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Vipin M. Vashishtha

@vipintukur

Dec 3

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/

Key finding:

➡️ People who recovered from COVID-19 showed significantly reduced inflammatory cytokines — IFN-γ, IL-2, IL-6, TNF-α — in response to both SARS-CoV-2 and MTB antigens.

➡️ Suggests prolonged immune downregulation after COVID-19. 3/

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Vipin M. Vashishtha

@vipintukur

Dec 1

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/

In contrast, post-flu patients mainly showed a decrease in CCR4 on naïve T cells, monocytes, and dendritic cells — a very different and less persistent pattern.

➡️ Flu does not drive the same long-term immune activation. 3/

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Vipin M. Vashishtha

@vipintukur

Nov 18

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/

Implications

➡️ This work maps a step-by-step causal chain:
CHCHD2 mutation → mitochondrial failure → metabolic shift → ROS buildup → alpha-synuclein aggregation → Parkinson’s pathology

➡️ It supports the idea that mitochondrial defects may underlie many forms of Parkinson’s, not just the inherited type.

➡️ Targeting oxidative stress, mitochondrial health, and energy pathways could offer new therapeutic strategies. 3/

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Vipin M. Vashishtha

@vipintukur

Nov 8

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/

The study also found anemia and hormone imbalances.
Women with LongCOVID had lower testosterone — a hormone that normally helps control inflammation.

➡️ Lower testosterone was linked to more fatigue, pain, brain fog, and depression. 3/

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Vipin M. Vashishtha

@vipintukur

Oct 27

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/

➡️ Results

-195 urinary peptides showed significant differences between PASC and controls.

-Most peptides were fragments of collagen alpha chains, suggesting altered collagen turnover, inflammation, and endothelial injury.

-The classifier, named #PASC195, achieved excellent diagnostic performance:
•AUC = 0.949 (training)
•AUC = 0.962 (validation)

-Computational analyses suggested potential benefits from exercise, GLP-1 receptor agonists, and mineralocorticoid receptor antagonists (MRAs). 3/

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Vipin M. Vashishtha

@vipintukur

Oct 22

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/

Current management:

- largely symptomatic—rehabilitation, pacing, and supportive therapies.

-Emerging treatments: under study — antiviral drugs, immune-modulating agents, microbiome restoration, and mitochondria-targeted therapies.

-Vaccination: reduces risk and severity of LongCOVID. 3/

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