Mild respiratory SARS-CoV-2 infection can cause myelin loss in the brain | Hacker News Reader

Mild respiratory SARS-CoV-2 infection can cause myelin loss in the brain

biorxiv.org

89 pointsbookofjoe49 comments

This is a paper in mice, and looks at a broad-spectrum markers or inflammation, focusing on CCL11, which has been associated with a large number of things, including allergic rhinitis:

https://www.sciencedirect.com/topics/immunology-and-microbio...

https://www.spandidos-publications.com/10.3892/etm.2020.9078

also cannabis use:

https://www.sciencedirect.com/science/article/abs/pii/S02785...

Importantly, they also note that the virus is not invading the neurons.

Be very cautious about extrapolating from this paper. They see up-regulation of microglial cells, which are macrophages (and are expected to be active during infection) and use that plus some other papers to make the claim. They show one figure concerning axonal myelin loss in mice showing a slight effect between groups, but that's a long way from any sort of link to a disease state, let alone in humans (I have updated this portion of my comment, after having more time to read the paper). Certainly, I wouldn't leap to any wild conclusions about other diseases related to myelin.

In short, they see some inflammatory signs in the brains of mice that are not associated with direct infection. That's interesting scientifically, but absolutely not worth panic or exaggeration.

This is a non sequitur. the idea that you expect brain inflammation when you get a mild cold is just dishonest.

This paper in the OP is pretty much confirmation of many presumptions that Physicians have had about COVID for the last few years.

Coronaviruses are adapting rapidly and are getting more creative in how they debilitate who they infect.

> This is a non sequitur. the idea that you expect brain inflammation when you get a mild cold is just dishonest.

I don't know what one "expects", but that's quite literally what the allergic rhinitis paper implies. It's also not the only paper that associates CCL11 with innocuous things.

The non sequitur is taking something like this and leaping to the conclusion that CCL11 is indicative of a severe problem.

Sorry OOT, would you mind commenting this https://news.ycombinator.com/item?id=30797582, thanks

There are several endemic coronaviruses that typically cause common cold symptoms. Viruses aren't "creative", and coronaviruses adapt slower than some other viruses such as influenza.

They seem to report results from human subjects as well.

> Human brain tissue from 9 individuals with COVID-19 or SARS-CoV-2 infection exhibits the same pattern of prominent white matter-selective microglial reactivity. [...] Humans experiencing long-COVID with cognitive symptoms (48 subjects) similarly demonstrate elevated CCL11 levels compared to those with long-COVID who lack cognitive symptoms (15 subjects).

Figure 3 shows some CD68 staining of a handful of human brain samples from people who died (not necessarily from Covid), and were subsequently found to test positive for Covid. The argument is that this is one sign of inflammation in the white matter (axons), but not gray matter (neural bodies) of these samples.

While this allows them to claim some connection to humans in a paper that is almost entirely about mice, it's so different from the bulk of the experiments that it is essentially a tangent.

Edit: Out of curiosity, I dug up the paper describing the people from whom these 9 samples were taken.

https://www.nejm.org/doi/full/10.1056/NEJMc2033369

These patients...let's just say they were not well prior to Covid:

> We performed conventional histopathological examination of the brains of 18 patients. Fourteen patients had chronic illnesses, including diabetes and hypertension, and 11 had been found dead or had died suddenly and unexpectedly. Of the 16 patients with available medical histories, 1 had delirium, 5 had mild respiratory symptoms, 4 had acute respiratory distress syndrome, 2 had pulmonary embolism, and the symptoms were not known in 3

I can't tell which of these patients' samples were used in this latest study, but...there's a lot going on. One of the patients was a meth addict, and another was a heroin addict, yet another was an alcoholic, and two others had recurrent seizures from prior head injuries:

https://www.nejm.org/doi/suppl/10.1056/NEJMc2033369/suppl_fi...

This just goes to show that you must dig into results like these before drawing any conclusion. If five of the nine samples used here were from people with drug addiction and chronic brain diseases, would it change your perception of the results?

"What Covid Can Do to Patients’ Brains": https://news.ycombinator.com/item?id=30753953

"Molecular imaging uncovers effects of Covid-19 on the brain": https://news.ycombinator.com/item?id=30710807

"Covid can shrink brain and damage its tissue": https://news.ycombinator.com/item?id=30592494

I wonder what other infections and substances we'd find that cause these sorts of issues if we looked hard enough?

I wonder that also. At this point, a lot of this seems like a situation of damned if you do damned if you don't. I saw a TikTok of a guy being able to show that whatever your preference, you can prove it through scientific papers. Seeing as COVID has been here for 2 years and even long haul COVID is exceedingly rare, I'm not too worried about any of it.

I'd love more data on this kind of thing in general. I developed a neurological disorder as a teenager with no apparent cause that affects me to this day, it's not like some bitter life-long crusade of having to know but I've always had a vague hunch it was a genetic disposition triggered by some external event and I'd be so curious to have that confirmed or debunked.

It's one of those ones that doesn't show up on an MRI but an fMRI shows characteristic changes, which suggests something wrong at a lower level I think.

We've been studying SARS-CoV2 a lot more than most other viruses, and in humans, it's often associated with confounding variables, so it's good to take studies with a grain of salt because the 200 common cold viruses probably haven't been studied this closely, and you have to be really careful to factor in emotional distress in human studies.

A lot. It'd be worth addressing. We see growing evidence of this.

Many are new too. Viral dynamics... changed with the rise of cities a few thousand years back.

Yes, this. COVID-19 is topical now, so we're looking hard, here. Is this something we've looked for with other diseases/conditions, in the past? If we go looking now, do we find that other insults that we thought we understood do this too?

Yes, this. COVID-19 is topical now, so we're looking hard, here.

I'd say more than 1 million confirmed deaths and over 81 million confirmed cases (in the US) in two years is more than just topical. We are approaching half a billion cases globally with over 6 million deaths.

Yes, there have been lots of Corona viruses in the past, some of which result in things as ubiquitous as the common cold.

It's called a novel Corona virus for a reason: humans had essentially zero immunity to this virus and its ability to evade the body's defenses and mutate so quickly at this scale is something we haven't seen before. Each major variant is more transmissible and more elusive than the previous one. BA.2 is now the dominant strain and the FDA just authorized another booster [2]. In many ways, we are still coming to grips with what we're dealing with.

We don't have a choice but to continue to look hard at COVID-19--the results of allowing it spread so widely are right in our faces and we have to deal with it.

[1]: https://www.worldometers.info/coronavirus/country/us/

[2]: https://www.fda.gov/news-events/press-announcements/coronavi...

I sense that we may me talking past one another. You seem to be focusing on my word choice and and justifying that we should spend resources studying COVID-19. My post does not dispute this at all.

What I'm saying is that to conclude that effect X (demyelination) is a cause for additional concern with respect to disease A (COVID-19), we should go back and see whether effect X is also present with respect to other diseases such as B, C, D (common cold, flu, etc). Because we may have found X linked to A because we are looking so hard at A, and not have found it previously with respect to B, C, D because we weren't looking as hard then.

Topical may imply temporary, which may have struck a chord with you, but this brings a genuine curiosity to the burning question, what are the conditions if any for returning to normal? I chuckle as I write this as living in western Canada, we just recently got the public place mask mandate removed so it's back to "normal" for some people even more, except we are dealing with record high inflation across the board (lumber too) -- c'est la vie...

Like, there have been mini-pandemics in the past (Spanish Flu is one I read a bit about), how do we "win" against it instead of just "minimize damage"? Herd immunity? Given headlines like OP, it makes one pause to think.

SARS-CoV-2 is sufficiently contagious that there will be no significant herd immunity effect to protect those who lack immunity. Everyone will be exposed. Fortunately the vaccines and other treatments are fairly effective at preventing deaths.

https://www.businessinsider.com/delta-variant-made-herd-immu...

https://www.medpagetoday.com/opinion/vinay-prasad/94646

The mask mandates implemented in most of North America were never an effective public health intervention. Areas which never had mandates, or removed them sooner, had similar outcomes. Correlations with death rates were weak at best, and confounded by multiple other factors.

Humans had a high level of immunity to COVID-19 before it even appeared. Many patients clear the infection entirely with the innate immune system, and suffer few or no symptoms. It's just like any other respiratory virus in that respect. Our species never would have survived so long if that wasn't the case.

The best evidence indicates we have seen something like this before, specifically in the 1889 pandemic. That was most likely caused by the HCoV-OC43 coronavirus (genetically very similar to SARS-CoV-2), although at this point we probably won't be able to prove the cause 100%.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7252012/

Additional boosters may be beneficial for some patients with defective immune systems. But they're not advised for the general population. We can't boost our way out of the pandemic.

https://youtu.be/jAjKQY0_BQA

Singulair (generic Montelukast) a prescription asthma medication is known to regenerate myelin.

https://www.cell.com/neuron/fulltext/S0896-6273(20)30716-9

Long covid patients have been seen to improve on montelukast and histamine blockers as well (loratadine & famotidine).

Just a note those are two different things/reasons.

The histamine blockers are for the common mast-cell reactions during/after covid.

But Montelukast is a leukotriene receptor antagonist which inhibits a specific enzyme.

https://en.wikipedia.org/wiki/Antileukotriene

Most of the multiple sclerosis protective compounds are generic pro-myelin drugs, e.g taking CDP-choline, melatonin megadoses, thymosin alpha 1, etc

'Can' or 'could'? And if 'could' how probable? Come one, this is HN!

Pretty sure I caught COVID March 2020, but wasn't tested. I lost my smell for 5 months and had chest pains. Just tried the trail making test and completed A in 20 sec and B in 52 sec, so seems like I don't have damage yet.

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