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Vipin M. Vashishtha

@vipintukur

Sep 24

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/

Immunohistochemistry further detected persistent SARS2’s S1 subunit antigen in the lungs of PASC (LongCovid) hamsters at 30 days post-infection, coinciding with marked neutrophil infiltration, which probably drove prolonged inflammatory responses. 3/

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Vipin M. Vashishtha

@vipintukur

Sep 20

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/

The researchers applied RNAtracker to a publicly available dataset of 16 human cell lines, in which newly made mRNAs had been chemically labeled and tracked over time.

This allowed them to identify genes whose stability varies due to specific mutations. Many of these genes are involved in immune system function—especially the innate immune system, the body's first line of defense against infections. 3/

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Vipin M. Vashishtha

@vipintukur

Aug 28

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/

Of the bacteria detected, oral viridans group streptococcal DNA was the most common, being found in 42.1% of coronary plaques and 42.9% of endarterectomies. Immunopositivity for viridans streptococci correlated with severe atherosclerosis (P<0.0001) in both series and death from coronary heart disease (P=0.021) or myocardial infarction (P=0.042). 3/

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Vipin M. Vashishtha

@vipintukur

Aug 22

According to a new study, SARS-CoV-2 virus hijacks the machinery of testicular cells that produce the hormone testosterone in order to replicate.

It also appropriates the metabolic pathways of these cells and cholesterol, a precursor of testosterone, thereby altering lipid metabolism for its formation. 1/

The study revealed the presence of SARS-CoV-2 particles in lipid inclusions and organelles responsible for testosterone production in Leydig cells for the first time.

In addition, the researchers described the mechanism by which the virus interferes with the functioning of these testicular cells.

The discovery helps explain why male patients with severe COVID-19 have lower levels of testosterone, and possibly cholesterol. 2/

After infecting the Leydig cells in the testicles, the virus uses lipid metabolism pathways and the cell structure to replicate, which impairs testosterone production.

This happens because these cells, responsible for producing testosterone, express high concentrations of the ACE2 receptor, facilitating the entry of the virus, 3/

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Vipin M. Vashishtha

@vipintukur

Aug 18

A COVID infection, particularly in women, may lead to blood vessels aging around five years!

➡️ Blood vessels gradually become stiffer with age, but the new study suggests that COVID could accelerate this process. Researchers say this is important since people with stiffer blood vessels face a higher risk of cardiovascular disease, including stroke and heart attack. 1/

Since the pandemic, we have learned that many people who have had COVID are left with symptoms that can last for months or even years. However, we are still learning what's happening in the body to create these symptoms. 2/

It is known that COVID can directly affect blood vessels. This may result in what we call early vascular aging, meaning that your blood vessels are older than your chronological age and you are more susceptible to heart disease.

If that is happening, we need to identify who is at risk at an early stage to prevent heart attacks and strokes. 3/

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Vipin M. Vashishtha

@vipintukur

Aug 14

A ‘universal’ antiviral for everyone!

🔥 A fascinating tale that reinforces the power of research driven by curiosity without preconceived notions.

➡️ For a few dozen people in the world, the downside of living with a rare immune condition comes with a surprising superpower—the ability to fight off all viruses.

➡️ An immunologist from Columbia discovered the individuals' antiviral powers about 15 years ago, soon after he identified the genetic mutation that causes the condition. 1/

At first, the condition only seemed to increase vulnerability to some bacterial infections. But as more patients were identified, its unexpected antiviral benefits became apparent.

The researcher soon learned that everyone with the mutation, which causes a deficiency in an immune regulator called IFN-I–stimulated gene 15 (ISG15), has mild but persistent systemic inflammation. 2/

The type I interferon (IFN-I) response is a conserved cascade of signaling and gene expression that, among other functions, confers protection of cells from viral infection.

After resolution of infection, the response is tamped down by regulators such as IFN-I–stimulated gene 15 (ISG15).

Cells from individuals lacking ISG15 are able to control viral infections in vitro as a consequence of maintaining a low-grade IFN-I response. 3/

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