Comment by timr | Hacker News Reader

Comment by timr | Hacker News Reader

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.

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?

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.

Reply on news.ycombinator.com