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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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Vipin M. Vashishtha

@vipintukur

Jul 31

In a small trial, researchers have found that a drug designed to treat celiac disease supported a more rapid return to normal activities for patients following COVID. The researchers found the oral drug #larazotide—an experimental drug originally designed to treat celiac disease—was both safe and effective in treating children with MIS-C. 1/

Current MIS-C treatments are limited. Some patients receive general anti-inflammatory drugs, but many experience a rebound of symptoms after completing a course. Such drugs are not designed to target the sticky SARS-CoV-2 viral particles that may persist in the gut. 2/

Enter larazotide, an orally administered drug that does target the gut. Larazotide strengthens intestinal barriers to limit the number of materials—like SARS-CoV-2 viral particles—that exit the intestines and enter circulation. 3/

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Vipin M. Vashishtha

@vipintukur

Jul 25

Researchers have discovered that gut bacteria produce a molecule that not only induces but also causes atherosclerosis, the accumulation of fat and cholesterol in the arteries that can lead to heart attacks and strokes.

This unexpected link between microbes and cardiovascular disease — the leading cause of death in humanity — is a paradigm shift. 1/

The new results show that some gut bacteria, in certain states, produce imidazole propionate, a simple molecule with six carbon atoms, eight hydrogen atoms, two nitrogen atoms, and two oxygen atoms (C₆H₈N₂O₂). This compound enters the blood, interacts with immature white blood cells, and triggers an inflammatory reaction in the arteries, which promotes the buildup of fatty plaques. Imidazole propionate induces atherosclerosis on its own. There’s a causal relationship. 2/

Furthermore, scientists observed elevated levels of imidazole propionate in one out of every five volunteers with active atherosclerosis, the type in which fatty plaques are more likely to rupture and form the blood clots that cause heart attacks and strokes. The new results demonstrate that atherosclerosis is not only a disease caused by fat, but that it also has an inflammatory and autoimmune component. 3/

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