This study was summarised using Gemini AI.

The study investigates how the SARS-CoV-2 accessory protein ORF7a manipulates host cell metabolism to create an environment that favors viral replication and immune evasion. Normally, healthy cells rely heavily on mitochondria to efficiently produce energy through a process called oxidative phosphorylation. However, the researchers discovered that the ORF7a protein essentially short-circuits this system, forcing the cell to rely on a less efficient, glucose-heavy energy pathway called glycolysis.

Cellular Changes Induced by ORF7a

Feature	Healthy Cell Baseline	ORF7a-Infected Cell
Primary Energy Source	Mitochondrial respiration	Glycolysis (Warburg-like effect)
Oxidative Stress (ROS)	Balanced by antioxidant defenses	Highly elevated due to depleted glutathione
PDK4 Enzyme Levels	Normal baseline	Significantly up-regulated
Mitochondrial Complex I	Fully active and assembled into supercomplexes	Functionally impaired and structurally disassembled

Key Mechanisms of Mitochondrial Sabotage

The researchers identified two primary ways that ORF7a breaks the cell's mitochondrial engine:

• The PDK4 Roadblock: ORF7a causes a massive increase in the enzyme PDK4. PDK4 then phosphorylates and turns off the Pyruvate Dehydrogenase Complex (PDHC). This effectively acts as a roadblock, stopping pyruvate (the cell's standard fuel) from entering the mitochondria to be burned for energy.
• Direct Complex I Impairment: Independent of the PDK4 roadblock, ORF7a selectively cripples "Complex I," a crucial piece of the mitochondrial electron transport chain. It also stops these respiratory complexes from assembling together properly.
• Irreversible Damage: When scientists treated the cells with a drug called dichloroacetate (DCA) to remove the PDK4 roadblock, mitochondrial energy production still failed to recover. This proved that the damage to Complex I is a separate, profound disruption caused by the virus.
• Oxidative Stress: Because the mitochondria are malfunctioning, they leak reactive oxygen species (ROS), and the cell's natural antioxidant buffers (like glutathione) are depleted, leading to severe cellular stress.

Key Takeaway

The SARS-CoV-2 ORF7a protein cripples the host cell's mitochondria via a "two-pronged attack"—blocking fuel entry by activating PDK4 and destroying the engine itself by impairing Complex I. This forces the cell into an inflexible, stressed, glucose-burning state that likely fuels the severe inflammation and metabolic complications seen in COVID-19 patients.

Link to 2026 study

This summary was made using Gemini AI.

The study is by Alain Moreau et al.

This study, published in August 2026 in the International Journal of Molecular Sciences, explores the biological reasons why Long COVID affects people so differently—specifically focusing on cognitive decline (often called "brain fog") after physical or mental effort. The researchers investigated whether a person's haptoglobin (Hp) phenotype—a genetic variation of a specific blood protein—could predict how severe their post-exertional symptoms would be.

How They Did It

The researchers compared 44 individuals with Long COVID to 20 control patients who had quickly and fully recovered from a COVID-19 infection. They analyzed the participants' genetics, blood metabolites, and physiological data both before and after a 90-minute post-exertional stress challenge.

Key Findings

The study revealed that a person's haptoglobin genetics strongly predicted their reaction to the stress test:

• The Hp2 Variant (Hp2-2 and Hp2 allele carriers): People with this genetic variant experienced worse overall fatigue, poorer physical function, and more severe symptoms after exertion. Immediately following the stress test, they showed a significant drop in cognitive performance. They also had lower levels of energy-related blood metabolites (like citric acid), which correlated directly with their poorer brain function.
• The Hp1-1 Variant: Individuals with this specific variant demonstrated "cognitive resilience". Their brain function did not decline after the stress test, and they had much better long-term cognitive trajectories. Their brains were also significantly better at extracting oxygen during the challenge compared to the Hp2 group.

The Takeaway

In short, your haptoglobin genetics might help explain why you might experience severe brain fog and crashes after exertion with Long COVID, while someone else might not. If validated in larger groups, a simple blood test to check your haptoglobin type could be used as a biological marker to classify Long COVID severity and eventually tailor personalized treatments based on your genetic profile.

Link to 2026 study

I’m using Stacher 7.1.11 on Windows 11 to download a YouTube video as MP3.

The download fails because YouTube returns an HTTP 429 Too Many Requests response, followed by “Sign in to confirm you’re not a bot.” Stacher/yt-dlp also reports that it cannot obtain the required GVS PO Token because Visitor Data is missing.

I have already reinstalled/updated yt-dlp and Deno, also reinstalled the app, but the problem remains. When retrying the same download it fails each time.

My current Stacher configuration extracts the audio as MP3, but the generated arguments do not include --cookies-from-browser or a cookies file. Has anyone encountered this in Stacher 7.1.11, and is browser-cookie authentication now required for normal public YouTube videos?

This summary was made using Gemini AI.

Study Overview

This study, published in BMC Immunology, investigates the cellular mechanisms behind Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). Specifically, it looks at why the immune systems of ME/CFS patients often function poorly, focusing on a specific ion channel in Natural Killer (NK) cells and how its malfunction starves the cells' mitochondria of vital calcium (Ca2+).

The Biological Context

To understand the study, it helps to know how a healthy cell operates:

• Natural Killer (NK) Cells: These are frontline immune cells responsible for destroying infected or harmful cells. To kill a target, NK cells require a precisely timed flood of intracellular calcium (Ca2+).
• TRPM3 Ion Channels: Think of TRPM3 as a specific "gate" on the surface of the cell. When the cell needs to attack, this gate opens, allowing Ca2+ to rush into the cell body (the cytosol).
• The Mitochondria: Known as the powerhouse of the cell, mitochondria do more than just make energy (ATP); they act like sponges that buffer and absorb this rushing Ca2+. This Ca2+ absorption directly powers the cellular energy required for the NK cell to execute its immune functions.

The Problem: Previous research established that in ME/CFS patients, the TRPM3 gates are broken, leading to a weak influx of Ca2+ into the cell. This study takes it a step further to see how this broken gate impacts the downstream mitochondria.

How They Tested It

• Participants: The researchers took blood samples from 10 ME/CFS patients (diagnosed using strict clinical criteria) and 10 healthy controls (HC).
• Isolation: They isolated the NK cells from the blood samples to study them directly.
• Live Imaging: Using special fluorescent dyes that light up when they bind to Ca2+, the researchers were able to visually track Ca2+ moving into the main cell body (using a dye called Fluo-8 AM) and specifically into the mitochondria (using a dye called Rhod-2 AM).
• Chemical Stimulation: They used a chemical called Pregnenolone sulfate (PregS) to artificially force the TRPM3 gates open, allowing them to measure exactly how much Ca2+ made it through.

Key Findings

The researchers found distinct differences in how ME/CFS cells handle Ca2+ compared to healthy cells:

1. The Cell Body (Cytosol) is Starved of Calcium

• When the TRPM3 channels were stimulated to open, the NK cells of healthy patients showed a robust, healthy flood of Ca2+ into the cell.
• In ME/CFS patients, both the total amount of Ca2+ entering the cell and the speed at which it entered were significantly reduced.

2. The Mitochondria Are Compromised

• Because the main TRPM3 gate was failing to let enough Ca2+ into the cell, the downstream mitochondria in ME/CFS patients were consequently starved. The Ca2+ making it into the mitochondria via TRPM3 activation was significantly reduced compared to healthy controls.
• Interestingly, when the researchers bypassed the TRPM3 gate and simply flooded the environment with standard Ca2+, the ME/CFS mitochondria absorbed it much faster and in higher amounts than healthy cells. The researchers theorise this might be a compensatory mechanism; because the mitochondria are usually starved, they rapidly suck up any Ca2+ they can get, which can inadvertently lead to dangerous mitochondrial calcium overload.

The Big Takeaway

The results of this study heavily support the theory that ME/CFS is a "channelopathy", a disease fundamentally driven by malfunctioning cellular gates (ion channels).

Because the TRPM3 channels in ME/CFS patients are impaired, their NK cells cannot generate the massive Ca2+ signals required for normal function. Without this Ca2+, the mitochondria cannot produce the energy necessary for the NK cells to kill threats, explaining the immune system dysregulation commonly seen in the disease. Furthermore, because TRPM3 channels are found all over the body (including the brain and nervous system), this cellular dysfunction could help explain the wide array of sensory, cognitive, and fatigue symptoms that ME/CFS patients endure.

Link to 2026 study - https://link.springer.com/article/10.1186/s12865-026-00849-1

This summary was made using Gemini AI.

The Biological Premise: Autophagy and ATG13

To maintain cellular health, our bodies rely on autophagy—a highly regulated degradation pathway that clears out damaged organelles and misfolded proteins. A specific form of this, mitophagy, targets defective mitochondria (the cell's ATP/energy producers).

ATG13 (Autophagy-related protein 13) is a critical signaling protein. It acts as the ignition switch for the ULK1 kinase complex, which physically initiates the formation of the autophagosome (the cellular "garbage bag"). The researchers wanted to observe the systemic consequences when this initiation step is genetically impaired.

The Experiment

The researchers utilized a genetically modified mouse model where ATG13 was chronically depleted. By knocking down this single protein, they created an in vivo (living organism) model of stalled autophagy to observe the downstream metabolic, immunological, and neurological effects.

The Pathological Cascade

Depleting ATG13 triggered a massive, multi-system domino effect driven by metabolic failure:

1. Mitochondrial Dysfunction & ROS Accumulation

Because defective mitochondria were no longer being recycled via mitophagy, they began to accumulate in the cells. These damaged mitochondria were highly inefficient: their ATP (cellular energy) production plummeted, and they started leaking massive amounts of Reactive Oxygen Species (ROS)—unstable molecules that cause severe oxidative stress and damage surrounding cellular structures.

2. Immunometabolic Shifting (SIRT1 and NF-κB)

The spike in oxidative stress (ROS) acted as an alarm bell for the immune system, specifically targeting macrophages in the spleen. This triggered a profound shift in gene expression:

• SIRT1 Downregulation: SIRT1 is a crucial enzyme that promotes metabolic efficiency and healthy aging while keeping inflammation in check. In these mice, SIRT1 levels collapsed.
• NF-κB Activation: With SIRT1 out of the way, NF-κB (a primary transcription factor that drives inflammation) was activated. This caused the macrophages to shift into a chronic, highly aggressive pro-inflammatory state.

3. Peripheral Neuropathy (Nerve Demylination)

The combination of chronic systemic inflammation and rampant oxidative stress eventually breached the nervous system. The researchers observed demyelination—the degradation of the protective myelin sheath—specifically in the peripheral nerves that innervate skeletal muscles.

The Clinical Translation: ME/CFS and Long COVID

This paper is highly significant because it successfully models the underlying pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Long COVID.

The hallmark symptom of both diseases is Post-Exertional Malaise (PEM)—a severe, disproportionate exacerbation of fatigue, cognitive dysfunction, and muscle pain following minor physical or cognitive exertion.

The Takeaway: This study provides a concrete, molecular explanation for PEM. If a patient's autophagic machinery (like ATG13) is compromised, their cells cannot clear the metabolic waste (damaged mitochondria and ROS) generated by exertion. This local cellular failure triggers a systemic inflammatory loop and damages the nerves connecting to their muscles, literally stripping the body of its ability to produce sustainable energy.

Link to 2026 study - https://link.springer.com/article/10.1007/s00011-025-02158-6

Paper Analysis and Summary Made Using Gemini AI.

Title: Identification of Altered Potassium Channels for Drug Repurposing in Long COVID Patients Authors: John P. George, Kiran Bharat Gaikwad, Jyoti Sharma

Date: June 19, 2026 (bioRxiv)

1. Background and Objective

Long COVID (LC) is a complex, chronic condition characterized by persistent multisystem manifestations, with a notably high prevalence of neurological symptoms (e.g., brain fog, persistent fatigue). Human ion channels (HICs)—and potassium channels in particular—are abundantly expressed in the nervous system and are critical for cellular homeostasis and signal transduction.

The authors hypothesized that the dysregulation of these channels during and after SARS-CoV-2 infection plays a role in LC pathophysiology. The study aims to identify altered potassium channels in LC patients to serve as potential targets for drug repurposing.

2. Methodology

The researchers utilized a computational biology and transcriptomic approach:

• Data Collection: They performed a meta-analysis of bulk RNA-Seq datasets, specifically comparing gene expression profiles between patients who fully recovered from COVID-19 and patients experiencing Long COVID.
• Network Analysis: They constructed co-expression networks to group genes into functional modules and identify the relationship between altered HICs and broader biological pathways.

3. Key Findings

• Three Significant Gene Modules: The network analysis revealed three primary modules of dysregulated genes involving HICs, lipid metabolism, and immune signaling.
• Pathway Associations: These modules were strongly associated with immune-driven mechanisms, specifically:
  • Antigen processing and presentation
  • Complement and coagulation cascades
  • Cytokine-related signaling pathways
• Specific Drug Targets Identified: The analysis isolated four specific potassium channels that were significantly dysregulated and possess existing, approved pharmacological modulators:
  • KCNA6 (Voltage-gated potassium channel)
  • KCNJ10 (Inward-rectifier potassium channel)
  • KCNN3 (Small conductance calcium-activated potassium channel)
  • KCNH4 (Voltage-gated, delayed rectifier potassium channel)

4. Drug-Target interactions

From the total differentially expressed HICs identified, 10 were found to interact with approved drugs (Supplementary File 4). Of these 10 HICs, KCNN3, KCNA6, and KCNJ10 were from the blue module, and KCNH4 was from the brown module. KCNN3 was observed to interact with dequalinium. KCNJ10 interacted with mitiglinide, glipizide, tolazamide, and chlorpropamide. Additionally, both KCNA6 and KCNH4 were found to interact with amifampridine, guanidine hydrochloride, dalfampridine, and amifampridine phosphate.

https://preview.redd.it/l33qlzt3no9h1.jpg?width=858&format=pjpg&auto=webp&s=8bac7a1dc2071f6dc7dfda49e6f549388adbbf4b

5. Conclusion and Significance

The study concludes that persistent disruption of potassium homeostasis—driven by underlying immune dysregulation and chronic inflammation—is a likely contributor to Long COVID's neurological and systemic symptoms.

By identifying KCNA6, KCNJ10, KCNN3, and KCNH4 as key molecular targets, the authors provide a viable framework for drug repurposing. Using already-approved drugs that target these specific potassium channels could accelerate the development of new therapeutic interventions for Long COVID patients, pending further experimental validation.

List of drugs in the supplemental material here - https://www.biorxiv.org/content/biorxiv/early/2026/06/19/2026.06.18.733062/DC1/embed/media-1.zip?download=true

Link to 2026 study - https://www.biorxiv.org/content/10.64898/2026.06.18.733062v1.full

This summary was created using Gemini AI.

The study is a pivotal piece of research published in the International Journal of Molecular Sciences (IJMS, May 2026) by Dr. Alain Moreau and his team at the Université de Montréal / Open Medicine Foundation.

It offers an objective molecular explanation for Post-Exertional Malaise (PEM)—the severe symptom crash ME/CFS patients experience after minor exertion—proving it is rooted in biological "gridlock" rather than simple exhaustion.

1. Summary of the Paper's Analysis & Findings

The researchers wanted to track how ME/CFS patients adapt to physical stress at a cellular level. They evaluated 92 ME/CFS patients against 44 healthy controls, measuring blood markers before and after a specialized 90-minute mechanical stress test used to trigger a controlled, temporary PEM state.

The Two Core Competitors

• Irisin: An exercise-induced messenger (myokine) released by muscles during contraction. In healthy bodies, it protects mitochondria, boosts energy production, and suppresses inflammation by binding to α Vβ 5 integrin cell receptors.
• Thrombospondin-1 (TSP-1): A protein released during tissue stress and injury. In this pathway, it acts as a molecular "bully" that blocks irisin from doing its job.

Proposed model of impaired irisin responsiveness in ME involving TSP-1, αvβ5 integrin, and extracellular HSP90α-dependent mechanisms.

Key Discoveries

• Blunted Response at Baseline: ME/CFS patients started with significantly lower baseline irisin, and their bodies failed to produce the normal surge of irisin during stress (p < 0.05).
• The "Irisin Resistance" Paradox: Paradoxically, in moderate-to-severe patients, baseline levels of both irisin and TSP-1 were elevated, and high irisin was a direct predictor of fatigue severity (β = 0.728, p = 0.018). This means the body is desperately producing irisin to cope, but the signal is being ignored or blocked.
• TSP-1 is the Blocker: Using advanced cellular spectroscopy, the team proved that TSP-1 directly binds to and shuts down irisin signaling in a concentration-dependent manner.
• The Molecular Framework: Irisin requires the help of an intracellular chaperone, HSP90α, and the receptor α Vβ 5. When the researchers experimentally blocked α Vβ 5  or inhibited HSP90α, the cells completely lost their ability to counteract TSP-1, mimicking the exact cellular defects seen in severe ME/CFS patients.

The Takeaway: PEM isn't a psychological aversion to exercise; it is an "irisin resistance" state. When a person with ME/CFS exerts themselves, an abnormal spike in TSP-1 essentially locks the cellular doors, preventing exercise-induced irisin from delivering energy to the cells and clearing out inflammation.

Link to 2026 study - https://www.mdpi.com/1422-0067/27/11/4770

Posted on X/Twitter here by user ME/CFS Science - https://x.com/mecfsskeptic/status/2063898792932347948

1. A research collaboration including Theoharis Theoharides and Nancy Klimas reports dramatically elevated levels of MMP-9, an enzyme that components of the extracellular matrix.

They previously reported similar results in Long Covid but I have doubts about their reliability.

2. MMP-9 was measured in serum (not in plasma) and there's a literature explaining why this isn't a reliable method. MMP-9 is released during the sampling and clotting process used to make serum.

3. One paper concluded for example "MMPs are released by platelets or leukocytes during platelet activation or sampling process, thus leading to artificially higher MMP-9 levels in serum..."

https://www.sciencedirect.com/science/article/abs/pii/S0009912006003237

4. The samples of ME/CFS patients and controls in this study were also handled and collected very differently. Patients were recruited at the University of Miami while the control samples were taken from an external biobank (bioBioIvt Elevating Science).

5. The authors note that "the samples had been stored for over ten years at -80 °C, which may have altered the fragmentation of certain biomarkers."

6. The 40 patients and 38 controls were all female but not properly matched (mean age was 51 in patients versus 43 in controls) and there's no info on other potential confounders such as BMI, medication use, etc.

7. So I have strong doubts about whether these results are reliable. The concentrations were 7 times higher in patients versus controls (126 versus 17 ng/ml), suggesting a technical artefact and differences in sample handling.

8 ) The authors also did a different experiment. They cultured mast cells and found that they release more MMP-9 when incubated with EBV-protein (representing viruses) or LPS (a component of the cell wand of bacteria).

9. In their Long Covid study they reported that MMP-9 was increased when cells from a microglia cell line where stimulated by Sars-Cov-2 spike protein.

Link here:

https://www.degruyterbrill.com/document/doi/10.1515/tnsci-2022-0352/html

10. Link to the paper:

Chinnapan et al. 2026. Elevated serum levels of interleukin-11 and matrix metalloproteinase-9 in myalgic encephalomyelitis/chronic fatigue syndrome.

https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2026.1827700/full

Dr. Liisa Selin, Dr. Ayano Kohlgruber, and Dr. Roshan Kumar received a Solve ME/CFS Catalyst Award for their study searching for the exact proteins recognized by T-cell receptors from a person with ME/CFS and a person with Long Covid.

These disease-associated T cells include “exhausted” CD8+ T cells and “double-positive” CD4+/CD8+ T cells (which are found in people with autoimmune diseases, too). The researchers hypothesize that these T cells recognize fragments of microbial proteins critical for developing the disease. The microbial protein fragments may overstimulate and exhaust the T cells.

Also, fragments of human proteins may resemble these microbial protein fragments; thus, the disease-associated T cells may cross-react with human proteins to drive an autoimmune response.

In this study, the research team will screen a library of protein fragments from microbes (viruses and bacteria) that are associated with developing Long Covid or ME/CFS (e.g., SARS-CoV-2, B. burgdorferi, enteroviruses), and a library of protein fragments from humans (to find self-antigens).

If successful, these deliverables would be important for understanding how much persisting pathogens or self-antigens can exhaust the immune system, and how dysfunctional and exhausted immune responses contribute to ME/CFS and Long Covid.

In this webinar hosted by Solve M.E. VP of Scientific Programs Dr. Jessica Maya, the panelists discuss the study and how this work could also produce new disease biomarkers and suggest new treatments for patient subgroups, as well as how the libraries of human leukocyte antigen–displayed microbial and human protein fragments established by this work could be valuable resources for future ME/CFS and Long Covid studies.

Review the presentation deck here: https://solvecfs.org/wp-content/uploads/2026/05/PDF-Deck-for-4.28.26-Selin_Kohlgruber_Kumar-webinar.pdf

Posted here by X/Twitter user #@ZdenekVrozina - https://x.com/ZdenekVrozina/status/2066526958842765474

New single-cell study, preprint and cross-sectional. The Long COVID group looks stuck in a loop it can’t switch off. The people who recovered had COVID too - and their immune cells are visibly winding the response down, finishing the job

The cohort is worth a flag. African Americans over 50, mostly women - a group almost absent from Long COVID biology. They profiled ~156,000 individual immune cells, 20 people with Long COVID vs ~18 recovered.

That same split - stuck vs resolved - shows up across every compartment they looked at. So the lesion may be less - too much immune activity - and more - an off-switch that won’t flip.

B cells (the antibody makers). In Long COVID even the naive ones run hot on BCR signaling - the receptor a B cell uses to recognize its target - long after the infection. Looks like chronic activation. It’s a gene-expression pattern here.

T cells go two ways. The central-memory pool - your reserve bench of future fighters - sits stuck in neutral, maturation blocked. The effector-memory cells - the veterans - look chronically exhausted. In recovered people the same cells mature normally and carry antiviral programs.

Monocytes - innate first responders. Are remodeled too - cranked-up migration and interferon signaling, but stalled maturation. So it’s not only the learning arm of immunity that’s off - the fast, innate arm is rewired as well.

The strongest single finding is in NK cells. More NK tracked with fewer symptoms!
In severe Long COVID the NK cells are exhausted, dying off, metabolically flat. In milder cases they’re metabolically fit, powerplants humming. This is a comparison within the Long COVID group, so it’s less confounded.

That flips the obvious move. You wouldn’t suppress NK cells across the board - you’d knock out the protective ones too. The better bet is restoring their metabolism and dialing down the AP-1 inflammatory switch. Still a hypothesis.

A snag in the framing - the antigen/reservoir story despite blood that comes up empty. The whole interpretation runs on persistent viral reservoir/antigen. When there’s nothing in the blood, they pivot to a tissue reservoir we can’t see here.

This ties to the study’s weakest piece - the virome scan. From leftover unmapped reads they report more Retroviridae and Poxviridae in Long COVID. But that method is contamination-prone and crucially, they found no difference in SARS2 or herpesviruses in the blood.

Retroviridae could be reactivated endogenous retroviruses (old viral fragments baked into our own DNA), or an artifact. It is not evidence of live virus.

What’s genuinely useful?
The failure to resolve frame, the NK functional axis, and the sign that the dysregulation may sustain itself through cell-to-cell signaling - together a real handle for biomarkers and targets, whatever kicked it off.

Small numbers, one timepoint, blood only - no tissue, exhaustion read from gene expression with no functional test, no identified trigger. Cross-sectional can’t rule out reverse causation - the signature might be a consequence of being chronically ill, not its cause.

By the figures this study cites, ~7% of infections lead to Long COVID, and fewer than 1 in 10 fully recover within two years. Not a fringe outcome. And it lands hardest on communities already carrying more - exactly also the kind of cohort here.

https://preview.redd.it/q67x9obdin7h1.jpg?width=1280&format=pjpg&auto=webp&s=1b29d94df41226b5928a01cd5986b166c0e922e2

2026 study - https://www.biorxiv.org/content/10.64898/2026.06.04.730206v1

Hey everyone, I’m really hoping someone here can help me out because I’m at my wits' end.

For the past two days, the site has become completely broken for me. It started after I left a few completely genuine, non-spam replies on a post. Ever since, I'm getting hit with:

"Rate limit exceeded. Please wait xx seconds" and "Server error. Try again later" every time I try to comment. I can barely even post this request for help.

To make it weirder, I also get a bright red banner saying "We had a server error..." every single time I just hover over or click on my own profile picture.

My Setup:

• OS: Windows 11 (fully up to date)
• Browser: Chrome (fully up to date)
• Note: I don't use the phone app at all, this is strictly on desktop.

It honestly feels like my account has been accidentally flagged as a bot or trapped in some weird glitch loop, and it's incredibly isolating. Has anyone dealt with this before? Any advice or help from a mod would mean the world to me right now. Thank you so much.