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/

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/

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/

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/

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/

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/

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/

A promising new COVID-19 vaccine candidate developed by researchers at the Centenary Institute and the University of Sydney has shown strong potential to protect against both current and emerging coronavirus variants.

By targeting features shared by a range of coronaviruses, the vaccine is designed to offer broader and longer-lasting protection as the virus continues to evolve. 1/ The new study shows that the vaccine candidate, named #CoVEXS5, protected mice from multiple coronaviruses, including the highly immune-evasive omicron XBB.1.5 variant and SARS-CoV-1, a relative of SARS-CoV-2 that was responsible for the 2002–2004 SARS outbreak. 2/

A new Yale study has found a promising target for treating the brain fog that can follow COVID-19 and offers new insight into a hypothesis about the origin of Alzheimer's disease.

Researchers obtained viable postmortem human retinal tissue and generated human retinal organoids that contain electrophysiologically active neurons.

They demonstrated that SARS-CoV-2 induced amyloid-β extracellular protein aggregates in human retinal explants and retinal organoids. 1/ While the etiology of Alzheimer’s disease remains unknown, there is growing support for the amyloid-β antimicrobial hypothesis.

Amyloid-β, the main component of amyloid plaques in Alzheimer’s disease, has been shown to be generated in the presence of microbes.

Entrapment of microbes by aggregated amyloid-β may serve as an innate immune response to pathogenic infections. 2/

A new study reviewed skeletal muscle adaptations & post-exertional malaise in #LongCOVID. People with LongCOVID show reduced skeletal muscle oxidative capacity, smaller muscle fibers & increased glycolytic activity, all which may explain fatigue & post-exertional malaise. 1/ Muscle biopsies revealed structural and metabolic changes similar to deconditioning, but also showed unique inflammatory and mitochondrial signatures, suggesting Long COVID involves distinct muscle pathology beyond simple inactivity. 2/

A new study finds that fragments of viral proteins, including SARS-CoV-2 spike peptides, can bind and either inhibit or activate human formyl peptide receptors (FPR1, FPR2, FPR3) which influences innate immune responses like neutrophil migration and NETosis. 1/ Formyl peptide receptors (FPRs) are pattern recognition receptors well-known for bacterial pathogen sensing. Researchers identified activator and inhibitor motifs for FPRs that are present on surface proteins of various viral pathogens. Peptides containing these motifs interact with all FPR family members and modulate various important immune functions in innate immune cells. 2/

Researchers used 3 RNA-seq datasets of 142 samples from Australia, the US and Russia to look at gene expression signatures in acute COVID infection and in #LongCOVID. They found that TNF-α/NF-κB pathway signatures could identify patients at risk of severe disease progression from acute COVID infection 1/ They also noted that OXPHOS and Myc pathway-associated signatures reflecting metabolic changes may be used as a biomarker for #LongCOVID diagnosis and severity stratification. 2/

Fibrinoloid (amyloid-containing) microclots are resistant to degradation and are found in a variety of diseases including #LongCOVID, ME/CFS, and sepsis. A NEW review looks at the use of laser speckle imaging (LSI) and laser Doppler imaging (LDI) to assess how fibrinaloid microclots can disrupt the microcirculation. 1/ The microcirculation typically refers to those capillaries less than 100 mm in diameter. Having shown that blood can clot into an anomalous amyloid form that is rather resistant to fibrinolysis, researchers have previously developed the idea that endothelial dysfunction can both lead to and be caused by the fibrinaloid microclots so formed, such that this can slow or block entirely parts of the microcirculation. 2/

A NEW study finds that infection with SARS-CoV-2 during the first year of the pandemic was associated with three to five times higher odds of cognitive impairment 2 years after infection. 1/ Survivors of the disease may require special attention from clinical doctors to diagnose and treat cognitive impairment, namely, those who were hospitalized for more than 15 days, in intermediate or intensive care units, and presented disorientation, changes in vision, gait or balance, during infection. 2/

A NEW study finds that anti-SARS-CoV-2 antibodies play a protective role against vital organ-related #LongCovid (LC) symptoms, especially cardiovascular symptoms, but are insufficient in preventing or limiting other highly prevalent LC symptoms, such as neurological, psychiatric and pulmonary. 1/ These data underscore the complexity of the potential involvement of anti-SARS-CoV-2 immune responses in either protecting against or contributing to the development of different #LongCovid phenotypes. 2/

A meta-analysis from Egypt of 125 studies involving over 4 million COVID survivors shows that months to years after infection, fatigue was the most common symptom at 43%. Around 27% of people experience cognitive impairment after COVID infection. 1/ Further, 28% experienced memory issues, 24% sleep disorders, 20% headaches, 16% dizziness, 14% depression, and 13% anxiety, with significant variability depending on follow‑up time, disease severity, sex, and BMI. 2/

A new review on neuroimmune pathophysiology of #LongCOVID explores how SARS-CoV-2 can cause lasting neurological symptoms through a combination of direct infection, immune dysregulation, and persistent inflammation. 1/ Key mechanisms include viral antigen persistence, autoimmunity, blood–brain barrier disruption, neurotransmitter imbalances, and glial cell dysfunction. The authors link these processes to cognitive impairment, fatigue, dysautonomia, and other Long COVID symptoms. 2/

I think, therefore I age!

As people get older, a growing population of cells starts to consume more energy — perhaps because the cells accumulate damage that leads them to rev up processes such as inflammation. 1/ An emerging hypothesis suggests that the brain accommodates these energy-hogging ‘senescent cells’ by stripping resources from other biological processes, which ultimately results in outward signs of ageing, such as greying hair or a reduction in muscle mass. 2/

A NEW study found that the SARS-CoV-2 nonstructural protein 15 (nsp15) helps the virus hide from the immune system in human lung and nasal cells. The nsp15 endoribonuclease is important in promoting virus replication and influencing disease severity. 1/ SARS2 variants lacking this activity exhibit impaired replication & cause milder disease, highlighting nsp15 as a key virulence factor. This underscores the importance of nsp15’s endoribonuclease activity in both promoting virus replication & influencing disease severity. 2/

Researchers developed a 23-amino acid peptide that mimics ACE2 and effectively binds the SARS-CoV-2 spike protein, preventing viral entry. 1/ The peptide demonstrated potent antiviral activity against both the original and Omicron strains, with a therapeutic index greater than 20, indicating strong potential for therapeutic use. 2/

A NEW preprint found that submaximal exercise in people with #LongCOVID caused large microclots to fragment into smaller microclots and this then triggered increases in inflammatory and vascular injury markers. 1/ The breakdown of large microclots, rather than clearing them from circulation, was linked to reduced oxygen uptake and heightened inflammation. 2/