Fascinating. It seems sensible (to a layman) that something would eat viruses but how would we construct tests (not trolling) to determine:
1. if the Halteria were not eating something_else, and that something_else was infected by the viruses?
2. if the Halteria themselves were not infected by the viruses?
3. are the Halteria trying to ingest the viruses, or are they just ingesting lots_of_things in the petri dish?
This observation seems interesting, assuming all other variables were constant and there was not some other interplay between the chlorovirus and other microbes which indirectly helped the Halteria grow:
>Halteria deprived of the chlorovirus, meanwhile, wasn’t growing at all.
Finally if the Halteria can ingest it and yet not be 'infected' by it then that seems awfully interesting as well.
Biophysicist here. Excellent questions – these are the kind of points peer reviewers would raise (though typically in far more esoteric and passive aggressive ways...).
(1) could be addressed in experiments where the algae-consumers in question are studied in monoculture (purified and grown in test tubes) with virus added artificially. This experimental design excludes the possibility that any middle man is present; if uptake is still observed, it must be direct.
(2) Measure viral replication, perhaps in a similar monoculture experiment as above. If the viruses are infecting (exploiting) the Halteria, they will have non-negligible replication (they are stealing the Halteria's resources to advance their own replication). Viral replication could be assayed by qPCR (counting viral genomes) or similar assays.
(3) This would require biochemical studies to determine the mechanism of uptake of viral particles. Typically, viruses are taken up (endocytosed) by cells as a result of interaction with receptors on the surface of target cells (prominently CCR5 in HIV, Ace2 for the COVID-19 causing virus). Of course, what biological systems are `trying` to do begs that we anthromorphize Halteria (or at least evolution), but one could conduct an evolutionary analysis to see if Halteria have progressively evolved receptors that improve viral uptake efficiency.
As an aside, the discovery of virovores hints excitingly (albeit remotely) at the possibility of creating virus sink cells/technologies that could eliminate viral particles in humans. An important question will be whether viruses, which evolve far faster than eukaryotes like Halderia (let alone than humans), can turn the tides in the evolutionary arms race and become the exploiters of the Halderia. Perhaps it's reassuring that we exist (mostly) symbiotically with our microbiota, despite their far faster evolution.
> these are the kind of points peer reviewers would raise (though typically in far more esoteric and passive aggressive ways...)
If you don't mind me asking, how do you deal with this kind of culture, where a normal process is being purposefully obstructed with such behavior from the reviewer?
Do you ever call people out who sprinkle their "reviews" with such passive aggression? What is their defense? What highlights does your profession have that make it worth putting up with this?
I have an i10 index of 2, h index of 3, 71 total citations. Not that impressive, but just goes to show I have some experience in this area.
So...
> If you don't mind me asking, how do you deal with this kind of culture, where a normal process is being purposefully obstructed with such behavior from the reviewer?
You just come to expect it. I realize this isn't the best answer or even a reasonable one, but it's how it is and there's really no controlling it.
> Do you ever call people out who sprinkle their "reviews" with such passive aggression?
No. Your field is dominated by experts who have a clique and run a crony network of influencers; getting mad at one of them is a great way to ensure you never hit tenure track / get punished on papers in the future (many journals are not blinded, or even if they are, it's fairly obvious who wrote a blinded paper given the subject matter in a niche field and/or timing attacks on the paper's submission + researcher's social media posts on the topics).
Sometimes - most of the time in my field - you have no idea who the reviewers were. I think this is typical for most science fields.
> What is their defense?
They suffered by much worse hands; really, they're being nice. (That's what they tell themselves.)
> What highlights does your profession have that make it worth putting up with this?
Very few. I work for a for-profit company, so the research we publish helps bolster the company's image, can be used in marketing, and so forth. Going from zero to one feels amazing. One day you're a guy with a dream that you'll publish an influential paper someday and give back to science, the next you have that publication credit - maybe even lead author credit - and going from 1 to N is just nowhere as interesting as going 0 to 1... like most things in life.
For some of us, science is in our blood, and it's our calling. Whether we like it or not. Most of the time, we don't. But we do it anyway.
To hopefully add to the discussion here. Not a scientist (professional), nor do i have a degree in anything (debt sucks), but AFA i see it, a reviewer shouldn't be evaluating a paper based on a popularity contest, but based scientific rigor and well reasoned approach that paper has. If the data is good, if their analysis is good, etc etc etc. On things that aren't dependent on being in a clique and/or popular.
That just smells of bad science, and make it not surprising the mainstream is "lagging behind". People actively stifling real scientific advancement, instead of letting it flourish.
I feel bad for people that do have that purity of purpose that either have to put up with that kind of BS, and people that have been victims of said behaviour.
I appreciate very much people who have it in their blood, their passion, like i have music and singing in my blood. You know you'll get someone who'll do the best job possible, and care about what sort of science is being done. Thank you for being you
I've read this post - broadly, I agree very much with it.
Unfortunately, inertia is a hell of a thing. Science is stuck with peer review for a few more decades at the very least. Many postgrads would do unspeakable things and commit various crimes to become a first author on a paper accepted into Nature, for example. It just means everything to academics.
arXiv is the biggest undermining threat to the professional peer review process, but in a weird way, it also bolsters it.
Anyway, at least Computer Science doesn't care much about academic journals. Hacker culture remains fairly strong.
I am a layperson but I guess arXiv moderation is not different from peer-review. Some authors have voiced concern over the lack of transparency in the arXiv screening process.
> If you don't mind me asking, how do you deal with this kind of culture, where a normal process is being purposefully obstructed with such behavior from the reviewer?
A huge part of the explanation is survivor bias IMO. The vast majority of undergrads who start in life science labs wind up leaving after a few months due to some bad experience (or at least lack of a sufficiently positive experience; life science is mostly failure). A large proportion of PhD students leave for industry jobs (tech, biotech, smaller subset to finance/consulting) because academic faculty jobs are very hard to come by and require making very little money for a long time. The only people left for the long haul are sufficiently motivated by the upsides (see below) to deal with the bureaucracy and problems of academic life.
> Do you ever call people out who sprinkle their "reviews" with such passive aggression? What is their defense?
Reviews are anonymous (this is now becoming controversial), and most people wouldn't jeopardize the acceptance of their paper just to call out a reviewer being an asshole. Slight saving grace is that the journal editor (who sits between authors and reviewers) has the final say, and can override unreasonable reviewers (in principle).
> What highlights does your profession have that make it worth putting up with this?
In fairness, some upsides if you make it: intellectual freedom (carte blanche to study anything you can get funded), sense of significance of advancing the frontier of medicine, freedom to work on and profit from startups if your tech is translatable (there is a surprising number of millionaire++ biology professors), very good job security, etc. Some would argue that many/most biotech companies take from 1 to N technologies that academic labs brought from zero to one. Some examples: mRNA vaccines, numerous cancer immunotherapies, CRISPR/Cas genome editing, recombinant insulin. Just look at the Nobel Prize in Medicine list – nearly all academic work.
My h index is around 20, which just means I have lots of experience with peer review.
Peer reviews are text, it is hard to accurately infer emotions or intention. What one person sees as passive aggressive another person might see as polite and deferential or even helpful.
Consider further that scientists come from all over the world and often have deep cultural differences, it becomes even less likely that you know the reviewer's intention.
Science is really hard and it's easy to fool yourself. Smart people want criticism to help validate and improve their work.
Agreed, as a counter/Devil's advocate point though, wouldn't what is being written by the reviewer be obvious whether or not it's just pettiness and other non-constructive criticism, versus something that was well considered?
Is “evolving faster” more like 3x-10x, or more like 100x-1000x… I guess what I’m wondering is, can we help the Halderia out somehow so it can keep pace, or is it just operating on a total different timescale than a virus.
Halderia would be 'lower eukaryotes'; we are 'higher eukaryotes'.
The idea of 'helping the halderia out' by increasing mutation rate is kind of funny; that would almost certainly kill them (this is largely how radiation kills us). You would need to be able to reliably and specifically introduce favorable mutations (i.e. those that increase fitness), which is far beyond current capabilities.
Why would we need to be able to specifically introduce favorable mutations rather than just induce random mutation and select for favorable ones?
We’ve been taking advantage of the latter with selective breeding for millennia and more recently through inducing random mutations with techniques such as irradiation the green revolution was quite famously kick started by new cultivars that where developed by irradiating seeds and selecting those which led to plants with favorable characteristics.
In general we can conduct 'directed evolution' (selective breeding is an example). In this example, however, we're talking about improving the resistance of Halderia to the possible future mutations the viruses could develop to exploit them. This is a much, much larger harder to search space; the cost function is not well defined.
A few fruits which are common were the product of “atomic gardens”. Grow plants around a fixed radiation source, plant the resulting seeds, and see what grows.
Ruby red grapefruit is an example you can probably find in your grocery store. I think they made it by irradiating cuttings for grafting.
Haha, ok. I was thinking by a totally inappropriate analogy — I mean, we “helped” dogs evolve in a direction that lets them work for us better, including things like defending our livestock from wolves and coyotes. But coyotes don’t evolve many orders of magnitude faster than dogs!
It isn't just mutation rate but generation time as well, even with the same mutation rate a virus that replicates several times a day would evolve faster. But there's certainly scope for us to artificially select for traits in virovorous organisms for our own purposes, we commonly do for crop plants to provide viral resistance or tolerance and viruses don't overcome them too quickly. Traditional methods have included x-ray mutagenesis where we crudely induce mutations in a lot of plants and see if any are useful afterward.
1. the parent raised questions in a neutral way. these questions seem essential for validating experimental design. why would peer reviewers present such questions in passive-aggressive ways, and how can we fix this?
2. could you kindly recommend services/consultancies to validate experimental designs? if not, would you be open to consulting and doing what you did here -- suggesting ways to control for key variables? experiments relate to cancer research. contact info in bio.
> 1. the parent raised questions in a neutral way. these questions seem essential for validating experimental design. why would peer reviewers present such questions in passive-aggressive ways, and how can we fix this?
Peer review is obviously a complex and controversial issue, but some key points (at least in life/medical sciences) include:
A. Your reviewers are very often your competition. Reviewers are supposed to be subject matter experts in your area of research, and academic science is a small world. The other subject matter experts are exactly the people competing with you for grants, to finish projects first, for trainees, prizes, etc. (You can typically ask that specific people do/don't review your paper, but it's at the editor's discretion. Some fields are simply too small to take such preferences into account.) You can often identify your (supposedly anonymous) peer reviewers because they respond with a critique that your paper should cite some specific papers, and they are the common name on the bylines of those papers.
B. Peer review is uncompensated work by academics, very often done for for-profit publishers. Hard to be thrilled with that paradigm (though some scientists feel it's a reasonable 'academic duty').
C. The mindset in peer review is often more about gatekeeping the journal hierarchy than about simply ensuring good experimental design. Publishing in top journals is often a career-making achievement. It is incredibly common for reviewers to ask for (often very time consuming) additional experiments based on their opinions about what is interesting, what a paper in the journal should look like, etc. There is a bias where reviewers don't want someone else to have an easier time publishing in X journal than they did.
D. Not exactly a critique of peer review, but I think it's important to realize that peer review is not even intended to address one of the major problems in science – irreproducible results and/or scientific fraud. Reviewers have to take all data presented on face value. At best, peer review is simply a check against poor experimental design, errors in reasoning, and authors making claims stronger than what the data supports.
> 2. could you kindly recommend services/consultancies to validate experimental designs? if not, would you be open to consulting and doing what you did here -- suggesting ways to control for key variables? experiments relate to cancer research. contact info in bio.
As mentioned, CROs are the companies in this space, though I'm not familiar with any that focus specifically on vetting experimental design.
Well, that's the fundamental difference between tech and science. With tech the 'truth' is entirely instrumental - is the product useful? (Not entirely accurate, as a product could be far less useful than the alternatives but still a commercial success).
In science sometimes the goal is instrumental value, but more often it is inferential insight where there isn't a simple 'it works or it doesn't' truth value and the role of methodology and review to control for sources of false positives and false negatives, misconduct, and unwarranted interpretation of data are important.
I'd argue that peer review aids breakthrough science overall, because where shoddy but splashy research slips through review, sometimes years of research effort and funding get funneled into avenues opened by such putative breakthroughs that turn out to have been bullshit all along. The misdirection into dead ends has the opportunity cost of the potential of making real breakthroughs.
> 2. could you kindly recommend services/consultancies to validate experimental designs? if not, would you be open to consulting and doing what you did here -- suggesting ways to control for key variables? experiments relate to cancer research. contact info in bio.
They are called CROs (contract research organizations). Pay them money and they will work on your experiments for you.
3 - or simpler, look at the ratio of virus to non-virus that's 'consumed'?
As a human I accidentally ingest a lot of 'bad bacteria', it's just dwarfed by the nutritious (or delicious..!) stuff. I think that's what GP's getting at - distinguishing 'accidental'/sife-effect consumption from intentional; not necessarily that it's great sentient or evolutionarily designed intent.
Virus sinks: did you see the recent paper published in Journal of Allergy and Clinical Immunology? [1] It cites lots of other studies showing that nasal epithelial cells create extracellular vesicles (blobs of stuff floating outside the cells) that have receptors for cold viri. Since the vesicles don't have DNA the virus can't replicate. Infected vesicles get swept up the rest of the immune system, so they're decoy Roach Motels for viruses. The study shows that when the nose gets colder fewer vesicles are created, and claims that's why cold and flu cases increase in the winter.
> An important question will be whether viruses, which evolve far faster than eukaryotes like Halderia (let alone than humans), can turn the tides in the evolutionary arms race and become the exploiters of the Halderia.
I'd assume that's the case, otherwise I feel like there would be more Halderia and/or less viruses
Viruses form a part of a control system for themselves and for higher and larger life forms. If any system becomes unstable, or if one organism starts dominating or growing out of control, the other organisms have an evolutionarily created self interest in bringing things back into balance. Viruses play a huge part in this self regulation mechanism.
Eliminating viruses would have the unfortunate effect of decreasing overall system stability for biological systems at every level.
Viruses as I understand it are generally fairly specific as to what they can infect. I don’t think there’s any reason to believe an algae virus infect ciliates. But again, I’m a programmer, not a microbiologist.
Cross-species infection usually happens (I think) due to mutation, rather than a single strain being able to target vastly different species.
However, there are some that do. For example, the Powassan virus. Ticks pick up the virus from woodland mammals, and then transfer it to humans. However, ticks do not transfer the disease from human to human [0].
I think the use of the word 'eat' is a bit non-specific. Macrophages cannot survive on a diet of virus. They can absolutely 'eat' it in the sense of taking it from outside the cell, breaking it down into constituent components inside the cell, and then putting it back outside the cell as waste, but they can't use viruses as a food source.
The classic biochemical way to do this would be isotopic labelling. You grow virus host cells in media with funny isotopes of carbon, nitrogen, phosphorous, whatever you like, use those to produce virions, feed the virions to Halteria growing in an isotopically normal environment, wait a while, then collect the Halteria, separate them into their component molecules, and use mass spectrometry to see which ones have funny isotopes in.
This doesn't entirely answer all the questions you posed, but it does definitively tell you whether the Halteria are incorporating material from the virions into themselves.
I would also wonder if Halteria could be genetically modified to consume PFAs and microplastics in the human body, assuming that our own immune system didn't attack and eliminate them on sight faster than we could replenish them.
Seems like it'd be super useful for maintaining a virus-free environment in an ongoing manner in a circumstance where they would contaminate your results, but where the virovores wouldn't. Maybe there's a virus that you're able to account for in your methodology that you feed the virovores with, and they stick around and clean up other viruses that get into your culture.
Or maybe in an industrial process they could help dampen the spread of viral outbreaks in your bioreactor.
Co-culture might be fine. But realistically it's probably a lot easier to add neutralizing antibodies or other peptides or chemicals which would block viral infection.
For an industrial process it would likely be easier to just genetically modify your organism to be resistant to the virus.
A nice benefit of the virovore though would be it would evolve to counter evolution of the virii. You could still treat with peptides &c but eventually they'll stop being effective. Against a highly adaptive organism it's probably best to employ multiple overlapping treatments. I'm not 100% sure it's this particular talk [1], but this researcher has a fascinating talk on this channel about using phage therapy in tandem with antibiotics such that bacteria resistant to the antibiotic are susceptible to the phage. Iirc they were able to clear up a life threatening antibiotic resistant infection in a patient's
aorta with a single treatment.
Genetic modification can be tricky in long-lived cultures, the organism you're cultivating may discard your modifications. There's things you can do to make this more difficult, but I can imagine a really general solution that works for many cultures could be super useful (say, for cultures you're speculating about productizing, but don't want to make too much of an investment in until you've characterized them better).
I ran some wild west style, open air algae bioreactors for a while, and I'd fantasize about productizing organisms like this for pest control. Crazy things can happen in that sort of environment; I wasn't around at the time but there was a story about a storm which blew in from the against prevailing winds, carrying some weird kind of rotifer not normally native to that environment, and across the state people woke up to their ponds turning pink. In that kind of environment you're unable to anticipate which organisms will invade your ponds. I think it's possible those kinds of cheap, low-control methods of production will become very important.
There was a 1st Season Episode of Star Trek Voyager called The Phage where a bunch of aliens whose organs were being eaten away by some virus had to continuously harvest fresh new organs from unwitting travelers to stay alive. Is that fictional disease related to the real world virophage?
In Greek, the word Phage or Fage means "to eat" so that might be the origin. Coincidentally, that's also the name of a pretty rich and thick yogurt, which I assume has nothing to do with viruses.
Would be fascinated to hear how the hell they do this microbiologically. This study just seemed to strongly indicate they do it.
I mean, as the consumER you'd have to (a) be resistant to getting infected by the virus in the first place, (b) encapsulate the virus in a way it can't broach, (c) deactivate and decompose it into nutrients you can use, no?
Which seems a tall order for something designed and continually evolving to breach your cell walls!
Granted, Halteria ciliates don't appear to be the virus' primary target, so potentially lack necessary binding points / are impenetrable to them, but that seems like playing with fire. Or eating plankton if plankton were carnivorous and rapidly evolving...
Although maybe it makes evolutionary sense if the Halteria:algae ratio is extremely low? I.e. it was never beneficial to target Halteria when more numerous food sources were colocated.
Viruses need far more than binding points to make use of a cell. They need to handle attachment, penetration, uncoating, gene expression, replication, assembly, and release. Some of these may leverage host machinery, or sometimes the virus packs their own. If they use the host, they typically need to have greater flux kinetics than the host. If they're able to do this, there's a chance they resemble a virus that the host already knows how to deal with. In that case, they'll also need to outmaneuver any existing intracellular defenses.
That's a lot of evolution that has to happen to fit your target.
I think from the article the viruses don’t target the ciliates at all but rather algae. That explains (a). I expect b and c are answerable with gradients and membrane mumbojumbo, but a programmer not a microbiologist. I actually like the study author am surprised that this hasn’t been observed before. I would have expected viruses are food for something - as it notes they’re little bundles of tasty proteins and useful elements.
> deactivate and decompose it into nutrients you can use
Viruses are just packages of protein, lipids, and nucleic acid, exactly like any other biological matter. It's not particularly surprising that enzymes which can digest bacteria (Halteria's usual food) can also digest viruses.
Love this mindset — “Given the sheer abundance of viruses and microorganisms in the water, he figured it was inevitable that — even setting aside infection — the former would sometimes wind up inside the latter.”
Very silly beginner question: Arent viruses non-alive? Arent virsus just DNA strands that if they fall into the right place in a cell mechanism, the cell mechanism will replicate them by mistake.
There's an ongoing debate, that when the cell is taken over by the virus, at that point the virus is kind of alive. the infected cell is the viruses' living form.
1) The infected cell, is no longer the same as the organism's other cells. If it's a single celled organism, the infected cell no longer the original organism.
2) Once the "infected cell" starts shedding the virus, that's when the virus is alive so to speak. the actual virus microbe thats shedded can be thought as a sex cell of sorts. (Like pollen or mammalian sperm or eggs, etc.)
Disclaimer. I'm not a virologist and as far as I know, *most* virologist conclude (last time i checked) that viruses are non-living microbes
It depends how you define "alive". Which is not really an interesting scientific question; biologists understand (roughly!) what viruses are and how they work, and defining them as alive or not doesn't contribute anything to that understanding, it just puts a label on it.
A virus is basically not a full cell. It doesn't do much until it enters a cell where it essentially feeds information to make the cell start doing things. Like creating more of the virus. It can't do that by itself. It relies on the host cell to do all the processing.
If you think of the cell as a computer and the virus of some kind of information carrier (tape, cdrom, etc.), you can answer the question by asking yourself whether a cd-rom is capable of doing computation. Which would be a good analogy for being alive. To which of course the answer is no.
So, by that analogy, viruses are not alive. They don't act by themselves. In the same way DNA is not alive. It's just a passive protein.
They are sometimes DNA and sometimes RNA. They also usually have proteins and lipids surrounding the genetic material, providing some protection and also the means of entering a cell. When replicating, both the genetic material and those proteins have to be replicated.
This reminds me of a question I have asked of those with more biology knowledge and not gotten a satisfying answer: Would there be adverse outcomes if we somehow killed all viruses?
Also unqualified but presumably similar to if you remove predators from an ecosystem; without negative feedback, fast replicating organisms get out of hand, biodiversity drops, eventually the ecosystem either crashes or evolves new feedback loops.
Consider that, if you pick a type of organism or of a hat - it is probably a virus (eg, for each kind of cellular organism, there are many kinds of virus targeting that organism). Getting rid of all the viruses would cut biodiversity by more than half, just on it's own. That's pulling a lot of rivets out of your airplane (https://en.wikipedia.org/wiki/Ecosystem_service#Ecology see redundancy hypothesis).
Heres an article about depriving an ecosystem of predators:
I enjoyed reading this article, which gives a glimpse of the life of "wet science" researchers and the two phases - in vitro vs. in vivo (cf. the last sentence).
The fact that a virus can be nutrition is an effect of it being part of the physical world: "it's made of stuff". Computer viruses, in contrast, are pure information, hence their ingredients cannot be eaten.
Viruses are interesting because they are not alive, yet they replicate, which is at least one property of life forms; they are physically encoded information in a crystal hull.
The peer review process, which is being debated here, is a bit like UNIX: some of it sucks but half a century later we still haven't come up with anything better or nearly as good. Peer review is important, and I'm concerned about the floods of pre-prints that are often cited as if they were (already) scientific publications - many will never be. What would help to take out sloppiness, nastiness and generally poor quality in peer reviews is if journals also always had meta-reviewers (reviewers that review the reviews) like the computer science conference do that I publish in. One might say that is the role of the editor, but I see the editor more as a Program Committee Chair, higher-level role. A paper rejected by all reviewers unisono would be rejected, a paper accepted by most reviewers would be rejected and papers with controversial reviews could go up to the editor after potential adding another reviewer first, who could be tasked to address specifically disagreements. Reviewing should be part of postgraduate education (I teach my doctoral candidates how to do it), but almost nowhere is, so there are many sub-par reviews by people who are not mentored properly. Overzealous reviews often come from younger postdocs or first-year PhD students, whereas older faculty members tend to be more generous, IMHO.
latin years in school flashback, but that word is malformed, because virus is Latin 4th declension and there's no -o stem in any case. seems "viruvore" would be more appropriate, and matches the forming of actual latin present active participle (think -ing in english) "virulens" (virulent).
Assuming "virus" is 2nd declension leads to a contradiction, in there is an -o stem in a case, but that assumption contradicts the centuries old "virulent" which wasn't written "virolent".
And the reason i mention all this is that i have no idea how one finds modern etymologies for classical words without knowing the languages (or subsets of course) outright.
I don't think virus is a 4th declension noun, and I've seen it described in multiple sources as a 2nd declension (meaning slime, poison, infection, mucus, or something thereabout). It is unusual in being a -us noun despite being neuter, but irregularities happen (other examples of neuter 2nd declension -us nouns being vulgus and pelagus). In classical Latin, it is a mass/uncountable noun, and only got the modern meaning (and the ability for form plurals) in recent times.
That said, your point about virulent vs virolent is interesting, but I don't know enough about sound changes, or how that word came to be and made it's way to us to know if this is counter evidence to being 2nd declension, or if it can be explained away otherwise.
It is not uncommon for a language to borrow two words from one source language in different centuries. The two borrowings can then follow different mechanisms, perhaps because something about the target language has changed in the meantime. Or maybe because knowledge of the source language was widespread in the target language community when one word was borrowed but not when the other one was borrowed.
i'm trying to think of an example. do you have an example?
i can come up with a composite word whose two parts are non obvious and obvious, but they're not loan words : were+wolf, with were germanic cousin to Latin vir and wolf obvious.
> Many words of French origin were borrowed twice or more. There were at least three periods of borrowing: one that occurred shortly after the Norman Conquest and came from Norman French, one in the thirteenth and fourteenth centuries from standard (Parisian) French at the time when English nobles were switching from French to English, and a third one during the sixteenth to nineteenth century, when France was at the height of its power and international influence. Examples of doublets from the first and second periods are catch vs. chase, cattle vs. chattel, and warden vs. guardian. More recent borrowings are often distinguished by maintaining the French spelling and pronunciation, e.g. chef (vs. chief), pâté (vs. paste), fête (vs. feast).
"contagion" while Greek in ending looks like con- (together) and a Greek analogue of "tango, tangere, ... , tactus" (touch). Like whatever happens with two things touching?
"Contagion" is not Greek in ending (or in any other part; e.g. the Greek equivalent of con- would be syn-). As you surmise, the word is directly derived from Latin contingo; the "n" which is present in the Latin stem, but not in the nominative singular form of the word, is realized in the English borrowing, just the same way it is in station / vision / legion / etc. etc. etc. etc.
This seems pretty cool! I wonder if we can extend this experiment for other viruses like HIV, Covid etc to see if this Halteria can consume it. That would be ground breaking.
It would not. Certainly you can't use that organism inside a Human body. Your immune system would object - violently.
Another problem about HIV is that there are so few Virus particles "floating around" at any time, which (among other things) makes it challenging to fight with vaccines or pharmaceutics. And all Viruses are hard to get to when they are inside a cell, which is why the immune system mainly uses cell targeting mechanisms to get rid of viral infections, rather than the "humoral" defense of free floating antibodies (simplifying by a lot here).
If you would compute the mass of a typical infection dose or even a full-blown infection and calculated the maximum caloric content in all the chemical bonds, I'm pretty sure it would amount to not much more than a grain of rice or similar.
It is conceivable and probable that some parts of viruses get broken down to keto bodies usable in the krebs cycle. The amino acids in the capsule for sure. Parts of the lipids of a viral membrane (which some virus have) maybe. But those aren't special mechanism and are used more as an accident to the destruction of viral particles rather than an intentional harvesting of energy. The energy expended to destroy the particles in the first part is also probably greater.
Can someone ELI5 no one ever thought to look for this in the first place? Viruses cause so many illnesses, would it be possible to release (possibly benign) bacteria that eat the illness causing virus into the body (assuming the bacteria themselves aren't attacked by the immune system)?
Also, is this an accidental discovery? Having read the article, I am under the impression that it is a bit of a chance find.
IDK why some smartasses, who probably have not taken Biology in HS, decided to bury your comment but some subtypes of T cells are indeed able to attack virus-infected cells.
I've been wondering recently, and probably naively, about a related question: does the human immune system have any kind of metabolic (digetsive) function? My understanding carries to the various ways that immune cells destroy non-self cells through processes like phagocytosis and lysis, and to the mechanisms for excreting waste products via, e.g., lymph. It seems like there would be opportunities to recycle components from bacterial or other cells, similar to how Halteria appear to be "eating" viruses. But I haven't found any references to this in a cursory search of pubmed (maybe because I just don't know the right keywords).
So my question for HN: do immune cells "digest" their prey?
Food is essentially just a bunch of molecules/chemicals. Digestion is essentially a word for breaking big complex chemicals (ie food) down into smaller simpler chemicals. And metabolism is just a word for any chemical process which takes food, digests it, and yields energy and/or raw materials to synthesize and sustain life functions.
All cells, including those which make up the immune system, need energy to function, and material to grow, and thus require a metabolism to sustain themselves.
As for whether immune cells "digest" their prey (meaning break them apart), the answer is yes. Neutrophils are known to ingest (eat) all sorts of pathogens, and are known to digest bacteria and fungi. I'm not so sure with viruses, as they are much smaller entities, but there are probably certain cellular circumstances in which they are also "digested". If you are wondering whether they are also utilized for energy/material upon digestion (ie "metabolized"), that is more complicated to say for sure, but the answer is likely yes under certain circumstances, and depending on a lot of things.
Thats because, cells metabolize energy in a lot of different ways. In fact, there are so many ways cells "metabolize", there are probably thousands of "metabolic pathways" [1]. And when you really dig deep into it; proteins, enzymes, viruses, cells, and even us, look to be nothing other than complicated molecular machines [2], just different in scale and complexity.
Neutrophils for example take up their "prey" in vacuoles and then merge those vacuoles with vesicles containing acid.
In some form there is a "digestion" happening. It's actually a non-trivial question to say if there is any form of energy that "escapes", for example in the form of keto-bodies, lipids, whatever, but it's certainly not very significant and certainly not the point of the digestion.
OP conflated digestion and metabolisis. Although macrophages 'digest' in that they break things they 'eat' into component parts, they do not use those parts for energy (metabolisis). This is the key novelty here, these virovores are metabolising the viruses (i.e.: using them as an energy source), rather than just breaking them down.
No, not really. T-Cells don't "eat" stuff. You may mean macrophages, neutrophils and so on. And those actually get their energy mainly from glucose, while they actually expend energy to destroy the stuff they take up.
1. if the Halteria were not eating something_else, and that something_else was infected by the viruses?
2. if the Halteria themselves were not infected by the viruses?
3. are the Halteria trying to ingest the viruses, or are they just ingesting lots_of_things in the petri dish?
This observation seems interesting, assuming all other variables were constant and there was not some other interplay between the chlorovirus and other microbes which indirectly helped the Halteria grow:
>Halteria deprived of the chlorovirus, meanwhile, wasn’t growing at all.
Finally if the Halteria can ingest it and yet not be 'infected' by it then that seems awfully interesting as well.