Researchers have mapped the interaction between SARS-CoV-2 proteins and human cells, showing which proteins are being activated and deactivated by coronavirus. The findings reveal how the virus can spread through the human body.
Men have higher concentrations of ACE2 in their blood than women. As ACE2 enables coronavirus to infect cells, the findings may explain why men are more susceptible to COVID-19 infection than women.
After natural killer immune cells kill virus-infected cells, T and B immune cells produce cytokines. This makes the immune reaction stronger and results in the cytokine storm associated with severe COVID-19 infection.
SARS_CoV_2, the virus responsible for COVID-19, can directly enter the nervous system. The virus can infect the brain, causing alterations in blood vessels and directly disrupt oxygen supply to the organ.
SARS-CoV-2, the virus responsible for COVID-19, can infect human neural progenitor cells and brain organoids. The findings back previous research, finding coronavirus can infect the human brain.
A new study seeks to explain why men infected by coronavirus generally show more severe symptoms and have an increased risk of death over women. Focusing on ACE2 receptors, researchers found the testes, along with the lungs and kidneys, were among areas of the body with the highest ACE2 expression. ACE2 could not be detected in ovarian tissue. The findings back up a previous study that reported male COVID-19 patients experienced impaired testicular function. This suggests the testes may be significantly affected when men develop coronavirus.
Smoking increases the gene expression of ACE2, a protein that binds to SARS-CoV-2, increasing the risk of coronavirus infection. Findings suggest long-term smokers could have an increase of ACE2 in the lungs, leading to higher rates of morbidity in COVID-19 patients.
Cholesterol-lowering statins show promise for the treatment of severe coronavirus infections. Statins lowered the death rate and decreased the need for mechanical ventilation in patients hospitalized for severe COVID-19.
From losing the sense of taste or smell to developing an increased risk of stroke, researchers investigate both the known and potential long-term implications of COVID-19 infection in the brain.
Smoking remodels the gene expression of lung cells so that the ACE2 gene is more highly expressed in goblet cells. The effects of smoking on ACE2 pulmonary expression indicates an increase in the overall entry points for coronavirus and increases the risk for viral binding and entry of COVID-19 into the lungs.
Some viral infections could increase intercellular spreading of protein aggregates associated with neurodegenerative disorders, increasing the risk for developing Alzheimer's, Parkinson's, and other neurodegenerative diseases.
Researchers explore why COVID-19 is more deadly compared to the flu and other viruses.
