A novel treatment for blocking SARS-CoV-2 entry into cells!
Researchers discovered #UNI418, a compound that effectively prevents the penetration of coronavirus. This compound works by regulating dielectric homeostasis, thereby inhibiting the virus's entry into human cells 1/
SARS-CoV-2 enters cells through endocytosis, a process whereby cells absorb material from outside by engulfing it w/ their cell membrane. They demonstrated that inhibiting specific proteins, PIKfyve & PIP5K1C during this process can prevent viral invasion. 2/
Genomic homeostasis is protective system that secures genetic information & allows it to be utilized when needed.
The team established #UNI418 supports genomic homeostasis while simultaneously preventing the infiltration and proliferation of coronaviruses within cells 3/
Existing treatments generally work by inhibiting viral proteins to prevent proliferation, but they are often less effective against mutant strains of the virus. 4/
This study represents the first evidence that #UNI418 can disrupt the virus's infection process, highlighting its potential as a treatment for mutant coronaviruses and other viral infections. 5/
There is a high likelihood that UNI418 can develop into a new treatment paradigm that effectively blocks various viral infections. 6/6
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/
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/
What the researchers found in animal models:
➡️ Giving a mucosal booster vaccine (delivered to the airways using an adenovirus-based vaccine) worked much better. It:
-Strongly boosted IgA antibodies in the nose and lungs
-Triggered local T-cells in the airways
-Provided stronger, longer-lasting protection against SARS-CoV-2. 3/
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/
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/
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/
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/