Long COVID
This paper from USA (2024-04-06) found that Glutamate and N-acetyl-aspartate levels were significantly higher in people with Long COVID and ME/CFS than in controls. They found no significant differences between people with Long COVID and people with ME/CFS in any of the neurochemicals they looked at.
They also found correlations between the amount of these neurotransmitters and the severity of the symptoms.
I think this is great news. It makes it more likely that they can come up with a treatment for it, and it means that a treatment for one disease will probably help people with the other disease.
This paper from Spain (2024-04-02) found that, 48% of people with Long COVID had episodic memory issues, 27% had impaired cognitive function. Compared to people who had had COVID-19 but recovered, the Long COVID cohort had thinner cortex in the left posterior superior temporal gyrus of the brain.
This paper from a completely different group in Spain (2024-04-04) reported on a very similar study. They found that 40% of long haulers had memory issues, 55% had attention difficulties, and 59% had executive function difficulties. They saw correlations between memory issues and thinning in the left parahippocampal and right caudal-middle-frontal regions of the brain compared to controls.
This paper from Italy (2024-03-06) found that long haulers’ impaired lung diffusion capacity came from decreased capiliary volume, not decreased alveolar capacity or alveolar function. This is yet another piece of data that supports the microclots theory of Long COVID.
There have been a fair number of papers in the past six months which have found biomarkers for Long COVID. I usually don’t post them here, because it’s not really news you can use. (What are you going to do with the knowledge that IL-1R2, MATN2, COLEC12, MATN2, CSF3, C1QA, SPON-1, NFASC, and SCG3 levels are elevated?) Just please take comfort in knowing that researchers are making progress.
Two recent papers were able to correlate the levels of proteins with specific Long COVID symptoms, which is even more exciting! It gets us that much closer to understanding and treatments. This paper from UK (2024-04-08) found that SCG3 was elevated in patients that had gastrointestinal symptoms. This preprint from Brazil (2024-04-09) also found that different proteins in the blood which correlated with Long COVID symptoms, although they found different proteins than the UK paper.
This Correspondence from UK and Norway using Norwegian data from 2018-2021 (2024-04-10) found that vaccines gave some protection against Long COVID, at least pre-Omicron. Vaccinated people got Long COVID at a rate of 0.09%, while unvaccinated people got it at a rate of 0.17%.
I was surprised at how low the study’s Long COVID rates were. Most papers use definitions which place it much, much higher. Partly that’s because it’s really difficult to measure, partly that’s because it’s difficult to define what is/isn’t Long COVID, and partly that’s due to not having control cohorts to compare to. It might be that this study undercounted Long COVID, but I assume they used the same criteria for Long COVID between the vaxxed and unvaxxed, so the big difference should still be valid!
Vaccines
There is something called Guillain-Barré syndrome (GBS) which is a known, nasty but rare side effect of vaccinations. (Any vaccination, not just COVID-19 vaccinations.) This paper from Israel (2023-10-16) found that the risk of GBS in people vaccinated (with Pfizer) in the previous six weeks was actually lower — only 41% of the risk of controls (who had neither tested positive for COVID-19 or been vaccinated in the previous six weeks). However, the risk of GBS for people with a documented COVID-19 infection in the previous six weeks was 6.30 times higher than for controls.
The anti-vax crowd frequently seizes upon sudden deaths of young people to bolster claims that vaccines are harmful. This report based on data from Oregon (2024-04-11) found that there were exactly three deaths in vaccinated young people in the 100 days after vaccination. Of those three, two were due to long-term chronic conditions. That left one whose death was undetermined (to the researchers, at least)… compared to thirty who died of COVID-19.
Transmission
This case studies paper from USA (2024-04-05) found (using whole genome transcription) that two hospitalized patients caught COVID-19 from an asymptomatic patient who had been in the room hours earlier. For one of the infected patients, they were infected 2.75 hours after the contagious person left; in the other case, it was 4.75 hours after the contagious person left.
(NB: I swear I read a paper a while back which found that patients who were put in a bed that had been previously occupied by a COVID-19 patient — and we’re talking about beds, i.e. the pieces of furniture, not rooms — were more likely to catch COVID-19 than patients whose bed had previously had a non-COVID patient in it… but I can’t find that paper now. If there was such a paper, it could mean that the patients in the case study above caught it from fomites on the bed and not from aerosols in the air.)
This paper from Qatar (2024-04-09) found that a COVID-19 infection is about 82.4% effective* in preventing symptomatic infection between three and six months later, but that wanes to a negligible level after a year. *I believe the comparison cohort was people who did not have a record of being COVID-19 positive, but the paper was not clear about the control cohort’s characteristics.
Pathology
This paper from Canada (2024-02-29) found that SARS-CoV-2 f’s up infected cells more than we knew. Not only does it hijack the cell’s machinery to make more SARS-CoV-2 virus, it actually prevents the cell from making the stuff it is supposed to be making! It does this in two ways: it blocks the body’s own mRNA (the instructions for what to build) and it jams up the copying machinery (the ribosomes). It’s almost like catching COVID-19 is a bad thing. :-/
This paper from USA (2024-03-04) found that SARS-CoV-2 in infects macrophages (an important player in the immune system) in the lung capillaries to really nasty effect. They also found that SARS-CoV-2 uses the CD209 receptor (instead of the more common and famous ACE2 receptor) to infect those macrophages. This is important because it could potentially lead to new treatments: if you can jam up the CD209 receptors, you could prevent SARS-CoV-2 from infecting more macrophages.
Recommended Reading
This blog post points out the COVID minimizers on both sides have pushed for herd immunity: the right side of the political pushed for herd immunity via near-universal infection; the left pushed for it via near-universal vaccination. Both sides were wrong. The post also dissects different mainstreamed anti-vax rhetoric in clear terms.