#LongCOVID (LC) shares striking symptom overlap with hypermobility spectrum disorders (HSD/hEDS): fatigue, brain fog, dysautonomia, pain—especially in women.

➡️ A new case series explores whether some “intractable” LC may reflect undiagnosed hypermobility disorders.

➡️ Five women with persistent LC symptoms were evaluated at an hEDS/HSD clinic.
All met Beighton score criteria for hypermobility.

➡️ 4 diagnosed with hEDS, 1 with HSD
➡️ 3 had dysautonomia

None had prior hypermobility diagnoses. 1/ All patients carried MTHFR polymorphisms (C677T or A1298C)—recently linked to hEDS/HSD.

➡️ Several also showed features of mast cell activation, suggesting immune dysregulation may unmask latent connective tissue disorders after SARS-CoV-2 infection.

➡️ Targeted management (physical therapy, methylfolate/B12, mast cell stabilization, pain interventions) led to clinical improvement in all cases.

🔑 Takeaway: Consider hEDS/HSD in women with refractory Long COVID, especially with multisystem pain and dysautonomia. 2/

🔥 A landmark study challenges the long-held belief that Alzheimer’s disease (AD) is irreversible.

➡️ Using advanced mouse models that mimic human AD pathology, researchers found that restoring and maintaining healthy levels of NAD⁺, a key cellular energy molecule, can not only prevent but also reverse advanced Alzheimer’s pathology and fully restore cognitive function in mice. 1/ The team showed that NAD⁺ deficiency is a central driver of AD pathology—leading to blood-brain barrier breakdown, neuroinflammation, oxidative damage, and impaired neurogenesis. 2/

As we age, our immune system becomes less effective, partly because key cells called CD8⁺ T-cells have trouble forming long-lasting memory.

A new study shows that a process called autophagy — the cell’s way of cleaning out old or damaged components — plays a central role in this problem. 1/ When a T-cell divides, it can make two daughter cells with different future roles: one becomes a long-lived ‘memory T cell’ that helps protect against future infections, and the other becomes a short-lived ‘effector T cell’ that fights the immediate infection.
For this to happen, the cell must sort its internal parts unevenly during division. 2/

A new review highlights how neurotropic viruses like SARS-CoV-2 reprogram the metabolism of brain immune cells — especially microglia and astrocytes — contributing to neuroinflammation and brain dysfunction.

➡️ Under normal conditions, glial cells use oxidative phosphorylation (OXPHOS) to support brain homeostasis and anti-inflammatory functions. But viral infection shifts them toward aerobic glycolysis, driving pro-inflammatory cytokine production and immune activation. 1/ This metabolic switch:

• increases inflammatory mediators (IL-1β, TNF-α)
• elevates oxidative stress
• impairs neuronal support
• disrupts the blood-brain barrier

All of which can exacerbate neuroinflammation and damage. 2/

Breakthrough in respiratory virus prevention (Flu, COVID & more)

➡️ Researchers have developed an AI-designed intranasal antiviral platform that could block multiple respiratory viruses—flu, COVID-19, and future variants—right at the entry point: the nose. 1/ The platform is based on interferon-lambda, a natural antiviral protein, redesigned using AI protein engineering to overcome major limitations: poor heat stability and rapid clearance from nasal mucosa.

➡️ Using AI, scientists strengthened unstable protein regions, improved solubility, and added glycoengineering—making the protein so robust it remained stable for 2 weeks at 50 °C. 2/

New study in International Journal of Infectious Diseases highlights persistent immune alterations after SARS-CoV-2 infection—providing further biological evidence for #LongCOVID as a genuine post-infectious condition.

➡️ Researchers found lasting changes in immune activation and regulation, even months after recovery from acute COVID-19—suggesting the immune system does not fully reset after infection. 1/ Key findings point to chronic inflammation, altered cytokine responses, and immune imbalance, which may explain prolonged symptoms such as fatigue, pain, and neurocognitive complaints.

➡️ Importantly, these immune changes were seen independent of initial disease severity, reinforcing that even mild COVID-19 can have long-term immunological consequences. 2/

A new Israeli study demonstrates why some people develop #LongCOVID.

➡️ By analysing immune responses, gene expression and plasma proteins in blood samples, scientists found that people with longCOVID show persistent chronic inflammation and disrupted immune signalling months after infection — patterns not seen in those who fully recovered. 1/ These immune differences help explain lingering symptoms — such as fatigue, brain fog and breathlessness — and point to specific inflammatory pathways that could be targeted for treatment. This work opens new avenues for better therapies for millions living with longCOVID. 2/

Can past COVID-19 weaken the body’s ability to fight tuberculosis?

➡️ A new study comparing immune responses to SARS-CoV-2 and Mycobacterium tuberculosis (MTB) suggests COVID-19 may dampen both antiviral and anti-TB immunity — even months later. 1/ Researchers tested immune cells from healthy individuals and COVID-19 survivors, both with and without latent TB infection (LTBI).

➡️ They stimulated the cells with SARS-CoV-2 Spike and MTB antigens and measured cytokine responses. 2/

A new study comparing immune profiles months after COVID-19 vs influenza shows that SARS-CoV-2 leaves behind distinct and longer-lasting immune abnormalities — very different from what is seen after flu. 1/ Post-COVID patients showed increased CXCR3 and CCR6 expression across multiple lymphocyte populations.

➡️ Punjabi This means their immune system is still sending signals for cells to migrate into tissues (especially the lungs) months after infection.

➡️ Persistent tissue-homing = prolonged inflammation. 2/

A new study provides some of the strongest evidence yet that mitochondrial dysfunction can directly cause #Parkinson’s disease, rather than being a consequence of neuron loss.

➡️ Researchers used a unique mouse model carrying a mutation in CHCHD2, a mitochondrial protein linked to a rare inherited form of Parkinson’s that closely mimics the common, late-onset form. 1/ Key Findings

➡️ Mutant CHCHD2 accumulates in mitochondria, making them swollen and structurally abnormal.

➡️ Cells shift away from normal energy production and develop oxidative stress due to buildup of reactive oxygen species (ROS).

➡️ Alpha-synuclein aggregation occurs after ROS rises, suggesting oxidative stress triggers Lewy body formation.

➡️ Human brain tissue from people with sporadic Parkinson’s showed CHCHD2 accumulation inside early alpha-synuclein aggregates, confirming relevance beyond the rare genetic form. 2/

New research in Cell Reports Medicine helps explain why women are more likely to develop #LongCOVID — and often experience more severe, persistent symptoms like fatigue, brain fog, and pain.

The key? Differences in the immune system, gut, and hormones. 1/ Researchers studied 78 people with LongCOVID (mostly mild initial cases) and compared them to 62 who recovered fully.

➡️ One year later, women with Long COVID showed clear biological differences — especially signs of gut inflammation and “leakiness.” 2/

Urine tells the story of #LongCOVID:

➡️ New study identifies a molecular fingerprint for #LongCOVID (PASC) — using just a urine test.

➡️ Researchers found 195 urinary peptides that can accurately distinguish Long COVID patients from healthy and ME/CFS controls (AUC > 0.95). 1/ Researchers used urinary peptidomics to identify a molecular fingerprint of post-acute sequelae of SARS-CoV-2 infection (PASC or LongCOVID).

➡️ Methods

-50 PASC patients (10 months post-infection) were compared with 50 controls (42 healthy + 8 with non-COVID ME/CFS).

-Capillary electrophoresis–mass spectrometry (CE–MS) was used to analyze urinary peptides.

-A support vector machine (SVM) model was built to distinguish PASC cases from controls. 2/

Understanding Long COVID

➡️ Long COVID isn’t one disease — it’s a complex web of immune, vascular, and metabolic dysfunctions.
From fatigue & brain fog to heart & lung complications, it stems from viral persistence, autoimmunity, and mitochondrial damage. 1/ Proposed mechanisms:

1️⃣ Persistent viral reservoirs or antigen remnants

2️⃣ Reactivation of latent viruses (e.g., EBV)

3️⃣ Immune dysregulation & autoimmunity

4️⃣ Endothelial injury and microclots

5️⃣ Gut microbiome imbalance

6️⃣ Mitochondrial dysfunction and energy metabolism impairment. 2/

Fathers’ COVID & offspring

➡️ New research shows that paternal SARS-CoV-2 infection before conception can alter sperm RNA — leading to anxiety-like behavior & brain gene changes in offspring.

A biological “memory” of infection may pass across generations. 1/ Beyond infection: inheritance

➡️ Male mice infected with SARS-CoV-2 fathered pups with altered hippocampal transcriptomes & higher anxiety.
Injecting sperm RNA from infected males reproduced the same effects — clear evidence of RNA-based inheritance. 2/

A new study provides new evidence to help us redefine steroid use in TB care

➡️ Given the renewed interest in the steroid dexamethasone, as a host-directed treatment during the COVID-19 pandemic, the Trinity College Dublin team provides evidence that treating patients with steroids may enhance the function of their macrophages to kill the mycobacteria, while diminishing pathways of inflammatory damage. 1/ The researchers goal was to determine whether dexamethasone impacts the macrophage's ability to fight TB. Although glucocorticoids can reactivate TB, they are paradoxically the only adjunctive host-directed therapies that are recommended by WHO for TB.

Steroids are given to patients alongside antimicrobials in certain circumstances; however, scientists don't fully understand the effect of these drugs on the immune system, especially innate immune cells such as macrophages. 2/

A NEW review explores how SARS-CoV-2 may influence cancer risk.

➡️ Unlike classical oncogenic viruses, it doesn’t insert viral oncogenes. Instead, its proteins:

-Inhibit tumor suppressors
-Activate growth, survival & inflammation pathways

👉 Potential role in cancer initiation & progression. 1/ Bioinformatic & experimental studies show direct interactions between viral proteins and host cellular components tied to cancer hallmarks.

➡️ These mechanisms could contribute to initiation, promotion, and progression of tumors, raising the possibility that SARS-CoV-2 may act as an oncovirus.

👇The figure illustrates various key oncogenic signaling molecules or pathways targeted by SARS-CoV-2 NSP, N, M and S protein. The activation of oncogenic pathways can lead to the conversion of a normal cell into a cancer cell. 2/

A new study from Karolinska Institutet shows that an unusual heart rhythm disorder, POTS, is particularly common in people with #LongevityPoweredbyGinseng COVID. The majority of those affected are middle-aged women. 1/ Postural orthostatic tachycardia syndrome, or POTS, is a condition where the heart beats abnormally fast when changing position from lying down to standing up. Standing up is a challenge for those affected who feel dizzy and would rather sit or lie down, so-called orthostatic intolerance. Their hearts may also beat faster than normal at rest and during exertion. 2/

New insights into #LongCOVID from a hamster model

➡️ Despite LongCOVID’s clinical significance, the mechanisms driving remain poorly understood.

Here, to address this, researchers utilized a Phodopus roborovskii hamster model to investigate the long-term effects of SARS-CoV-2 infection compared with influenza A virus.

➡️ While 46.25–47.50% of hamsters survived SARS-CoV-2 or influenza A virus H1N1 infection, 13.75% of SARS-CoV-2 survivors exhibited impaired weight recovery, severe lung pathology and significant neutrophil accumulation, defining the LongCovid (PAŚĆ) group. 1/ Single-cell RNA sequencing of bronchoalveolar lavage (BAL) fluid, lung and spleen at 30 days post-infection revealed hallmark LongCovid (PASC) gene signatures uniquely upregulated in the PASC group.

➡️ This was accompanied by elevated neutrophil levels and reduced macrophage populations, indicative of disrupted myeloid cell differentiation. 2/

It is currently debatable whether mucosal vaccination is still warranted given that most individuals in developed countries have established a hybrid immunity from vaccination and infection.

➡️ In a new study, researchers studied how our immune system in the airways (the “mucosal” immune system) responds to COVID infection, vaccines, and special mucosal booster vaccines. 1/ What they found in people:

➡️ Having both vaccination + prior infection (“hybrid immunity”) gave only a modest increase in protective antibodies (IgA) in the nose and lungs compared to infection or vaccination alone. 2/

How quickly #mRNA degrades is linked to autoimmune disease risk!

➡️ We usually think of gene activity in terms of how much mRNA is produced. But a new study shows another key factor: how fast mRNA degrades. 1/ UCLA scientists built RNAtracker, a tool to tell whether changes in gene expression are due to production or breakdown of mRNA.

➡️ Testing across 16 human cell types, they found that many “unstable” mRNAs come from innate immunity genes.

➡️ Crucially, UCLA scientists built RNAtracker, a tool to tell whether changes in gene expression are due to production or breakdown of mRNA.

➡️ Crucially, these unstable mRNAs are linked to genetic variants tied to autoimmune diseases like:
•Lupus
•Type 1 diabetes
•Multiple sclerosis
•Allergic rhinitis 2/

A pioneering study has demonstrated for the first time that myocardial infarction may be an infectious disease. This discovery challenges the conventional understanding of the pathogenesis of myocardial infarction and opens new avenues for treatment, diagnostics, and even vaccine development. 1/ According to the study, an infection may trigger myocardial infarction. Using a range of advanced methodologies, the research found that, in coronary artery disease, atherosclerotic plaques containing cholesterol may harbor a gelatinous, asymptomatic biofilm formed by bacteria over years or even decades. Dormant bacteria within the biofilm remain shielded from both the patient's immune system and antibiotics because they cannot penetrate the biofilm matrix. 2/