SARS-CoV-2 S protein may compete for the same processing protease with EnaC-alpha, a sodium permeable ion channel that controls fluid reabsorption at the air–liquid interface.
Acute COVID-19, Long COVID, Post COVID-vaccination Syndrome & Other Body Systems-Experimental Studies
Latest content
SARS-CoV-2 spike protein was co-localized with increased expression of vascular and autophagy markers in the placental tissue of unvaccinated infected women
Increased expression of VEGF and the endothelial cell marker CD34 indicates alterations, disarrangements, or remodeling of normal vasculature, associated with vascular endothelial injury and endothelitis.
SARS-CoV-2 enters human erythrocytes but does not affect the development of Plasmodium falciparum
SARS-CoV-2 enters human erythrocytes, but in a low percentage of cells (10.9%) compared to SARS-CoV-2 permissive cell lines. The presence of SARS-CoV-2 in blood culture did not affect the survival or growth rate of the malaria parasite.
Other Entries
The BNT162b2 mRNA vaccine alters the activity of human ovarian granulosa cells (possible link with menstrual disorders)
The BNT162b2 mRNA COVID-19 vaccine directly affects the activity of ovarian granulosa cells, which is a unique, independent mechanism for vaccine-related menstrual abnormalities.
Intranasal infection of mice with SARS-CoV-2 led to retinal inflammation and elevated viral titers in the lungs and brain
The prolonged presence of SARS-CoV-2 S protein in ocular tissues (thirty days after the intravitreal injection) resulted in microaneurysms, retinal atrophy, and retinal vein occlusion.
SARS-CoV-2 preferentially infects intestinal cells via their apical side and causes damage to the intestinal epithelial barrier
Inoculation of SARS-CoV-2 at the apical pole resulted in the severe damage to the integrity of the intestinal epithelial barrier, suggesting that the virus present in the intestinal lumen could damage the intestinal epithelial barrier, enter the blood vessels and spread to various organs.
SARS-CoV-2 binds to kidney injury molecule-1, which is highly expressed upon kidney injury
The receptor binding domain (RBD) of SARS-CoV-2 binds to kidney injury molecule-1 (KIM1), which is highly expresed only upon kidney injury.
SARS-CoV-2 can infect hepatocytes and stimulate hepatic glucose production through gluconeogenesis
SARS-CoV-2 can infect, replicate, and produce infectious viral particles in primary human hepatocytes and stimulate their production of glucose through gluconeogenesis.
