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
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/
🔥 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/
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/
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/
An exceptional study from Stanford found that lymphocytes from ME/CFS & #LongCOVID patients show elevated oxidative stress, disrupted redox balance, and mitochondrial damage.
These abnormalities lead to excess energy use by immune cells, which may contribute to severe fatigue and other symptoms. 1/
The researchers identified increased lipid peroxidation and glutathione metabolism changes, indicating shared metabolic dysfunction in ME/CFS and LongCOVID.
Females show higher mitochondrial ROS levels and insufficient antioxidant levels (GSH), while males show mitochondrial lipid oxidative damage. These findings suggest that the pathophysiology for ME/CFS and LC are distinct between sexes. 2/
The group also tested ROS-targeting therapies. Metforminshowed some benefit on CD4 T cell proliferation in vitro, and the findings suggest oxidative stress could be a target for diagnosis and therapy. 3/
New gene discovery may change cancer and autoimmune treatment!
Researchers have identified the #SDR42E1 gene as crucial for absorbing vitamin D from the gut and metabolizing it into the active hormone calcitriol, which is essential for bone health, immune function, and cellular processes.
They used CRISPR/Cas9 gene editing to disable SDR42E1 in HCT116 colorectal cancer cells, resulting in a dramatic 53% reduction in cancer cell viability while leaving healthy cells unharmed. 1/
The gene disruption triggered widespread molecular changes affecting over 4,600 downstream genes involved in sterol metabolism and cancer-related signaling pathways.
A specific mutation in #SDR42E1 on chromosome 16 has been linked to vitamin D deficiency, causing the protein to be cut short and rendered inactive. 2/
This discovery opens potential new avenues for precision medicine, including targeted cancer therapies and treatments for autoimmune diseases where vitamin D plays a regulatory role. 3/