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wubwub t1_jdlp338 wrote

Oh the ironicness. After hearing antivaxers say the are avoiding the vax because it changes your DNA.


[deleted] t1_jdlqmv8 wrote



wubwub t1_jdm0tq4 wrote

I know the word is "irony" but I deliberately said "ironicness". It's a _very_ old (can't believe it is 23 years now!) reference to a Daily Show bit about a deer crashing through the window of a taxidermy place.

Ever since then I love using the word "ironicness"


AlexHanson007 t1_jdlitu8 wrote

Would anyone be kind enough to tell me what this means in Layman's terms please?


BananaResearcher t1_jdlku8r wrote

Lots of viruses make use of the host's DNA for their own purposes. This study looked at how SARS-CoV-2 affected host DNA, on a large scale. [more in-depth: DNA is a giant, giant molecule. It's so big that its overall organization itself is really important and affects all kinds of things. A very simple example is that expression of a certain gene may rely on activation of a region on the DNA that is, in 1-dimension, extremely far away. But just like you can loop a rope back on itself to bring two points close together, these points can be extremely far in 1 dimension (along the DNA chain) but right next to each other in 3 dimensions.] This study found that SARS-CoV-2 does indeed modify infected cells' DNA on large scales, and this is important not just for acute infection but can cause lasting impacts after the infection is cleared.

ELI5: The virus bends the DNA around so the cell can't fight the virus as effectively


AlexHanson007 t1_jdllfj2 wrote

Thank you very much.

So, is that saying this could be the cause of "long covid" or that it makes us vulnerable to other viruses in future?


BananaResearcher t1_jdllrpa wrote

From the authors, my emphasis

>Epigenetic alteration is known to exert long-term effects on gene expression and phenotypes37,38. Given the increasingly realized high incidence of post-acute SARS-CoV-2 sequelae (long COVID39), understanding the viral impacts on host chromatin and epigenome will not only provide new strategies to fight SARS-CoV-2 in the acute phase, but also pave the way for unravelling the molecular basis of long COVID for its intervention.


AlexHanson007 t1_jdllvji wrote

Thanks. You're very kind. I'm sure others will appreciate it too.


priceQQ t1_jdn8hp5 wrote

Long COVID has been studied quite a bit in large studies, so rather than saying “might” it’s better to look at what’s actually been linked to it.



AlexHanson007 t1_jdncwt4 wrote

Thank you for linking that. However, it's 36 pages of technical medical language that I don't think I will have the expertise to follow! :)


weird_elf t1_jdlje36 wrote

>Here we characterized the 3D genome and epigenome of human cells after
SARS-CoV-2 infection, finding widespread host chromatin restructuring
that features widespread compartment A weakening, A–B mixing, reduced
intra-TAD contacts and decreased H3K27ac euchromatin modification
levels. Such changes were not found following common-cold-virus
HCoV-OC43 infection.


Abeyita t1_jdljpwh wrote

I have no idea what that means.


AimlessZealot t1_jdnj41u wrote

I don't spend a lot of time on genetics but as I remember it:

Compartment A weakening- Active chromosomes being weakened.

A/B mixing - Inactive and active chromosomes coming in contact and potentially affecting each other when they are supposed to be kept in separate compartments to avoid that.

Intra-TAD contact - Genes that exist to help enhance, promote or silence specific other genes can affect genes they were not intended to, thanks to the isolating boundaries being broken.

Decreased H3K27ac modification - (This one I kinda remember) This reduces the likelihood of DNA correctly copying sections when signalled (enhanced) and causes some genes to not be enhanced. This is a problem because sections like our opposable thumbs and brain development have been linked to enhancer genes doing their thing, of which many depend on H3K27AC modification to help.

Hope that helps.


y0nm4n t1_jdlklrm wrote

This is…not layman’s terms?


terekkincaid t1_jdmefxd wrote

Viruses do all kinds of things to hijack a cell's machinery. The question is, how long do those cells survive? Are there SARS-CoV-2-infected cells that don't die and avoid detection by the immune system? Are they reverting to normal or semi-normal function after infection? Most cells are a lost cause after viral infection for any number of reasons. Is there a reason they expect these cells to survive and somehow cause "long COVID"? Is there a proposed mechanism?


3rddog t1_jdmh7en wrote

I think the paper basically hints that it’s a potential cause of long Covid but the exact mechanism is not understood at this point.

>… will not only provide new strategies to fight SARS-CoV-2 in the acute phase, but also pave the way for unravelling the molecular basis of long COVID for its intervention.


terekkincaid t1_jdn74zk wrote

That's kind of my point. These cells wouldn't stick around long enough to be involved in long COVID. It's like saying peanut butter is found in crunchy and creamy varieties. This might help us unravel why waffles are so popular. If you're going to speculate in your discussion, you have to have some kind of hypothesis that links them logically (that leads to your next paper).


dumnezero t1_jdm7s0j wrote

Is this a risk for oncogensis?


chemicalysmic t1_jdmp99d wrote

Intuitively I want to say it is possible - any modification to DNA can potentially promote oncogenesis depending on how that affects gene expression and regulation of transcription. In this case, we don’t know yet.


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Darksaint91 t1_jdmtk65 wrote

Is this why there’s were many reports of diabetes in young adults and kids after getting covid? The virus changed some cells causing the immune system to attack them which then caused diabetes, specifically T cells and type 1 diabetes?