are go then the presence/viability of the virus on the surface can be determined by looking for activity of one or more viral genes.
I can't give you landmarks for HPV, and the exact sequence of events is unknown for any of the viruses I know anything about, but in general viruses tend to be non-viable before you can no-longer detect genetic material. Exactly how long each of these takes depends highly on the virus. For instance, take two quite topical viruses - SARS-CoV-2 and influenza, both enveloped (less stable) RNA viruses with similar size and structures and similar routes of transmission. Viable influenza persists for about 2 weeks on stainless steel, but only 1 week on cotton, but you can detect the RNA for up to 17 weeks, while CoV-2 only persisted for 1 week on steel, but RNA could be detected for the full duration of the study (though I can tell you personally from my CoV-2 as yet unpublished results >14 days on some surfaces under some conditions at room temp).

That was quite an elaborate answer. This discussion of HPVs in water environment could be a great addition - recent discovery of HPV's presence in urban wastewaters and surface waters has led to hypotheses of water-borne transmission. Although it claims there is little data reg the fate/stability or waterborne transmission of HPVs - waterpathogens.org

Thank you for a very elaborate answer indeed. Does the quote from the research published in Nature, cited above, establish any sense of an upper boundary for HPV-16 in the environment?

@PrashantBharadwaj I noticed the article you mention while looking into this subject. It would be a rather frightening vector for the disease but hopefully one that may be mitigated in the standard water treatment process if it turns out to be viable.

'The virion is composed of 72 copies of the structural protein L1' it's 72 capsomers, each of which has 5 copies of L1. So 360 copies total: https://link.springer.com/content/pdf/10.1007/s00705-006-0798-8.pdf

@timeskull - you are quite right I will edit to correct.

bob1's answer is good, but I was already working on this one so I'll go ahead and post the parts that aren't redundant:
What does it mean for a virion to lose infectiousness?
To be 'infectious' a  virus particle perform a set of tasks that result in more virus particles. A simplified list for HPV could be: attach to receptor on host cell > enter cytoplasm > enter nucleus > make proteins > copy DNA > assemble new virions from protein and DNA > exit cell. The first four tasks must be performed by proteins in the virion; if enough of these are degraded, the corresponding task cannot be completed, and the virion cannot infect a cell. This means that there are many different routes by which any particular virus might be inactivated. One of the references in the question suggests HPV can be inactivated by gunk from dead cells sticking to the otherwise-viable virions:

The greater inactivation of the virions in the extracts at 56 C may be due to denatured cellular protein, which visibly aggregated at 56 C and above, interfering with infection.

Viruses are not metabolically active on their own!
This means that damage cannot be repaired, and also that a functional protein cannot be 'reset' after it changes shape. To use the SARS-2 spike protein as an example, the spikes have energy stored in them like a mousetrap. If the transition from open to closed is triggered while the spike is bound to ACE2 on a host cell's membrane, the motion of the spike protein changing shape will bring the viral membrane in contact with the host membrane, fusion occurs, and the virion contents enter the host cytoplasm. If the transition is triggered before the spike is bound to a host receptor, that spike is 'dead'. SARS-2 virions have many spikes, but if all of them trigger prematurely, the virion as a whole becomes uninfectious. The transition from the high energy 'prefusion' state to the lower energy 'dead' or 'postfusion' state has to be energetically accessible in order to be triggered by the new host cell. This means that the risk of premature triggering is inescapable. Therefore, damage or premature transition of all copies of some viral protein that changes shape to allow cell entry is a likely candidate for inactivation for any viral species. This hasn't been investigated systematically, though, so there's no reference I can cite for this.
In papillomaviruses:
Unlike coronaviruses, HPV doesn't have a membrane that can fuse with the host's for cytoplasm entry. Instead, it is absorbed by endocytosis, then the capsid disassembles, and L2 disrupts the endosome membrane. The details of how this happens aren't known, but it's likely that L2, which is protected inside the capsid most of the time, becomes exposed by structural changes to L1 which occur in the endosomes. This suggests to me that degradation of L1 is the main cause of viral inactivation outside of the cell. That hypothetical structural change of L1 would need to be identified before you could start to investigate if it's present in inactivated particles.

Thank you for contributing to an already full answer with additional technical detail and in an accessible manner. Do either of you have any perspective to share on the process of decay of viruses outside the body, and a sense of  their "life expectancy"?

there's no data on that as far as I know. The proteins are probably degraded fastest by UV rays, then chemical attack by oxygen. 'Life expectancy' can't be predicted yet. Even fairly similar viruses might have different rates of survival. Viruses that transmit through a fecal-oral route are usually tough, and blood-transmitted viruses are usually fragile. Viruses with a lipid envelope usually degrade faster than ones without. But there are a lot of exceptions.


text:
Disposing biohazardous material
I had conducted some disc diffusion tests with E.coli and S.epidermidis.
Now, I wanna dispose these petri dishes and was wondering the correct way to do it. Many websites mention adding bleach to the agar and disposing them in biohazardous waste bags right away.
I've decided to do the same. But, the lid for all the petri dishes I have are very loose. If I simply dispose the petri dishes in waste bags, I think that the lids are gonna come off and the bacteria may infect the waste bags.
Should I seal the petri dish with some tape like a parafilm so the lids won't come off or is it not a problem that the bacteria may come out onto the waste bags?
(No websites mention the issue of loose lids while disposing, so I wonder if this is a problem at all)

You don't have an autoclave available?

No, I'm not a professional researcher, a high school student. I just did this exp. at home...so I don't have one

Autoclave is standard, but bleach can be used. In your case, you'll want all the culture media and dish surfaces to have contact with the diluted bleach solution. I would prepare diluted liquid bleach as described in the link below and pour some in a plastic wash tub to a depth where you can put all your petri dishes etc in and have them fully submerged. Let them sit for at least 30 minutes in the solution, then recover the solids and put them in trash, and dispose of the bleach solution with MUCH dilution down the toilet. Pay attention to the safety suggestions and warnings in the link!
This U of Toronto web page has good info on disinfecting using bleach.


text:
Does the current phylogenetic system classify only Algae as Thallophytes?
I am studying the current system of division of plants.
While studying Thallophytes, I came across some sources which said that Thallophytes consist of Fungi, Algae, and Lichens. Some others (https://asm.org/Articles/2021/January/Three-Reasons-Fungi-Are-Not-Plants), however, stated that Fungi are no longer considered plants.
My question being, which statement is the truth?
It would be quite helpful if I could get an answer, as none of the sources I have visited are intercepting this problem.
There may also be shortcomings in my knowledge, for which I apologise in advance.