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‘It’s something I have never seen’: How the Covid-19 virus hijacks cells (statnews.com)
114 points by onemoresoop 13 days ago | hide | past | web | favorite | 25 comments





This was a bit dense in some paragraphs for me as a layperson, but the conclusion sounded like we may have found a more reliable (read understood) way to tackle this virus. Is that the case? (I realize a lot more work would have to be done for effective drugs and vaccines)

It talks about two processes that happen.

The first is cells emit a signal to other cells that it's infected, which causes the cell receiving the signal to shutdown replication facilities.

The second message sends out a call for the cops.

Covd2 stops the first signal but allows the second.

Suppressing the first signal means it can replicate faster because the cells in the area didn't stop their replication facilities.

Allowing the second means you get tons of cops showing up because every cell is now calling the hotline. So many cops in one area causes problems of its own.

The cops can't kill them fast enough because the cells aren't slowing down replication. So you get tons of virus cells and tons of host immune cells, and not enough organ cells doing whatever they do.

Anyway they're saying possibly manually taking replication inhibitors would substitute for cells 1st message not working, and allow the runaway infection to be killed by the cops.

There are issues with just blindly taking drugs for this. So they'd have to find out when its appropriate.


There would likely be consequences to forcing your cells to stop replicating for an extended period too.

doesn't chemotherapy does something similar to this:

"The ability of chemotherapy to kill cancer cells depends on its ability to halt cell division. Usually, cancer drugs work by damaging the RNA or DNA that tells the cell how to copy itself in division. If the cancer cells are unable to divide, they die."

So wouldn't a low dose chemotherapy work on this drug?


It might, though the viral replication factories aren't necessarily the ones that are used for cells to replicate. If they do work, well, you'd have all those side effects of stopping cell replication that the parent mentioned - all those horrible side effects of chemo. Maybe it would be worth it, but it would have to be pretty darn effective to be worth those side effects.

> Suppressing the first signal means it can replicate faster because the cells in the area didn't stop their replication facilities.

The article also says this suppression is "stronger than the original SARS virus or influenza viruses".

The article touches on how this might connect with the severity of the disease. But I'm curious if it could also have something to do with how easy it is to transmit. If your lungs contain many times more viruses (than they'd have with most other diseases), then perhaps when you cough, many times more viruses float out into the air.


I read it the opposite way- am also a layperson but have memory of reading similar distilled versions of the research into HIV.

With COVID updates like this come every week; in the 1990s with HIV it was more like every few months there was some new report/observation. But those- like these were framed with the similar- holy shit, this virus does stuff we have never seen before.

I would caution to not infer that anything like a viable solution at scale on either the preventative side or the treatment side is anywhere near deployment.


Yes. In vitro (petri dish), this method appears effective; and we have a solid understanding of why it works.

In practice, this does not always translate to effective treatments in actual people. Further, this type of treatment is known to have risks and side effects, so we will likely not be able to give it to everyone as a preventative measure. Further, it is not clear how early in the disease's progression one would need to take such a drug to get a significant benefit.


> the conclusion sounded like we may have found a more reliable (read understood) way to tackle this virus.

No, but it gives doctors another thing to try with the possibility that it might work.

Interferon treatment isn't pleasant, so you won't do it without justification. This gives some justification to actually try it in humans if things are really bad.


At least they're not advocating AZT...

Hmmmm, Mr. President? I have this new experimental therapy you might want to try...


I’m against animal cruelty, but for that baboon?

I wonder how novel the attack vector of Covid-19 is, in comparison to other viruses.

HIV slowly kills you, by infecting your blood. But it requires blood contact.

Ebola quickly kills you by liquefying your internal organs, and you die in a hemorrhagic fever. It requires fluidic contact, or maybe via droplets too.

SARS-1 was transmitted via airborne and aerosols.

Covid-19 is airborne, even though they keep saying it’s via droplets.

So, the transmission is very contagious by being airborne. And it hides itself better, meaning not everyone infected will show symptoms, so there can easily be silent spreaders. And for those infected, it won’t show up for a few days, and you can transmit it without know you’re actually infected.

Then, it kills you by slowly wearing you down, until your other organs fail, and you technically die of organ failure.


the surname of the researcher, tenOever, seemed really odd to me, but I found an interview he did a few years back and looks like he's a real person.

https://www.youtube.com/watch?v=_WCXuaLXHP4


The capitalization is a bit odd, but it's not an uncommon Dutch surname. Usually spelled in two words: "Ten Oever". That would probably be "Banks" in English, as in a river bank.

While I'm on the subject, the Dutch (as in the nationality, not the language) are a bit unusual when it comes to surnames. It's common to capitalize every word in a name in many parts of the world, but the Dutch usually don't capitalize words like "ten" or "van" ("from", "of"), which can make for weirdly capitalized names like "Jan ten Oever". Were the same person to live in Belgium, the same Dutch name would become "Jan Ten Oever".


My favorite example of this is the famous physicist Gerard 't Hooft. His last name (by which I mean, the way you would refer to him in a formal situation like a citation) is "'t Hooft" — yes, that starts with an apostrophe and a lower-case T.

However, like many names which have a prefix, it is properly alphabetized under "H", not "t" or "'". This is an example of why linguistic tagging is often necessary, not just nice-to-have. A Dutch author "van Dijk" should be sorted under D, but an American (or, perhaps, Belgian) author "Van Dyke" should be sorted under V. The same is traditionally true of Scottish names starting with Mc/Mac, as I understand it. The rigid FIRSTNAME LASTNAME model of human names breaks down in very, very many places.


Very interesting. Same happens with some Spanish names, for example "del Rio" ("of the River"), "del" is a conjunction of "de" and "el" ("of" and "the"). But most people have accepted their names being "wrongly" capitalized - in the example "Del Rio".


Why was it odd to be a surname?

Maybe I'm wrong, but when translated it's more probable to be a surname than anything else.


One thing that threw me off is that sometimes people artificially construct names or modified forms of names. For example, "k8e" is an alternative form of "Katie".

Not being familiar with this surname, the first thing I noticed was that "ten" and "ever" are both English words. So I tried reading it as "ten oh ever" or "ten zero ever". I couldn't understand what that would mean, but it was the best interpretation I could think of.

In my experience, smart people are more likely to be idiosyncratic, so I wasn't inclined to dismiss the possibility.

I tried putting "tenOever" into Google, but the first two pages of results just take me back to him and his research. I tried Wikipedia too and search results there were also dominated by his work.

It wasn't until I came to the comments here that I was able to find the real answer.


I have a question that I hope someone in medical research might be able to guide me to understanding.

Suppose we had a 'good enough' vaccine today. It's side effects are rare enough and/or minor enough that it can be used on the general population, and it is effective in enough people to be worth using. However we don't yet know both of these things.

What would be the likely timeline from lab, to small feasibility trials to safety trials to population trials to large-scale distribution?

My guess based on the risk of distributing a vaccine that could have long-term risks down the line and the large population that would be taking it is that this could be multiple years of slowly increasing the population using it. Is this correct?


Vaccines in general are believed not to have long-term risks beyond those caused by the desired immune response - there's just not really a plausible mechanism that would allow them to. If it's proven to be effective and safe over O(months), scaling up distribution will be the only blocker.

(And note that this isn't quite a "suppose"; we have a lot of vaccine candidates today, and most experts expect some of them will prove to be good enough.)


Thanks, I didn't know either of these things.

New York Times says at least 12-18 months.

Source: https://www.nytimes.com/interactive/2020/04/30/opinion/coron...


It's so exciting to see science begin to gain such a deep understanding of the mechanisms at play. I'm hopeful we'll get an effective treatment long before the vaccine is available.

quote all virologists about every virus studied.



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