Sydney scientists think they've discovered what causes long COVID symptoms

#longcovid #symptoms #brain_health #news

Sydney scientists think they've discovered what causes the debilitating symptoms of long COVID - and their research is being recognised around the world. @MarkWBurrows #9News

MORE: https://t.co/Z5KQ60AIAP pic.twitter.com/CgJvl2sPIj

— 9News Sydney (@9NewsSyd) June 8, 2023

Sydney scientists believe they have discovered the cause of the debilitating symptoms of Long COVID, and their research is gaining recognition worldwide.

Long COVID induces severe symptoms, but its cause has not been well-understood. Here, more research from Sydney scientists is presented.

Researcher Ole Tietz, who is suffering from Long COVID, began contributing to the research to understand what Long COVID is and how it is caused.

His fellow researchers have discovered that the COVID-19 virus can cause brain cells to fuse together, leading to malfunction and cessation of function.

This could explain some of the neurological symptoms like loss of smell or brain fog.

They created "mini-brains" in vitro using human 📁 Supplements 💊/⚗️ Pharmacology (Notes)/Stem Cells to mimic what could be happening to patients' brains.

The mini-brain was infected with COVID, and fused neurons were found. In 10% of the experimental conditions, neuronal activity completely stopped.

Researchers don't have a way to unfuse the neurons, but they have developed a drug to reduce the viral load and alleviate the effects of Long COVID.

Sources:

• https://www.science.org/doi/10.1126/sciadv.adg2248

Read more here:

• SARS-CoV-2 infection and viral fusogens cause neuronal and glial fusion that compromises neuronal activity

The study investigates the impact of viral fusogens on neuronal fusion, using SARS-CoV-2 as a model. Here's a summary of the key findings:

1. Investigation using 3D Brain Organoids:

   • Human embryonic stem cell (hESC)-derived 3D brain organoids were infected with SARS-CoV-2 to study its pathogenesis.
   • Post infection, neuronal syncytia (fusion) was observed, similar to what was seen in 2D neuronal cultures.

2. Viral Fusogens and Neuronal Fusion:

   • Two viral fusogens, the spike S protein of SARS-CoV-2 and p15 from baboon orthoreovirus (BRV), were studied.
   • p15 induced neuronal fusion in embryonic mouse primary hippocampal neurons.
   • Spike S protein required the hACE2 receptor to trigger fusion, and its expression alongside hACE2 led to neuronal fusion.

3. In Vivo and In Vitro Experiments:

   • Transgenic Caenorhabditis elegans strains expressing p15 showed neuronal fusion, with additional GFP-positive cells observed.
   • In adult mice, p15 expression led to neuronal fusion in both hippocampus and cortex.
   • In human-derived neurons, both p15 and spike S induced fusion, forming clusters of interconnected cells.

4. Implications:

   • The fusion led to a temporary or permanent diffusion of cytoplasmic material between cells.
   • Neuronal fusion was observed in vivo in both C. elegans and mice, and in vitro in human-derived neurons.
   • The findings suggest that viral fusogens can induce neuronal fusion, which may have implications for understanding viral pathogenesis and developing potential therapeutic interventions.

This study provides a detailed examination of how viral fusogens, particularly from SARS-CoV-2, can induce neuronal fusion, expanding the understanding of viral interactions with the nervous system.