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Nick #AirborneCovidExhaustsTCells😷 Anderegg Profile picture
Nick #AirborneCovidExhaustsTCells😷 Anderegg
@NickAnderegg
DevRel, Coder, Writer, Raconteur. Masked #LongCovid ally/loudmouth. 🇺🇸in🇨🇦, he, cis, bi/queer. Tweets: public health, cognition, linguistics, ADHD, tech
Perpetual Mind Profile picture Guus Brugman 💙 Profile picture Just Here For The News Profile picture 4 subscribed
Jul 8 • 20 tweets • 8 min read
OOHHHH WOW! New preprint on the host immune response in Long Covid was just posted (few hours ago), and it's more significant than the 3-gene signature!

They found reactivation of viral herpes (EBV/CMV/HSV2) and CONFIRMED PERSISTENT SARS-CoV-2 INFECTIONS! Here's a summary...

1/ Preprint Title: "MENSA, a Media Enriched with Newly Synthesized Antibodies, to Identify SARS-CoV-2 Persistence and Latent Viral Reactivation in Long-COVID." Abstract: "Here, we use MENSA, Media Enriched with Newly Synthesized Antibodies, secreted exclusively from circulating human plasmablasts, to provide an immune snapshot that defines the underlying viral triggers. [...] Applying the same principles for long-COVID patients, MENSA is positive for SARS2 in 40% of PASC vs none of the COVID recovered (CR) patients without any sequelae demonstrating ongoing SARS2 viral inflamma... IMO, this is a hugely important study, so I'm going to do my best to explain it in detail, in a way that everybody can understand!

The headline here is that a persistent/reactivated infection of (one or more of) SARS2, EBV, CMV, and/or HSV2 were found in 60% of LC patients!

2/ "In summary, MENSA is a novel immune diagnostic which captures unique signatures of the early-minted ASC in the blood to reveal the cause of illness. In chronic conditions such as PASC where serum antibody titers are high, MENSA is an independent matrix that identifies persistence of SARS2 viruses or antigens and can also recognize the reactivation of latent herpes viruses, such as EBV, CMV, and HSV2 in 60% of patients. This host immune snapshot reveals the fundamental drivers of viral persistence and reactivation in this chronic disease." That means 60% of LC patients have one o...
Jul 7 • 27 tweets • 10 min read
GUESS WHAT?! A new study has shown SARS-CoV-2 infection is DISTINCT from common respiratory viruses!

Unequivocally, COVID is NOT "just a cold."

These findings are HUGELY significant, for multiple reasons! Here's a breakdown of the study (written for a general audience)...
1/16 SARS-CoV-2 infections—both symptomatic and asymptomatic—produce distinct host immune responses compared to human rhinovirus infections (the common cold), influenza virus infections, and RSV infections. That is, SARS-CoV-2 induces a set of changes in gene expression with significantly higher magnitude of change compared to other common respiratory viruses. For each of the four viruses, the column on the left shows differential gene expression (relative to controls) for symptomatic infections, while the column on the right shows differential gene expression for asymptomatic infections. Note... The paper is fairly complicated, so I'm going to start with the high-level takeaways before explaining everything in more detail.

Overall, they found a 3-gene signature that distinguishes SARS-CoV-2 infections from common viral infections—long before PCR test positivity!

2/ A T-Cell-Derived 3-Gene Signature Distinguishes SARS-CoV-2 from Common Respiratory Viruses Abstract: ..., we performed a multi-cohort analysis with integrated bioinformatics and machine learning. We collected 3730 blood samples from both asymptomatic and symptomatic individuals infected with SARS-CoV-2, seasonal human coronavirus (sHCoVs), influenza virus (IFV), respiratory syncytial virus (RSV), or human rhinovirus (HRV) across 15 cohorts. First, we identified an enhanced cellular immune response but limited interferon activities in SARS-CoV-2 infection, especially in asymptomatic cases. Se...
Jun 3 • 37 tweets • 13 min read
SIGNIFICANT new study has found a potential mechanism of ALS pathogenesis (with broader implications for other unexplained/idiopathic/"functional" neurological conditions?!)

This thread is pretty long, because I try to explain *everything* in a way anyone can understand!

1/many Endogenous Retroviruses are Dysregulated in ALS doi: 10.1016/j.isci.2024.110147 Amyotrophic Lateral Sclerosis (ALS) is a universally fatal neurodegenerative disease with no cure. Human endogenous retroviruses (HERVs) have been implicated in its pathogenesis but their relevance to ALS is not fully understood….. Using different methods of feature selection, including differential expression analysis and machine learning, we discovered that transcription of HERV-K loci 1q22 and 8p23.1 were significantly upregulated in the spinal cord of individuals with ALS. Additionally, we identified a subs... The short summary is that an endogenous retrovirus (HERV-K) is highly expressed in the brain and spinal cord of ALS patients, and may lead to neuroinflammation which leads to neurodegeneration.

These next several tweets are the background needed to understand the results!

2/ Image
May 27 • 19 tweets • 7 min read
HOLY SHIT. These mechanistic findings about covid's impact on immune signaling seem potentially HUGE!

Let's dig in...

(And I'm honestly ecstatic right now, because this paper seems to support my hypothesis about *how* I personally avoided LC.)

1/ SARS-CoV-2 Selectively Induces the Expression of Unproductive Splicing Isoforms of Interferon, Class I MHC, and Splicing Machinery Genes A plethora of respiratory viruses, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), strategically manipulate the host’s RNA processing machinery to circumvent antiviral responses….. Our findings explore a suggested but uncharacterized mechanism, whereby SARS-CoV-2 infection induces the predominant expression of unproductive splicing isoforms in key IFN signaling, interferon-stimulated (ISGs), class I MHC, and splicing machinery gene... When a cell is infected, the MHC-I protein presents antigens from the virus to the immune system to signal that the cell should be destroyed.

When infected with SARS-CoV-2, some genes involved in creating MHC-I are suppressed *by the virus* and form defective proteins.

2/ SARS-CoV-2 Promotes Unproductive Splicing of Class I MHC Genes Pathways associated with antigen presentation through class I MHC exhibited greater upregulation among unproductive isoforms compared to productive isoforms (Figure 2A)…. Genes encoding core class I MHC complex elements, such as B2M, HLA-A, and HLA-B, also displayed a higher unproductive fold change. The HLA-B gene revealed five distinct overexpressed retained intron isoforms in ACE2-MOI2.0 cells (Figures 2F and S2C). This upregulation of unproductive isoforms could potentially decrease HLA-B protein production in SARS-CoV-2-in...
May 18 • 6 tweets • 3 min read
When I had covid in Jul 2020, it was the worst experience of my life... but it was only *four days* of severe symptoms with an abrupt onset and resolution. Then a paper came out in October saying my symptoms strongly predict LC (93.5%)!

So how did I avoid chronic symptoms??
1/
The model using only the “top eight” symptoms predicted ME/CFS development most accurately. The top eight features are shown below in Table 2 along with the corresponding symptom domains: 1. Fatigue/extreme tiredness 2. Mentally tired after the slightest effort 3. Feeling unrefreshed after you wake in the morning 4. Minimum exercise makes you physically tired 5. Next-day soreness or fatigue after non-strenuous, everyday activities 6. Needing to nap daily 7. Dread, heavy feeling after starting to exercise Excerpt from: Hua, Schwabe, et al. (2023). Predicting Myalgic Encephalomyelitis/Chron...
Predicting Myalgic Encephalomyelitis/Chronic Fatigue Syndrome from Early Symptoms of COVID-19 Infection Highlighted portion of abstract: "Early symptoms, particularly those assessing post-exertional malaise, did predict the development of ME/CFS, reaching an accuracy of 94.6%. We then investigated a minimal set of eight symptom features that could accurately predict ME/CFS. The feature reduced models reached an accuracy of 93.5%. Our findings indicated that several IOM diagnostic criteria for ME/CFS occurring during the initial weeks after COVID-19 infection predicted Long COVID and t... I think I avoided LC by random genetic chance

I put my 23andMe data into Promethease, and it turns out I have a gene that occurs in about 9.7% of white people, and it's associated with better control of viruses in general, incl. HIV, herpes, and hep C:
2/ omim.org/entry/142840#m…
SNP: rs9264942(C;C) Description: 90% reduction in HIV viral load The rs9264942(C;C) genotype is reported to be associated with a 90% reduction in viral load in HIV-infected individuals. [] See also rs9264942 and HIV.
May 6 • 13 tweets • 3 min read
I don’t know how to say this without sounding fear-monger-y, so here goes:

Brace yourself for things to get really bad, really fast.

In this case, “things” refers to *everything*, including public health and the climate. I think that,… In multiple ways, certain patterns that were governed by self-limiting processes have fallen apart, because the context in which those patterns existed have slipped too far out of homeostasis.

But that’s not even my biggest concern.
Apr 15 • 22 tweets • 8 min read
Oh shit, continuing in the theme of "everything is inflammation, it turns out"…

A GROUNDBREAKING research paper shows seasonal variation of systemic inflammation in Bipolar Disorder, explaining just… so, SO MANY ASPECTS of the disorder, including treatment resistance!

1/ New Study on Systemic Inflammation and Bipolar Disorder: "Higher Seasonal Variation of Systemic Inflammation in Bipolar Disorder" Dallaspezia, S., Cardaci, V., et al. (2024). “Higher Seasonal Variation of Systemic Inflammation in Bipolar Disorder.” International Journal of Molecular Sciences, 25(8). doi: 10.3390/ijms25084310 They present a clear hypothesis, test it in a way that accounts for multiple potential confounding factors, and their conclusion is clear: seasonal variations in systemic inflammation are associated with Bipolar Disorder (BD)

Many fascinating immune system connections, too!

2/ Figure 1. Changes in systemic inflammation across seasons in participants, divided according to diagnostic groups. Left: neutrophil to lymphocyte ratio. Right: systemic immune-inflammatory index. Points are means; whiskers are standard errors of the mean.
Apr 14 • 10 tweets • 4 min read
I just read through the (automatically translated) Dutch LC guidelines and they are… somehow simultaneously aware of the worst consequences AND absolutely divorced from reality. Just contradictory, gaslighting nonsense. Let’s take a tour!

(This thread is gonna be enraging.)

1/
Okay, so first off, this is an automatic translation, and it translates some of the medical words literally. For example, “gloomy” is used a bunch, which I think is supposed to be “melancholy,” an older term for “depression.” But it makes everything sound more absurd!

2/ Anxiety, gloomy symptoms, sleep problems and other psychological complaints Ask for: • nature, seriousness and course • a possible relationship with the acute phase, or other long-term complaints post-COVID-19; think of anxiety, coughing or thoracic complaints as a reason for poor sleep. • Consider using the 4DKL. • Consider whether there may be anxiety disorder or depression (see the NHG Standards Anxiety and Depression). • For sleep problems, see also the NHG-Standard Sleep Problems and Sleep Aids.
Apr 13 • 26 tweets • 10 min read
Oh, cool, a new systematic review on the pathophysiological mechanisms of Long COVID was published today. Here's a summary (well, more like a play-by-play) of the paper.

I gotta say, I love when thorough papers exactly match my mental model of LC! This paper covers it all!

1/ Title card for the thread "New Systematic Review on the Pathophysiological Mechanisms of Long COVID," for a study published on April 12, 2024. The title of the study is "Pathophysiological Mechanisms in Long COVID: A Mixed Method Systematic Review," and the following text from the abstract is highlighted: Overall, the quality of reporting across the studies included in this second review was moderate to poor. The pathophysiological mechanisms with strong evidence were immune system dysregulation, cerebral hypoperfusion, and impaired gas transfer in the lungs. Other mech... For this review, they were intending to do a meta-review, but they found that the existing systematic reviews were lacking, so they just had to do their own. Overall, I think their methodology was pretty thorough.

2/ Conducting a systematic review in this diverse and fast-moving field is never going to be ‘definitive’, but we believe the time is right for a systematic and transparent synthesis of the literature that aMempts to integrate the findings across different domains into a causal network to help identify suitable therapies. We originally intended to conduct a meta-review to inform our research. However, existing systematic reviews were found to be of low quality, and we found recent narrative reviews to be speculative and not grounded in a systematic approach to finding and assessing recent research....
Apr 8 • 21 tweets • 9 min read
Why the hell is HPAI H5N1 doing that?!: A Brief Twitterature Review.

This thread is going to be a summary of *past* knowledge of influenza dynamics, and the *recent* bafflement at HPAI A(H5N1) that scientists have been expressing in the literature.

1/ Title card for this thread, and screenshot of the abstract for the paper "Recent Changes in Patterns of Mammal Infection with Highly Pathogenic Avian Influenza A(H5N1) Virus Worldwide". The abstract says: We reviewed information about mammals naturally infected by highly pathogenic avian influenza A virus subtype H5N1 during 2 periods: the current panzootic (2020–2023) and previous waves of infection (20032019). In the current panzootic, 26 countries have reported >48 mammal species infected by H5N1 virus; in some cases, the virus has affected thousands of individual animals. The... Currently, we seem to be facing an unprecedented threat when it comes to Influenza A(H5N1) infections in mammals. There is, of course, increased interest in emerging pathogens, but the sheer quantity of mammal infections is a concern.

2/ We found 59 scientific articles on mammals infected naturally by H5N1 virus, 23 from previous waves of infection (up to 2019) and 36 from the current panzootic event. The articles reporting mammals infected naturally in previous waves were published during 2004–2018, whereas those addressing the current panzootic were published during 2021–2023. The current panzootic has thus generated more articles in 3 years than all the previous waves of infection (published over a 15-year period). This fact suggests increased general interest in emerging pathogens affecting biodiversity and mammals (wil...
Apr 7 • 25 tweets • 11 min read
Someone asked for my recommendations on elastomeric respirators, so is a guide to selecting the right one for you!

Three key points:
- They all meet the same SAFETY standard
- You get what you pay for in terms of COMFORT
- Ensure all the components you buy are COMPATIBLE

1/
A preview of all the things that will be discussed in this post, including (in clockwise order starting from the blue respirator): - MSA Advantage 900 half-mask respirator - MSA Advantage 420 half-mask respirator - Honeywell North 7700 half-mask respirator - Honeywell North HM500 half-mask respirator - Honeywell P100 Particulate Filter cartridges - Honeywell Volatile Organic Vapor cartridge - Honeywell Filter Cover with N95 Filter Pad - MSA Advantage P100 Particulate filter cartridge Just three quick notes:
- I hardly actually *use* elastomerics, preferring Vitacore and 3M N95s.
- The prices are what I actually paid for each item (in Canadian dollars), included as relative prices.
- Some alt texts include extra info.

2/
Apr 2 • 20 tweets • 7 min read
Here's a thread about a paper that build a more accurate model of depression—as an outcome of PHYSIOLOGICAL factors! I'm genuinely impressed by the robustness of their method, and I'm usually nitpicky as fuck about research methods!

They come in HOT in the abstract…

1/ Towards a major methodological shift in depression research by assessing continuous scores of recurrence of illness, lifetime and current suicidal behaviors and phenome features They point out that, fundamentally, it's a mistake to represent a complex spectrum of factors with a single binary metric.

When they actually account for these complex factors, they end up with a robust statistical model that explains how the factors interact.

2/ "The binary major depressive disorder (MDD) diagnosis is inadequate and should never be used in research. ... The study’s objective is to explicate our novel precision nomothetic strategy for constructing depression models based on adverse childhood experiences (ACEs), lifetime and current phenome, and biomarker (atherogenicity indices) scores. ... The outcome of depression should not be represented as a binary variable (MDD or not), but rather as multiple dimensional scores based on biomarkers, ROI, subclinical depression traits, and lifetime and current phenome scores including SBs.&...
Apr 1 • 19 tweets • 6 min read
Well, would ya look at that.

Yet another condition—one that is primarily marked by 1) psychological symptoms, 2) chronic fatigue, and 3) chronic pain—is found to be neuroinflammatory in origin!

This paper is FASCINATING, because the condition is associated...

1/11
Screenshot of "In major dysmood disorder, physiosomatic, chronic fatigue and fibromyalgia symptoms are driven by immune activation and increased immune‐associated neurotoxicity" published in Scientific Reports (a Nature journal).
Highlighted text: "Major depressive disorder (MDD) is accompanied by activated neuro‐immune pathways, increased physiosomatic and chronic fatigue‐fibromyalgia (FF) symptoms. The most severe MDD phenotype, namely major dysmood disorder (MDMD), is associated with adverse childhood experiences (ACEs) and negative life events (NLEs) which induce cytokines/chemokines/growth factors. ... Physiosomatic, FF and gastro‐intestinal symptoms belong to the same factor as depression, anxiety, melancholia, and insomnia. The first factor extracted from these seven domains is labeled the physio‐affect... ...with a history of traumatic events (including emotional trauma).

This shows that—even for psychological disorders that are known to directly result from psychological trauma—the etiology of the disorder is PHYSIOLOGICAL, not "mental."

2/11
Mar 14 • 39 tweets • 13 min read
Here's a thread about a paper I recently read that made me genuinely *furious*.

It's a paper from 1980.

You know... 40 years before the pandemic began.

You wanna know the title?

"Coronavirus Infections of Man Associated With Diseases Other Than the Common Cold"

1/ If you're now thinking "well, it probably can also cause pneumonia and acute respiratory distress syndrome," you'd be correct. If you guessed another major LC issue, neurological symptoms, YOU'RE CORRECT AGAIN.

But it gets worse! Let's take a little tour of the method...

2/
Mar 13 • 19 tweets • 6 min read
I want to point out some highlights from this piece that totally surprised me while researching it. A bunch of things were offhandedly mentioned in a paper, and then when I looked at the source, it opened up a tanker-truck-sized can of worms People with an asymptomatic acute infections can develop Long Covid. The risk from asymptomatic infections is definitely *lower* than symptomatic infections, but it's NOT ZERO.

What the hell, amiright? However, the damage done by COVID-19 is cumulative (Bowe et al., 2022). Even someone who recovers from an asymptomatic (Ma et al., 2023) or mild case (Novak et al., 2022) of COVID-19 is at risk of developing one or more PCCs. In fact, a recent review by Boufidou et al. (2023) noted that those who were reinfected were more prone to developing long-term symptoms—in comparison to those who were only infected once—and more prone to “various complications, including potential cardiac, pulmonary, or neurological problems” (p. 7). Even asymptomatic SARS-CoV-2 infections can result in long-term sy...