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Nick #AirborneCovidExhaustsTCells😷 Anderegg Profile picture
@NickAnderegg
Jul 7 • 27 tweets • 10 min read • Read on X
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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...
Because the signature:

1. is SPECIFIC to SARS-CoV-2,
2. is an EARLY indicator of infection,
3. is a DISTINCT pattern from other infections, and
4. even accurately identifies Omicron infections,

this discovery may be useful as a diagnostic tool AND a direction for treatment!

3/ "The 3-gene signature offered two major improvements to SARS-CoV-2 infection triage: specificity and early diagnostic power. ...showed superior diagnostic performance only in SARS-CoV-2 ... achieved excellent diagnostic performance in Omicron patients ... showed exceptional performance to identify SARS-CoV-2 infection before detectable viral RNA on RT-PCR testing.... ... The bioinformatics methods, including DEGs and WGCNA, provided biological insights into the stable SARS-CoV-2 specific candidate genes. The machine learning approaches on these candidates offered a better extrapolation po...
One of the major limitations of this study is that it's unknown how applicable this signature will be for immunocompromised individuals. Why?

Because T cells were the major source of this 3-gene signature being expressed! This is important, because...

4/ "Hence, we could not assess how the 3-gene signature would perform in patients with comorbidities, especially immune system-related disorders. Future studies validating the 3-gene signature should focus on addressing these limitations. In summary, our study aimed to uncover the unique pathogenesis of COVID-19 by investigating the differential host responses to prevalent viruses. We systematically identified a SARS-CoV-2-specific 3-gene signature that could independently distinguish asymptomatic and symptomatic individuals infected with SARS-CoV-2 from other respiratory viral infections. ...
This is YET ANOTHER study showing SARS-CoV-2 adversely impacts the immune system.

Monocyte abnormalities (decreases) were found in BOTH symptomatic and asymptomatic SARS-CoV-2 infections! Because monocytes INCREASE in normal immune response, this suggests monocyte infection!

5/ "In addition, the results of CIBERSORTx revealed a reduced level of monocytes in SARS-CoV2 infection, while other viruses introduced an elevated level of monocytes, especially in the symptomatic group (Figure 3A). SARS-CoV-2-related monocytic abnormalities have been observed in both symptomatic [53] and asymptomatic cases [17]. The possible mechanism might be that the monocytes could be directly infected with SARS-CoV-2, leading to pyroptosis [54]. Moreover, attention should be paid to the boosted levels of IFNG and TNF in COVID-19 (Figure 3B), as synergism of TNF-α and IFNG triggers i...
This study also found the same odd immune response patterns found by other studies: The immune system is STRONGLY activated (especially the inflammatory response), but the pathway responsible for signaling *targeted* attacks on infected cells is suppressed!

6/ "Host responses resulting in SARS-CoV-2 infection differed from several common respiratory viruses. These results were in line with previous in vitro studies [9] (Figure S5). Although part of ISGs (i.e., IFI27) were enhanced in SARS-CoV-2 infection (Figure 2A), moderate IFN responses have been a sign of COVID-19 (Figure 2C). The improved cellular immune response, such as strong T cell responses and high secretion of TNF, were observed, surprisingly in these asymptomatic subjects (Figures 2 and 3). It has been reported that asymptomatic SARS-CoV-2-infected individuals might develop an effi...
As shown in Figure 2C, BOTH symptomatic and asymptomatic SARS-CoV-2 activate identical cellular pathways, but with less inflammatory signaling for asymptomatic infections.

That is, even asymptomatic SARS-CoV-2 impacts processes usually unaffected by the other studied viruses!
7/ Figure 2C from the paper. This shows the pathways implicated by "differentially expressed genes" in symptomatic and asymptomatic cases of different viral infections. This shows that for both asymptomatic and symptomatic SARS-CoV-2 infections, there are many different cellular pathways that are strongly activated; there is usually much less activation of these pathways for HRV, IFV, and RSV in *symptomatic* infections than there is for SARS-CoV-2 in *asymptomatic* infections. This isn't good news. It suggests that the impacts of asymptomatic infections are likely similar to sympto...
This study strongly suggests that there are "distinct molecular mechanisms" at play during SARS-CoV-2 infections, relative to other common respiratory viruses.

It *unambiguously* shows, however, that even asymptomatic SARS-CoV-2 infections are NOT "just a cold."
8/ "Discovery and validation of SARS-CoV-2-specific host response genes have been calling [26]. To address this issue, an ideal dataset for biomarker discovery should include not only SARS-CoV-2 infections but also other respiratory infections (Figure 4). Therefore, we co-normalized datasets HRA000786 and GSE17156, which included both asymptomatic and symptomatic cases. With integrative bioinformatics and machine learning approaches, we identified that the combination of CLSPN, RBBP6, and CCDC91 was robustly associated with SARS-CoV-2 infection in both discovery and validation datasets. Col...
The authors validated their discovery with a longitudinal study that was able to detect even asymptomatic Omicron infections with high accuracy, long before a given patient is able to test positive with RT-PCR testing.

9/ "Research on the host responses to respiratory viruses could help develop effective interventions and therapies against the current and future pandemics from the host perspective. Here, we leveraged the substantial biological, clinical, and technical heterogeneity in publicly available respiratory virus datasets and identified a 3-gene (CLSPN, RBBP6, and CCDC91) host response signature for identifying the SARS-CoV-2 infection at either an asymptomatic or symptomatic stage. We validated this 3-gene signature in an independent longitudinal follow-up study and demonstrated that it performs ...
That's all the highlights! The study is Open Access and available at

The rest of this thread is going to be commentary/analysis of the details of the study...
10/16mdpi.com/1999-4915/16/7…
So what role do these genes play?

It seems to be a cascade that highjacks the innate and adaptive immune responses in a way that's advantageous for the SARS-CoV-2 virus itself. That's not to say that the virus *directly* increases expression of these genes...

11/ "We proposed that the upregulation of CLSPN, RBBP6, and CCDC91 by SARS-CoV-2 in T cells might create a cascade of effects that alter both the innate and adaptive immune responses. First, CLSPN plays a significant role in genomic stability during DNA replication [56]. ... CLSPN might help T cells manage the stress and damage induced by viral replication. Second, ... RBBP6 is involved in cell cycle regulation, apoptosis, and ubiquitination processes [58]. RBBP6 has been reported as a negative regulator of Ebola virus replication by mimicking the viral protein [59]. ... RBBP6 might preven...
Rather, these are the common product of the cascade of dysfunctional processes triggered by SARS-CoV-2 infection. This study identified a unique signature of *differentially expressed genes*, but there's not a 1:1 cause and effect for differential expression of a given gene!

12/ "Although there is limited specific information on the expression changes of CCDC91 in response to viral infections, CCDC50, a related gene to CCDC91, negatively regulated the type I IFN signaling pathway initiated by RIG-I-like receptors (RLRs), the sensors for RNA viruses [60]. Together, these genes may in concert with T cells not only respond to viral infections effectively through cellular immunity but also regulate the immune response to avoid excessive inflammation or autoimmunity. Further experimental validation and research would be essential to elucidate these proposed mechanisms...
The methods were thorough, in that they cross-validated all of their findings multiple ways to ensure they weren't picking up on some spurious signal in the data. Even if the genes turn out not to be meaningful for *pathogenesis*, they're VERY meaningful for *diagnosis*!

13/ Image
IMO, there's one big error. Figures 2A and 2B have slightly different Y-axes, likely because the graphs were generated separately, but it actually has the effect of shrinking a range that is *unexpectedly* larger.

I aligned the scales on Figures 2A and 2B here

14/ Image
When symptomatic and asymptomatic gene expression for each virus are put side by side, it's clear that SARS-CoV-2 has a wildly different pattern compared to the other viruses, and a vastly larger magnitude of effect.

Differential expression INCREASES in asymptomatic covid?!

15/ 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...
Most notably, T cells are the PRIMARY type of cell where the 3-gene signature is most differentially expressed... and it's specifically a pattern that will lead to T cell exhaustion through overactivation.

Say it with me: "COVID is airborne and exhausts T cells!"

16/end 3.4. T Cells Are the Primary Source of the 3-Gene Signature We used single-cell RNA sequencing (scRNA-seq) profiles of 15,639 cells from PBMC samples of 7 individuals (4 SARS-CoV-2 infections, 3 Controls) to identify the cell types that express the 3-gene signature. Visualization using UMAP illustrated the infection status (Figure 5A) followed by cell type (Figure 5B). T cells had the highest scores (Figure 5C), and 3-gene signature scores were significantly higher in T cells from patients with SARS-CoV-2 infection (Figure 5D), especially in activated CD4 T cells, mucosal-associated invarian...
Afterthought: The bit about “discovery should include not only SARS-CoV-2 infections but also other respiratory infections” is an echo of another paper about HCoV-OC43… from 1980! There, the author also complained about lack of dataset diversity



17/16
Discovery and validation of SARS-Co V-2-specific host response genes have been calling 26]. To address this issue, an ideal dataset for biomarker discovery should include not only SARS-CoV-2 infections but also other respiratory infections (Figure 4). Therefore, we co-normalized datasets HRA000786 and GSE17156, which included both asymptomatic and symptomatic cases. With integrative bioinformatics and machine learning approaches, we identified that the combination of CLSPN, RBBP6, and CCDC91 was robustly associated with SARS-CoV-2 infection in both discovery and validation datasets. Collect...
I’m not sure if it would, because at least one of the genes is involved in one type of cell entry, and there’s evidence that persistent infections may use *different* methods to move between cells that possibly wouldn’t engage that gene!

18/16
2. Lots of things can cause lymphopenia! () It's just usually *temporary* with most non-HIV causes.

1. Like the HIV patients on death's door in the 90s, who are alive today thanks to HAART, recovery may be possible

19/16
en.wikipedia.org/wiki/Lymphocyt…

The most common cause of temporary lymphocytopenia is a recent infection, such as the common cold.[citation needed] Lymphocytopenia, but not idiopathic CD4+ lymphocytopenia, is associated with corticosteroid use, infections with HIV and other viral, bacterial, and fungal agents, malnutrition, systemic lupus erythematosus,[3] severe stress,[4] intense or prolonged physical exercise (due to cortisol release),[5] rheumatoid arthritis, sarcoidosis,[6] multiple sclerosis,[7] and iatrogenic (caused by other medical treatments) conditions. Lymphocytopenia is a frequent, temporary result from man...
Simply put, if the cause of dysregulation is removed, the immune system can *likely* recover.

Time is the enemy, in this case! Cancer is a huge concern here, because without immune cells, cells with defective DNA will be ignored and grow into tumors
20/16
Opportunistic infections are the biggest concern with a compromised immune system (lack of defenses), but when an individual has effectively zero immune system, the body isn't able to perform basic janitorial tasks that clean up random defective processes!

21/16
@willrye8 Oh, and they did include seasonal CoVs in their discovery analysis
Sure! Here's a meta-annotated version of the graph with simplified explanations of each element. The graph itself is fairly noisy, but the takeaways are simple!

tl;dr: larger graph = more intense response

[Quoted tweet was referring to the graph]
22/16

Image
Lack of symptoms may not even be because of immune system *destruction*! Symptoms of cold and flu are driven by interferon signaling, which SARS-CoV-2 suppresses.

But the end result is the same: lack of effective immune response!

23/16
The immune system has a vast range of functions spread across different systemic and cellular mechanisms.

It's likely that there are many people walking around with a compromised innate immune system, who don't realize it as leftover adaptive defenses fight infections

24/16
This discovery seems to have a clear path to commercialization, because this discovery is purely a new method of *analyzing* the results of existing types of Nucleic Acid Amplification Tests (NAAT), including RT-PCR and LAMP testing. It's software!

25/16
The advantage here is that, rather than requiring detection of a specific viral protein (which may be present in the body but not the swab location), it requires detection of elevated levels of HOST PROTEINS that indicate active viral infection!

26/16

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Nick #AirborneCovidExhaustsTCells😷 Anderegg Profile picture
Jul 8
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...
Simply put, they looked at the antibodies produced by "Antibody-Secreting Cells" (ASCs), a type of short-lived immune response cells!

The primary types of antibodies stay in the blood. In contrast, ASCs peak *shortly* after infection, then rapidly decline! (see screenshot)

3/ From "The Antibody-Secreting Cell Response to Infection: Kinetics and Clinical Applications" (2017): "In this review, we summarize previous studies that have used techniques to enumerate ASCs during infection. We describe the emergence, peak, and waning of these cells in peripheral blood during infection with a number of bacterial and viral pathogens, as well as malaria infection. We find that the timing of antigen-specific ASC appearance and disappearance is highly conserved across pathogens, with a peak response between day 7 and day 8 of illness and largely absent followi...
Read 20 tweets
Nick #AirborneCovidExhaustsTCells😷 Anderegg Profile picture
Jun 3
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
So, DNA… it's a *language* that encodes the instructions a cell uses to build proteins out of smaller molecules.

Like written language, different symbols are used to indicate when segments start and stop (i.e. capital letters, spaces, punctuation in human language).

3/ Visualization of gene structure from Wikipedia. The structure of a eukaryotic protein-coding gene. Regulatory sequence controls when and where expression occurs for the protein coding region (red). Promoter and enhancer regions (yellow) regulate the transcription of the gene into a pre-mRNA which is modified to remove introns (light grey) and add a 5' cap and poly-A tail (dark grey). The mRNA 5' and 3' untranslated regions (blue) regulate translation into the final protein product.
Read 37 tweets
Nick #AirborneCovidExhaustsTCells😷 Anderegg Profile picture
May 27
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...
The result of the suppression is that infected cells are *unable* to present an antigen to the immune system, allowing infected cells to evade the immune system.

The authors view their result as indication of SARS-CoV-2 promoting unproductive splicing of key MHC-I genes.

3/ Similarly, melanoma cells possess a mutation at the 5 ′ splice donor site of intron 2 of the HLA-A2 gene, causing the absence of the HLA-A2 antigen and likely protecting these cancerous cells from immune surveillance. Our findings indicate that SARS-CoV-2 infection may also lead to the loss of class I MHC antigens due to intron retention, potentially rendering infected cells incapable of presenting viral antigens to the immune system. Reduced expression of HLA-DR in monocytes represents a molecular hallmark of severe COVID-19. Other studies have demonstrated that SARS-CoV-2 ORF6 inhibits c...
Read 19 tweets
Nick #AirborneCovidExhaustsTCells😷 Anderegg Profile picture
May 18
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.
But the interesting thing is that it seems to increase the expression of MHC-I receptors, related to the functionality of T cells and NK cells, and generally fine-tunes the immune response, I think?



3/ ncbi.nlm.nih.gov/gene/3107
HLA-C major histocompatibility complex, class I, C "Class I molecules play a central role in the immune system by presenting peptides derived from endoplasmic reticulum lumen. They are expressed in nearly all cells. ... The HLA system plays an important role in the occurrence and outcome of infectious diseases, including those caused by the malaria parasite, the human immunodeficiency virus (HIV), and the severe acute respiratory syndrome coronavirus (SARS-CoV). The structural spike and the nucleocapsid proteins of the novel coronavirus SARS-CoV-2, which causes coronavirus disease 201...
Read 6 tweets
Nick #AirborneCovidExhaustsTCells😷 Anderegg Profile picture
May 6
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.
In the last 75+ years of limitless growth, so little thought was given to things in the long-term. I think we’re approaching a tipping point on all the cans we’ve kicked down the road. Now, for example, the U.S. has so many buildings and other structures that were…
Read 13 tweets
Nick #AirborneCovidExhaustsTCells😷 Anderegg Profile picture
Apr 15
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.
Let's dive in!

Interestingly, epidemiological data already shows seasonality to BD symptoms, correlated with changes to neurotransmitters related to changing light. On top of this, there has been a convergence on the neuroinflammatory model of mood disorders more recently!

3/ …clear seasonal effects in the pattern of recurrence of severe illness episodes and hospitalization in bipolar disorder (BD), with excess depressive and mixed episodes in autumn and spring, and mania in summer. Changes in mood… parallel to the effects of changes in the photoperiod…, with serotonin (5-HT) release increasing, and the serotonin transporter density decreasing, together with the amount of daily light,… and associated with the severity of depression in winter…. In recent years, an unprecedented amount of evidence has supported immunoinflammatory mechanisms as a point of converge...
Read 22 tweets

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