Oral Cavity Serves as Long-Term COVID-19 Reservoir with Increased Periodontal and Viral Disease Risk:
-COVID-19 history significantly correlates with severe oral health complications while vaccination reduced but did not eliminate these issues. 1/
A NEW study identified oral associated #LonhCovid primarily manifested as periodontal (gum) disease (COVID +ve: 73.1±18.9% vs COVID -ve: 33.1±14.3%)
Covid19 positive cases correlated w/ higher rates of dry mouth (57.5%), taste disturbance (47%) & smell loss (20%). 2/
Vaccination reduced oral LongCovid (PASC) in COVID-19 positive subjects; however, periodontal disease indicators persisted compared to the COVID-19 negative group. 3/
Notably, 3-6 months post-infection, while SARS-CoV-2 Spike (S) transcript was rarely detected in saliva (∼6%), its protein was commonly detected (∼70%) in the COVID-19 positive subjects indicating incomplete viral clearance. 4/
This correlates with significantly higher salivary expression of viral entry receptors (ACE2, and TRMPSS2), and inflammatory mediators (IL-6, IL-8 and MMP-8), in COVID-19 positive subjects. 5/
This finding was further supported by higher prevalence of other oral viruses including Epstein-Barr Virus (70.5%), Herpes Simplex Virus (8.1%), and Human Papillomavirus (17.5%) in COVID-19 positive subjects. 6/6
SARS-CoV-2 spike protein may directly amplify brain inflammation.
➡️ Researchers found that spike proteins can colocalize with amyloid-β (Aβ) and trigger distinct inflammatory responses in microglia — the brain’s immune cells.
➡️ This raises important questions about potential long-term neurodegenerative consequences of COVID-19. 1/
Researchers developed advanced “expansion microscopy” techniques that physically enlarge human brain tissue, allowing scientists to see disease-related structures at near-nanoscale resolution using ordinary microscopes. 2/
Applying this method to brains from some COVID-19 patients revealed tiny amyloid-like protein clusters closely associated with SARS-CoV-2 particles in a small subset of cases, suggesting a possible link between COVID-19, neuroinflammation, and abnormal protein aggregation in the brain.
The study highlights how ultra-high-resolution imaging could uncover previously hidden mechanisms of neurological disease. 3/
👉 The lungs may remain biologically altered long after acute infection resolves. 1/
A new review highlights how persistent immune activation in LongCOVID may lead to:
• Fibrosis-like lung changes
• Endothelial dysfunction
• Microvascular injury
• Ongoing respiratory symptoms
COVID may end clinically—but not biologically.
#LongCOVID #Pulmonology 2/
LongCOVID respiratory sequelae may result from a “perfect storm” of:
COVID-19 may be, in part, a mitochondrial disease.
➡️ A Cambridge review shows SARS-CoV-2 disrupts mitochondrial function in lung cells—driving inflammation and worsening pneumonia.
➡️ Emerging studies suggest even after the active infection is resolved, residual viral proteins, particularly SARS-CoV-2 spike protein, may linger and continue to cause damage to the mitochondria by increasing oxidative stress and disrupting energy metabolism, offering a plausible mechanism for #LongCOVID. 1/
H/T: @CatchTheBaby
COVID-19 is not just viral—it’s metabolic.
SARS-CoV-2 hijacks mitochondria →
↓ Energy production
↑ Inflammatory signaling
A key pathway worsening lung injury. 2/
Mitochondria may link acute COVID → #LongCOVID.
Viral disruption of mitochondrial function can persist, sustaining oxidative stress and immune dysregulation even after infection. 3/
New study shows SARS-CoV-2 directly damages heart cell mitochondria—key energy engines—offering a mechanistic link to #LongCOVID cardiovascular symptoms. 1/
#LongCOVID may be a mitochondrial disease: electron microscopy reveals structural damage & myofilament breakdown in cardiomyocytes. 2/
Biopsies from LongCOVID patients confirm myocarditis with mitochondrial disruption—mirrored in infected animal models. Strong biological plausibility for persistent cardiac symptoms. 3/